Transcript ULCERUL PEPTIC

PEPTIC ULCER DISEASE
PATHOGENY
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Low PGE2 secretion
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Low secretion of mucus and bicarbonate
Decreased vascular flow in the mucosa
Low epithelial proliferation
Low resistance to aggresion
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Endogenic factors (HCl, pepsine, biliary salts)
Exogenic facotrs (NSAIDs, alcohol, etc)
Helicobacter pylory
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90% in duodenal ulcer and 75% gastric ulcer
G- bacili
Produce ureasis
Asociated with antrala gastritis
Mechanism
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Toxic products that produce local injury
Induces a local imune response
Increases the acid secretion
NSAIDs
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Low trophicity of the mucus layer
Low synthesis of PGE2
SPECIAL SITUATIONS
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Gastrinoma - sdr. Zollinger-Ellison
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Hypercalcemia
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2x risk
Steress
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3x risk in first degree relatives
Smoking
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Acid hypersecretion
Gastrine hypersecretion
Genetic factors
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Pancreatic isle tumor
Very high secretion of gastrine
25% MEN I
Increases the acidic secretion
Alcohol and diet
PATHOLOGY
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UG şi UD
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Gastrine, Calcium, acid output?
Detection of HPylori
 Endo biopsy
 Urea breath test
 Immunological detection Ab
TREATMENT
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MEDICAL
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goals– relieve symptoms, heal, prevent recurrence and
complications
1. Avoid substances that induce ulcer
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NSAID, smoking, stress
2. Antiacide medication
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1-3 ore after meal and in the evening → buffers acid output
Mg → diarea; CIND in chronic renal disease
Al → constipation → hipophosfatemia
Ca → rebound acid secretion, hipercalcemie, hipercalciuria
TRATAMENT
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3. Inhibit acid secretion
H2 blockers on the parietal cells → inhibition of acid
secretion
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Cimetidine , Ranitidine → side effects: ginecomastia, impotence,
antiandrogenic effect
Famotidine, Nizatidine – much better
Healing achieved in 8-12 weeks in 80-90% patients
Recurrence rate 25-40% at 6 2weeks
PPI
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Omeprazol, Lansoprazol, Pantoprazol, Rabeprazol, Esomeprazol
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PPI blockage for 24 hours
Also indicated in long term treatment of ZE syndrome
TREATMENT
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4. agents with barrier effect
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Sucralfat
complex of AlOH şi sucrose sulfate → stimulates the
endogenous synthesis of PG
 effect – barrier on the base of the ulcer
 Inhibits the action of pepsin
 Binds pepsin and biliary salts
 No neutralizing effect
 SE – prevents absorption of other drugs
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5. PGE
Inhibits secretion of acid and increases the mucus
protection of the duodenal mucosa
 Misoprostol
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TREATMENT
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6. Anti H. Pylori treatment
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IPP+claritromycine +amoxiciline ± metranidazol
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7 days + 14/28 days
Indications
H.pylori pozitive
 In vitro sensitivity for recurences
 Test for eradication 4-6 weeks or if required
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TREATMENT
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SURGICAL
Indications
Inefficient medical treatment +/ Complications
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perforation
 obstruction
 bleeding
 penetration
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Operative mortality in elective cases <1%
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10% - recurence after
or during therapy due
to HPylori
Not used any more
History + patients
with resections in
PMH
BLEEDING ULCER
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5-20%
> 75% managed with medical therapy
INDICATIONS FOR SURGERY
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Massive bleeding with shock
Repeated 6 units of blood in 24 h
Recurrent bleeding during therapy
Old persons may require it earlier
endoscopy – local treatment
Angiography - embolisation
SURGERY
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In situ hemostasis
Resections
Biopsy
Evaluation for other sources of bleeding
PERFORATION
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nonoperative– Taylor
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Nasogastric tube + ATB + watch
High risk patients
operation
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Simple suture ± omentum or glue
Excision suture ± omentum or glue
Omental patch
+/- resection +/- VT
PENETRATION
OBSTRUCTION
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Vomiting
Gastric stasis
Sndr Darrow
Alcalosis, hypoCl, HypoK, HypoNa
MALIGNANT TUMORS OF
THE STOMACH
LYMPHOMA
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Gastric location – the most frequent
2% of all
<15% of all gastric tumors
>50 y
3 types
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Difuse B cell lymphoma 55%
MALT (mucosa associated lymphatic tissue L) – 40%
L Burkitt – 3%
Lymphoma
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Pathogeny
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Imunodeficiency
Hpylori
Epstein Barr infections
Staging
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Std I – T limited to digestive tract
Std II– regional LN
Std III – extraregional LN
Std IV – other intraabdominal organs/extraabdominal
extension
Lymphoma
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Diagnostic
Clinical
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Nonspecific
Paraclinic
Endoscopy+biopsy
CT, RMN,
echoendoscopy – stage
Imunohistochemistry –
characterization of
phenotype
Lymphoma
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TRATAMENT
CHT + RXT + biological therapy
Surgery
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NO – only in emergency or missdiagnostic
HPylori eradication
MALT early stage
 Limited extension diffuse B cell lymphoma
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PROGNOSTIC
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5y survival
95% - std I
 75% - std II
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SARCOMA
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3% din TM gastrice
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GIST more frequent – special
characters
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60-70% of all sarcomas
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PATOGENIE
Cajal cells (pacemakers)
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In the muscle layer
Expresses protooncogenic KIT (CD117) CD34 mutation
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Mitotic index
Staging of GIST
<5 mitosis/ 50 HPF – benign behavior
 > 5 mitosis/ 50 HPF – malignant behavior
 >50 mitosis/ 50 HPF – very aggressive
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Malignant behavior
T>5 cm
 Cellular atypies
 Necrosis
 Local invasion
 c-KIT mutation
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Benign:malign=3-5:1
Even “benign” phenotype can produce metastasis
GIST
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Diagnostic
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dispepsia, bleeding
Endoscopy+biopsy
CT
Imunohistochemistry
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Treatment
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Surgical (excision)
RXT + CHT not good
Imatinib mesylate
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Competitor inhibition of tirozine
kinaze associated with KIT
INDICATIONS:
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High risk
Non resectable
Metastatic
BENIGN TUMORS
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3-5% from all gastric tumors
Any origin
40% mucosa şi 40% muscularis
Types
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Polyps sporadic
Polyps associated with genetic
diseases (FAP, sdr. Peutz-Jegers)
Leiomioma
GIST
Fibroma, fibromioma
Lipoma
Ectopic pancreas
Vascular, neurogenic
Cysts
Mucocel
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Hiperplastic
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28-75%
<1,5 cm
Associated with atrophic gastritis with
HP
2% can develop malign
Fundic
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POLYPS
47%
Sesil, 2-3 mm
Never transform malignant
On healthy mucosa
Asociated with FAP, Gardner sdr)
Adenomatos
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10%
Risk to develop cancer – 21%
> 4 cm 40% risc of ADK
If present: high risk for cancer on any
part of stomach
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Diagnostic
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Clinical
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Asimptomatic
Endoscopy: by chance
Can produce obstruction,
torsion, bleeding
Paraclinical
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Endoscopy +biopsy
Echoendoscopy
Imunohistochemistry
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Treatament
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Observation
Endoscopic excision
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Small<2 cm
Adenomatos, hiperplastic
Polips associated with sdr.
Peutz-Jegers, Gardner,
Cronkhite-Canada, juvenile
poliposis)
Small stromal tumors
Surgical
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Excision
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Complicated tumors
Unclear diagnostic
Rezection
GASTRIC VOLVULUS
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Volvere (lat)= rotated around axis
 Pathology
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To be able to rotate with 180º only if significant
laxity.
Special anatomy
Clasification
ethiology
idiopatic
 secundary(75%):
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1.associated with HH
 2.associated with other diaphragmatic hernias
 3.pyloric obstructi
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GASTRIC VOLVULUS
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Classification
 organoaxial- axis = cardiapylorus
More frequent
 Majority with acute
presentation
 Associated with HH or
diaphragmatic deffects
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mezentericoaxial-axis
perpendicular on the
precious
More often partial
 Not very frequent
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GASTRIC VOLVULUS
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How much:
total
 partial
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Severity
acute: obstructio + vascular problems (gangrene) –
very unusual ischemic due to complex irrigation
 chronic, recurrent more frequent
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DIAGNOSTIC
 Clinical:
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chronic:
Asymptomatic – discovered during barium meal
 Light unspecific symptoms: meteorism, burping,
vomiting, pain.
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acute:
Major emergency
 1.severe pain with abdominal distension
 2.try to vomit but vomiting is impossible
 3.impossible to pass a naso-gastric tube
 Necrosis, bleeding, respiratory failure, shock
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TREATMENT
 Only
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if simptomatic
Chronic:
Careful for associated problem or anything that can mimic
 Laparoscopy: local evaluation
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Primary (idiopatic) gastropexy –
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fixation of stomach to the diaphragm and
mediogastric, in order to prevent further volvulus
TREATMENT
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Secondary: treat the underlying pathology. If easy
to fix
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Secondary with difficult to treat conditions
(ligamentary laxity, diaphragmatic hernia, etc)
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Partial gastrectomy
Fixation of transverse colon
Acut:
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Naso-gastric tube: immediate reduction (unusual).
Surgery
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necorsis = resections
Treat de cause
Prevent reucrence: gastropexie, etc
SURGERY FOR MORBID
OBESITY
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>300 milions –
2-7% all medic al spendings
USA >50% of adults are obese or overweighed,
5% morbid obesity
CHIRURGIA OBEZITĂŢII MORBIDE
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IMC>40kg/m2
IMC
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Normal 20-24,9
Overweight 25-29,9
Obesity 30-34,9
Morbid obesity 35-39,9
TREATMENT
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Approaches:
Change life style
 medication
 surgery
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Life style changes
Low calory diet (800-1200 kcal/day): goal: 8% loss with a
decrease of fat tissue over 6 months
 Exercise, 3-7 sessions/wk for 30-60 min 2-3% decrease in
body weight
 Behavioral therapy: change life style (identification of
stimuli, autoevaluation, support group)
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TREATMENT
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Medication
When life style changes do not help
 sibutramine, inhibits serotonine reabsorbtion
 orlistat, inhibits pancreatic lipase
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6-10% reduction in body weight in 1 year (rebound after
stop)
SURGERY
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Indications
IMC>40
 IMC>35 with comorbidities
 After at least one year of medical therapy
 Obesity should be stable or worsening in the last 5 years
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Contraindications
Psihiatric problems
 Thyroid or adrenal problems
 Chronic inflammatory pathology of digestive tract
 Drug or alcohol abuse
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SURGERY
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A. Restrictive procedures
Diminishes the gastric reservoir to 15-20 ml, limiting
the ingestion of solids and inducing early feeling of
being full
Two procedures
Gastric banding
 Calibrated vertical gastroplasty .
 Resection of the major curvature
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B. Malabsorbitve procedures
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Biliopancreatic diversion +/- duodenal switch
SURGERY
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C. Mixt procedures
Restriction + malabsorbtive procedure
 Gastric by-pass with „Y” loop. The gold standard
in surgical procedure for obesity
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POSTGASTRECTOMY
SINDROMES
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Long term incidence 20%
Mechanical
Alkaline reflux gastritis
 Aferent loop syndrome
 Blind loop syndrome
 Recurent ulcer disease
 Bezoars
 Carcinoma
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Functional
Dumping (early or late)
 Diarheea
 Malnutrition
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Alkaline reflux
gastritis
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Causes
Very frequent after
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Not often
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Billroth I
GEA
Unusual
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BillrothII
VT+GEA
VT+P:
Not after
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PCV
Alkaline reflux
gastritis
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Simptoms
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Nausea, vomiting (bile)
epigastric pain, loss of
weight
Not better after antiacide
medication or food. May
be better after vomiting
Diagnostic
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Endoscopy
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See the reflux
Lesions: eritema,
ulcerations
Biopsy
Alkaline reflux gastritis
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Treatment
Medical
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Prostaglandine
Metoclopramid,
cisaprid???
Colestiramine
Surgical
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GJA Roux (Y)+VT
Afferent loop syndrome
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Cause
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Simptoms
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Billtoth II
RUQ pain
Sensation of abdominal fulness
Simptoms better after vomiting
with bile and food
Diagnostic
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US
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Rx with barium
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Dilated afferent loop and
duodenum
Barium enters the aferent loop
and duodenum which are
distended Tratament
Treatment: conversion
Billroth II in Billroth I
Blind loop syndrome
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Complete obstruction of aff erent
loop
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Technical error
Adhesions
Internal hernia, invagination, volvulus
Anastomotic ulcer, cancer
Bacterian proliferation –
deconjugation of bile salts, lipolisis,
diarhea, weigh loss, malabsorbtion of
fat and B12
Simptoms
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Violent abdoinal pain
Vomiting (not with bile)
Jaundice
Pancreatitis
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Diagnostic
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Blind loop syndrome
Rx abdominal plain
Rx contrast
Endoscopy
US
Treatment
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Atb, pancreatic enzyme
supplemets
Surgical correction
Coversion to Billroth I
DUMPING
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Cause
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Pathogeny
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by-pass or excision of pilorus
GEA+VT, total gastrectomy
Sudden decrease of plasmatic
volume due to sudden increase of
osmotic pressure in the small
bowell
Consequences
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Rapid gastric emtying + rapid
intestnial passage
Jejunal distension
Low pasmatic volume
Tachicardia
Low blood pressure
Low serum K
EKG changes
DUMPING
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Simptomatoms
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gastrointestinal
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neurovegetatitve
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Weekness, dizziness, pale, vertigo, palpitation sweating
Triggered by food rich in carbohydrates
Early Dumping
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Epigastric discomfort, fulness, bloating, crampy abdominal pain,
vomiting, diarrhea.
Often symptoms start very early after eating or during eating
Relieved within 1 hour
Late Dumping
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1-2 hours after meal
Due to hypoglicemia
DUMPING
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Diagnostic
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Simptoms
i.v. glucose makes symptoms better
Exclude other diseases
Treatment
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2/3 will feel better without treatment,
diet
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medication
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Main alternative for 80% pt
Meals with lots of proteins and carbohydrates in small quantity
No drinks during meal (not to solve hypertonic liquids) 35-40 minutes later
antihistaminics, sedative, serotonine antagonists, parasimpatomimetics, verapamil,
octeotride and somatostatine
surgical
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Piloric reconstruction
Conversion GEA in Billroth I
Jejunal interposition
Late dumping
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Initial hyperglicemia → excess insulin → rapid metabolism
→ hypoglicemie
Simptoms
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Diagnostic
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Senzation of hot, sw2eating, tremor, diziness
Often 1 hour after meal for as long as 10-20 minutes , unusual it can
produce convulsion
Severe hypoglicemia
Treatment
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Frequent eating with low content in carbohydrates
Medication: late glucose absorbtion - pectina, diazoxid, octeotride
Surgery
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Antiperistaltic loop between stomac and duodennum
Pyloric reconstructio
Conversion GEA in Billroth I
Postvagotomy Diarrhea
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Not clear mechanism
After truncal vagotomy
Diarrhea
1-3-8 /zi
 Explosive diarrhea without worning +/- incontinence
 May last 3 months potop
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Treatment
diet: avoid coffee, and foods associated with diarrhea
 Medication: :colestiramina,codeine 1-3 hours before meal,
verapamil, octeotride
 Surgery:
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Pyloric reconstruction
 Antiperistaltic loop 48-135 cm from Treitz.
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MALNUTRITION
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Malabsorbtion
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Typical
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Total/Subtotal gastrectomy
Reconstructions that favor rapid transit
Diagnostic
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Weight loss, steathorea, anemia, osteoporosis, osteomalacia
Causes
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Fat, liposoluble vitamines, proteins, B12, Fe, Ca, Po4, folic acid
Low serum level of de Ca, Fe, vitamine
Stool - steathorea
Test Schilling B12 absorbtion
Juejunal biopsy
Treatment
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Diet – vitamine, minerals, pancreatic enzimes
Surgical correction
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Blind loop
Billroth II in Billroth I
Recurent ulcer
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Causes
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Close to or on the anastomosis
Simptoms
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Peptic ulcer
Diagnostic
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VT (inadequat???)
1-2% after antrectomy +VT
Antral stasis
Incomplet resection???
Rx barium, endoscopy, serum level of Ca şi gastrinei
Treatament
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Medical – IPP, etc.
Surgical – not anymore
Bezoars
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Insoluble vegetable fibers fitobezoars
Causes
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Low acid output
Digestion in stomach limited
Low proteolitic activity
Changes in gastric motility
Dental problem or mastication
insuficient
Simptoms
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Up to 10 years from operation,
unspecific symptoms
Eary senzation of fulness bed
odor in respiration
May produce intestinal obstruction
if pasage in small bowell
Gastric outlet obstruction not
possible (floats)
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Complications
 malnutrition
 gastritis
 ulcer
 bleeding
 Intestnal
obstruction and
perforation
Bezoars
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Diagnostic
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Rx. + barium: filling defect ~ cancer
Endoscopy
Obstruction – may mimic adhesions or anything
Tratament
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Conservative
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Surgery
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Gastric lavaj
Endoscopic mechanic destruction
Enzimatic disolution
Gastrotomy and removal
Profilaxis
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Good dentition
Low fiber
Cancer formation
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High incidence after any
operation
5y after cance roperation =
second cancer
Risk increases after 10 y
localisation
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Close to anastomosis, usually
without involving the jejunum
Proximal part of gastric
remnant
Cancer should be searched
for for any new symptoms
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Diagnostic
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Endoscopy: multiple biopsies
+/- citology with brush
Treatment
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Gastric resection