This document provides an overview of peptic ulcer disease (PUD) and its management. It discusses the types and causes of PUD, including Helicobacter pylori infection and NSAID use. Complications of PUD like bleeding, perforation, and obstruction are also covered. The management of PUD focuses on medical treatment with acid suppressants, H. pylori eradication therapy, and long-term maintenance to prevent recurrence. Surgical treatment may be needed for complications that do not respond to medical management.
Definitions of GI bleeding
GI Bleeding include Upper and Lower of GIB
Causes of GI bleeding
Pathogenesis of GI bleeding
Diagnosis of GI bleeding
Clinical of GI bleeding
Management of GI bleeding
Recommendation of GI bleeding
Clinical guideline of GI bleeding
Obstructive jaundice is one of the important surgical topics. In this playlist I have discussed the introduction, choledocholithiasis, Carcinoma Pancreas and biliary atresia. If you watch all these videos together you will become confident in Managing obstructive jaundice.
Definitions of GI bleeding
GI Bleeding include Upper and Lower of GIB
Causes of GI bleeding
Pathogenesis of GI bleeding
Diagnosis of GI bleeding
Clinical of GI bleeding
Management of GI bleeding
Recommendation of GI bleeding
Clinical guideline of GI bleeding
Obstructive jaundice is one of the important surgical topics. In this playlist I have discussed the introduction, choledocholithiasis, Carcinoma Pancreas and biliary atresia. If you watch all these videos together you will become confident in Managing obstructive jaundice.
Intestinal fistulas pose the greatest challenge to the General Surgeon. The presentation provides abrief guideline for management of this complex problem.
Intestinal fistulas pose the greatest challenge to the General Surgeon. The presentation provides abrief guideline for management of this complex problem.
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Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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7. Surgical importance of rich gastric blood
supply
• At least two of the four can be ligated or occluded
• rich venous interconnections in the stomach,
distal splenorenal shunt(splenic vein and lt renal
vein)
effectively decompress esophagogastric varices in portal
hypertension
10. …cont
Function in stomach
• In the stomach the vagus nerves
• affect secretion (including acid),
• motor function
• mucosal bloodflow
• cytoprotection.
11. extrinsic sympathetic nerve supply
• originates at spinal levels T5 through T10
• There may be more intrinsic gastric neurons(myenteric
and submucosal plexuses) than extrinsic neurons, but
their function is poorly understood
12. …cont
• epinephrine is important in the sympathetic nerves,
• Others..
• cholinergic,
• Adrenergic
• peptidergic (e.g., substance P
and somatostatin).
13. …cont
• Proximal gastric distension stimulates the acid secretion
by vagovagal reflex(which is abolished by truncal or HSV)
• Antral distention also stimulates antral gastrin secretion.
• Acetylcholine stimulates gastrin release
and gastrin stimulates histamine release from ECL cells.
14. Basal acid secretion
• Interprandial basal acid secretion is 2 to 5 mEq
hydrochloric acid per hour
• 10% of maximal acid output (MAO),
and it is greater at night
• contributes to the relatively low bacterial counts found in
the stomach.
• Basal acid secretion is reduced 75% to 90% by vagotomy
or H2 receptor blockade.
15. …cont
• H2 receptor knockout mice do not secrete acid in
response to gastrin implies the pivotal role of ECL cells in
acid production
• Somatostatin inhibits histamine release from ECL cells
and gastrin release from antral G cells.
• Helicobacter pylori infection, inhibits D cells and this leads
to an exaggerated acid secretory response (see section
Helicobacter pylori Infection).
17. …cont
• TV and HSV significantly affects receptive relaxation and
gastric accomodiation phases
• result in decreased gastric compliance, shifting the
volume/pressure curve to the left
• Increases liquid emptying rate,
• But increases dumping symptoms after vagotomy
18. …cont
• Proximal gastric tone also is decreased by duodenal
distention, colonic distention, and ileal perfusion with
glucose (ileal brake)
• vagotomy abolishes phase II of the
gastric MMC but has little influence on phase III(present in
autotransplanted stomach)
19. MMC(fasting)
• Phase I(about half the length of the entire cycle) is a
period of relative motor inactivity. High-amplitude
muscular contractions do not occur
• Phase II (about 25% of the entireMMC cycle) consists of
some irregular, high-amplitude, generally nonpropulsive
contractions.
• Phase III, a period of intense,regular, (about three per
minute) propulsive contractions, only lasts about 5 to 10
minutes begin in the stomach, and the frequency
approximates that of the myoelectric gastric slow wave.
• Phase IV is a transition period.
20. PUD
• focal defects in the gastric or duodenal mucosa
that extend into the submucosa or deeper.
• They may be acute or chronic
• imbalance between mucosal defenses and acid/peptic
injury
22. Pathophysiology and Etiology
• H. pylori infection and/or NSAID use
• final common pathway to ulcer (“no acid, no ulcer”
remains true).
• The previous thought of all duodenal ucer dueto
hyperacidity and all gastric ulcer dueto loss of mucosal
protection is not true today
23. …cont
• (beneficially)
decreased H. pylori infection prevalence ,
better medical therapy
increased outpatient management;
• (detrimentally)
NSAIDs and
aspirin use in aging population
.
27. Southern Ethiopia
• Peptic ulcer disease in south Ethiopia is strongly
associated with Hebcobacter pylori
• Helicobacterpylori infection was detected in 93% of 174
patients with a peptic ulcer compared with 63% of 116
patients with normal findings
32. Acid Secretion and Peptic Ulcer
• duodenal ulcer more than gastric ulcer
• There is no correlation between acid
secretion and the severity of the ulcer
disease
• 70% of patients with duodenal ulcers have
an acid output within
the normal range
33. …cont
• Duodenogastric reflux may play a role weakening the
gastric mucosal defenses(bile, lysolecithin, and
pancreatic juice)
• NSAIDs and aspirin
• Impaired feedback mechanism of gastrin level
• associated with H. pylori infection
• increased rates of gastric emptying
• decreased duodenal bicarbonate secretion(decreases the
buffering capacity
34. NSAIDS
• Inc. risk of peptic ulcer disease about 5-fold
• Inc. upper GI bleeding about 4-fold
• risk for bleeding and ulceration is proportional to the daily
dosage of NSAIDs
• Complications of PUD (hemorrhage and perforation) are
much more common
35. …cont
• overall risk of significant serious adverse GI events in
patients taking NSAIDs is more than three times that of
controls
• NSAIDs Vs cyclooxygenase enzymes Vs PGs(rate
limiting)
• NSAID-induced ulcers are more often found in the
stomach
36.
37. Age more 60 years old(on NSAID)
• risk of complication increases to five times in patients In
elderly patients taking NSAIDs,
• require an operation related to a GI complication is 10
times that of the control group
• will die from a GI cause is about four and half times higher
38. Smoking
• smokers are twice as likely to develop PUD as
nonsmokers
• increases gastric acid secretion and
duodenogastric reflux
• decreases gastroduodenal prostaglandin production and
pancreaticoduodenal bicarbonate production
39. Stress
• Both physilogic and psychologic
• Curling ulcer(burn)
• Cushing ‘s ulcer(head trauma)
• Stressful life events increase the occurrence of PUD
comlications
• NB…. Alcohol is commonly mentioned as a risk factor for
PUD, but confirmatory data are lacking
43. mortality
• duodenal ulcer was 3.7%
• 2.1% for gastric ulcer of the admitted
• High rates of hospitalization and mortality in elderly
patients for the peptic ulcer complications of bleeding
and perforation.
• use of NSAIDs and aspirin in this elderly cohor
• H. pylori infection.
44. Clinical Manifestations
• 90% of patients with PUD complain of abdominal pain
• Reffered pain signifies penetration into the pancrease
• nonradiating, burning in quality, and located in the epigastrium
• DU pain >>2 to 3 hours after a meal and at night
• pain that awakens them from sleep(2/3rd )
• nausea,
• bloating,
• weight loss,
• stool positive for occult blood,and anemia
45. …cont
• Duodenal ulcer is about twice as common in men
• incidence of gastric ulcer is similar in men and women
• gastric ulcer patients are older than duodenal ulcer
patients
• GU incidence is increasing in the elderly(NSAID and
aspirin)
46. Diagnosis of PUD
• In the young patient(clinical Dx)
• empirical PPI therapy for PUD without confirmatory
testing after pt counseling of small possibility of an
alternative diagnosis
.
47. Routine laboratory studies include
• complete blood count;
• liver chemistries;
• serum creatinine,
• serum amylase
• calcium levels.
• A serum gastrin level(ulcers that
are refractory to medical therapy or require surgery)
• H.pylori(urea breath test, serum,stool Ag).
48. …cont
• The two principal means of diagnosing duodenal ulcers
flexible upper endoscopy(need to perform a biopsy to R/o
malignancy, upper endoscopy has replaced upper GI
radiography all with
Age > 45 years old, all patients, regardless of age, should
have this study if any alarm symptoms
49. Biopsy(gastric ulcer)
• >>>H.pylori(urease assay,culture)
• >>> histologic evaluation
• first biopsy >>only a 70% sensitivity
in detecting gastric cancer
• four biopsy specimens increased this yield to 95%
• taking seven specimens increased it to 98%
50.
51.
52.
53. Medical Treatment of Peptic Ulcer
Disease
• Acid supressants>>>PPIs, high doseH2RAs
• Protective>>>sucralfate
• H.pylori>>> ABCs
• Iv PPIs for admitted patients+ lifelong PPI on discharge
• acid supressive therapy for 3 months(if underlying cause
resolved)
• Avoid alcohol,smoking NSAIDs
• Pt on NSAIDs is a must, always take concomitant PPIs or
high dose H2 receptor blockers
54. …cont
• Treat documented H. pylori infection
• give eradication Tx if H. pylori testing is negative and
ulcer symptoms persist
• H. pylori eradication will decrease of elective surgical
procedures and decline complications and mortality from
emergent complications
55. long-term maintenance
PPI
• all patients admitted to hospital with ulcer complications,
• all high-risk patients on NSAIDs
or aspirin (the elderly or debilitated),
• all patients with a history of recurrent ulcer or bleeding
56. Complications of PUD
• bleeding,
• Perforation
• Obstruction
• Interactablity
• >>>>>>>7% of hospitalized patients need surgery
57. Bleeding peptic ulcer
• present with melena and/or hematemesis
• NG tube aspirate Is diagnostic
• Abdominal pain is quite uncommon
• Shock could be the presentation
• Early endoscopy is important to diagnose the cause and
manage
58. …cont
• Three-fourths of the patients who come to the hospital
with bleeding peptic ulcer will stop bleeding with acid
supression ,resuscitation and NPO
• one fourth will continue to bleed or will rebleed after an
initial quiescent period(all mortalities of UGIB)
59. high-risk group
• Shock,
• hematemesis,
• transfusion requirement exceeding four units in 24 hours
• endoscopic stigmata (active bleeding or visible vessel)
• these patients benefit from
endoscopic therapy to stop the bleeding
60. …cont
• most common endoscopic hemostatic modalities used
• injection with epinephrine
• Electrocautery
• Clipping
• Persistent bleeding or rebleeding afterendoscopic therapy
is an indication for operation(vs repeat endoscopic
treatment)
61. …cont
• elective operation even after initially successful
endoscopic treatment in elderly patient, especially if they
have a high-risk ulcer.
62. high-risk lesions
• Deep bleeding ulcers on the posterior duodenal bulb ()
gastroduodenal vessel erosion
• Bleeding at lesser gastric curvature(left gastric vessels
erosion)
• early operation should be considere since not
amenable for conservative control
71. …cont
• operation for ulcer perforation is much more common than
operation for bleeding ulcer
• suture ligation of the bleeder;
• Suture ligation and definitive nonresective ulcer operation
(HSV or V +D)
• gastric resection (usually, including vagotomy and ulcer
excision).
• Take biopst of gastric ulcer if not resected.
72.
73. Surgery indication for bleeding PUD
• similar to the approach to a trauma patient(ABCs)
• massive hemorrhage unresponsive to endoscopic control,
• transfusion requirement of more than four to six units of
blood despite attempts at endoscopic control
• Lack of availability of a therapeutic endoscopist,
• recurrent hemorrhage after one or more
attempts at endoscopic control,
• lack of availability of blood for
transfusion,
74. …cont
• Age more than 60 years of age
• Shock at presentation,
• more than four units of blood in 24 hours or eight units of
blood in 48 hours,
• rebleeding,
• ulcers >2 cm in diameter
75. …cont
• repeat hospitalization for bleeding ulcer
• concurrent indications for surgery(perforation or
obstruction)
• Bleeding from posterior duodenal ulcer or lesser curvature
gastric ulcer
77. …cont
• initial pyloromyotomy incision allows access to the
bleeding posterior duodenal ulcer
• expeditious Kocher maneuver allows the surgeon to
control the hemorrhage with the left hand .
• Heavy suture material
• figure-of-eight sutures or U-stitch to securethe bleeding
vessel at the base of the posterior duodenal ulcer.
• Multiple sutures are usually necessary
79. Perforated PUD
• second most common complication of peptic
ulcer
• a more common indication for operation
than bleeding
• sudden onset of the excruciating abdominal pain
• Previous Hx of PUD
• Phases of peritonitis
chemical peritonitis develops from the gastric and/or
duodenal secfretions
bacterial peritonitis supervenes within hours
80. Clinical examination
• marked involuntary guarding
• Rebound tenderness is evoked by a gentle examination
• Upright chest X-ray shows free air in about 80% of
patients
81. Management approach
• NGT insertion
• Analgesic
• Antibiotic
• Resuscitation with isotonic flids
• Take to OR
82. surgery
• Supraumblical incision
• 1st portion of duodenum
• Those <1 cm can generally be closed primarily
• buttressed >>>wellvascularized omentum.
83. …cont
• larger perforations or ulcers ,a Graham patch repair
with a tongue of healthy omentum is performed.
• stay sutures are placed that incorporate a bite of healthy
tissue on the proximal and the distal side of the ulcer.
• The omentum is placed underneath these sutures,
85. …cont
• very large perforations (>3 cm)
Primary closure is difficult
The defect should be closed by the application of healthy
tissue(omentum or jejunal serosa from a Rouxen-Y type
limb)
bypass the duodenum (Billroth II or
Roux-en-Y fashion)
several weeks, the pyloric exclusion stitches or staples
give way
86. …cont
• simple patch closure
• patch closure and HSV
• Patch closure and V + D
• biopsy
• Simple patch closure, currently the most
commonly performed
• laparoscopy appears to be the superior approach in
patients with duodenal perforations who are
hemodynamically stable
87. …cont
• should be done in patients with hemodynamic instability
and/ or exudative peritonitis signifying a perforation >24
hours old
• Vagotomy procedures are ommited this days even in
stable patients because of the availablity of PPIs
• Perforation has the highest mortality rate of any
complication of ulcer disease, approaching 15%
88.
89. Post OP care
• stomach is decompressed until bowel activity
returns
• Drains should be kept in place until patients have eaten
without a change in drain output or quality
• A routine contrast radiograph
• H. pylori–positive patients should undergo eradication
with appropriate triple-therapy
90. Nonoperative management
of perforrated PUD
• Surgery is a rule
• objective evidence that
the leak has sealed (i.e., radiologic contrast study)
• The absence of clinical peritonitis
91. perforation in an inopportune location
• Patch closure with biopsy
• local excision and closure
• biopsy (for gastric ulcers if not resected)
• closure
• truncal vagotomy and drainag
92. Gastric outlet obstruction
• 5% of patients with PUD
• due to duodenal or prepyloric ulcer disease,
• may be acute (from inflammatory swelling
and peristaltic dysfunction) or chronic (from cicatrix)>>do
not need surgery
• Significant obstruction from chronic ulceration will require
some sort of more substantial intervention(baloon
dilitation,surgery)
94. …cont
• Other causes of GOO must be ruled out(pancreatic,
gastric, or duodenal malignancy)
• ulcer disease is now less common than obstruction from
cancer
95. operation for obstructing PUD(GOO)
• Most managed with endoscopic dilitation
• Surgery is for refractory cases
• Vagotomy and antrectomy.
• vagotomy and gastrojejunostomy(difficult duodenal
stump)
• HSV and gastrojejunostomy (curable gastric or duodenal
cancers can be missed)
96. Intractable or Nonhealing Peptic Ulcer
• failure of an ulcer to heal after an initial trial of 8 to 12
weeks of therapy
• patients relapse after therapy has been discontinued
• unusual indication for peptic ulcer operation
• The surgeon should review the differential diagnosis of
nonhealing ulcer before any
consideration of surgery
97.
98. Endoscopic and UGI radiography
features that suggest malignancy
• Intraluminal location
• Irregularity and nodularity
• Surrounded by asymmetric mass
• Clubbed mucosal fold
• Ulcers in the fundus(rare but malignant if they present)
• Larger ulcers
• irregular or heaped edges
99. …cont
• With single-contrast radiographic techniques, 50% of
duodenal ulcers missed
• double-contrast studies, 80% to 90% of ulcer craters can
be detected
100. Surgical Treatment of Peptic Ulcer
Disease
• The indications for surgery in PUD
bleeding,
perforation,
Obstruction
intractability or nonhealing
Non compliant to medical Tx
Refractory H.pylori inf.
thin or marginally nourished individual(relative C/I)
101. Goal of surgical therapy
• to reduce gastric acidsecretion
vagotomy,
gastrin-driven secretion >>antrectomy
Vagotomy decreases peak acid output by
approximately 50%
vagotomy plus antrectomy decreases>> 85%
102. Surgical options
• Highly selective vagotomy(HSV)
• vagotomy and drainage (V+D),
• vagotomy and distal gastrectomy
• Taylor procedure(posterior truncal vagotomy and anterior
seromyotomy)
103. …surgical options
Depends on
• Typeofulcer(duodenal,gastric,recurrent,marginal)
• condition of the patient,
• surgeons experience
• Superimposed lesions(duodenal scarring/inflammation,
adhesions,
or difficult exposure),
104. …surgical options
• the ulcer diathesis status of the patient,
• H. pylori infection
• NSAID therapy, previous treatment
• future compliance with
105. Indications for surgery
• nonhealing or intractable PUD
• multiple recurrences,
• large ulcers (>2 cm),
• complications
• Obstruction
• perforation,
• Hemorrhage
• suspected malignancy
106. Surgery types for interactable ulcers
• lesser operation
• avoid truncal vagotomy and/or distal gastrectomy
• HSV with or without gastrojejunostomy
• distal gastrectomy (to include the ulcer)
• don’t add a vagotomy in patients with type I or type IV
(juxta-esophageal) gastric ulcers
107.
108. • Type IV gastric ulcers may be difficult to resect as part of
a distal gastrectomy,special procedures are used
109.
110.
111. summary
Stomach is a pear shaped,1st intra abdominal organ of
the digestive tract followed by duodenum
It has its own protective mechanism from its own acid
secretion
PUD occurs when the protective mechanism fail to control
the stress usually dueto the undelying
causes(H.pylori,NSAIDs,ASA)
112. …summary
• PUD can complicate if its not treated
Bleeding
Perforation
GOO
Interactablity
• The need for admission and surgery comes when it
complicates
• Surgery is the last(not the first) management for PUD
113. References
1. Schwartz principle of surgery,10th Ed, P1050-1090
2. Sabiston text book of surgery,20th Ed, P1200-1240
3. Harrison’s prinsiple of Internal medicine,19th edition
4. Uptodate 20.1
5. Netter Atlas Of Human anatomy,6th Edition
the right gastroepiploic artery is second largest artery to the stomach
It arises consistently from the gastroduodenal artery behind the first portion of the duodenum.
The left gastroepiploic artery arises from the splenic artery together with the right gastroepiploic artery, forms the rich gastroepiploic arcade along the greater curvature
Left gastric artery(largest)
Right gastric artery
Left gastoepiploic artery
Right gastroepiploic artery(2nd largest)
Short gastric artery
veins draining the stomach generally parallel thearteries
left gastric (coronary vein) and right gastric veinsusually drain into the portal vein, occasionally into the splenic vein.
The RGE vein drains into the SMV near the inferiorborder of the pancreatic neck,
left gastroepiploic vein drains into the SMV.
From the vagal nucleus in the floor of the fourthcerebral ventricle,through the neck and carotidsheath
Mediastinum(gives off the recurrent laryngeal nerve)
Then divides into several branches aroundthe esophagus.
These branches come together again above theesophageal hiatus and form the left (anterior) and right (posterior) vagal trunks (mnemonic LARP)Near the GE junction the anterior vagus sends a branch (or branches) to the liver in thegastrohepatic ligament,
Then the left(ant) vagus continues along the lesser curvature as the anterior nerve of Latarjet
posterior vagus sends branches to the celiac plexus and continues along the posterior lesser curvature.
The nerves of Latarjet send segmental branches to the body of the stomach before they terminate near the angularis incisura as the “crow’s foot,” sending branches to the antropyloric region.
In 50% of patients, there are more than two vagal nerves at the esophageal hiatus
The branch that the posterior vagus sends to the posterior fundus is termed the criminal nerve of Grassi.
This branch typically arises above the esophageal hiatus and is easily missed during truncal or highly selective vagotomy (HSV).
Most of vagal trunks have afferentnerves(from viscera to brain)
Vagal fibers originating in the brain synapse with neurons in Auerbach’s myenteric plexus and Meissner’s submucosal plexus.
acetylcholine is an important neurotransmittermediating vagal function,
the start of these trends all predated the use of H2 receptor blockers, or proton pump inhibitors, fiberoptic endoscopy, and highly selective vagotomy decreased hospital admission and death rate(past 30 yrs) but not as dramatically as expected
NSAID use causes ulcers predominantly by compromise of mucosal defenses. gastric ulcer was viewed as a disease of An increased understanding of peptic ulcer pathophysiology has blurred this overly simplistic distinction saying increased acid-peptic action causes duodenal ulcer , weakened mucosal defenses causes gastric ulcer
The gold standard for diagnosisof H. pylori is mucosal biopsy performed during upper endoscopy,but noninvasive tests offer an effective screening tool and do notrequire an endoscopic procedure. If endoscopy is to be performed,evaluation of biopsy samples with either a urease assay or histologic examination offers excellent diagnostic accuracy. Evaluationof serum antibodies is the test of choice for initial diagnosis whenendoscopy is not required but has the drawback of remainingpositive after treatment and eradication of infection. For monitoring treatment efficacy, stool antigen and urea breath testing arebetter choices.
In the United States, probably more than 90% of seriouspeptic ulcer complications can be attributed to H. pylori infection, NSAID use, and/or cigarette smoking
Pts infected with h.pylori produces more acid with small gastrin stimulation than the normal ones
weakening the gastric mucosal defenses, and a variety of components in duodenal juice, including bile, lysolecithin, and pancreatic juice, have been shown to cause injury and inflammationin the gastric mucosa. NSAIDs and aspirin
NSAIDs are absorbed through the stomach and small intestineand function as systemic inhibitors of the cyclooxygenase enzymes.Cyclooxygenase enzymes form the rate-limiting step of prostaglandin synthesis in the GI tract
Lesser curve, incisura.
II. Body of stomach, incisura + duodenalulcer (active or healed).
III. Prepyloric.
IV. High on lesser curve,near gastroesophageal junction.
V. Medication-induced (NSAID/acetylsalicylic acid), anywhere in stomach
Approximately 60% of ulcers are in this location and areclassified as type I gastric ulcers. These ulcers are generally notassociated with excessive acid secretion and may occur with lowto normal acid output. Most occur within 1.5 cm of the histologictransition zone between the fundic and antral mucosa and are notassociated with duodenal, pyloric, or prepyloric mucosal abnormalities. In contrast, type II gastric ulcers (approximately 15%)are located in the body of the stomach in combination with aduodenal ulcer. These types of ulcers are usually associated withexcess acid secretion. Type III gastric ulcers are prepyloric ulcersand account for approximately 20% of the lesions. They alsobehave similar to duodenal ulcers and are associated with hypersecretion of gastric acid. Type IV gastric ulcers occur high on thelesser curvature, near the GE junction. The incidence of type IVgastric ulcers is less than 10%, and they are not associated withexcessive acid secretion. Type V gastric ulcers can occur at anylocation and are associated with long-term NSAID use. Finally,some ulcers may appear on the greater curvature of the stomach,but the incidence is less than 5%.
Antacids differ greatlyin their buffering ability, absorption, taste, and side effects. Magnesium antacids tend to be the best buffers but can cause significant diarrhea, whereas acids precipitated with phosphorus canoccasionally result in hypophosphatemia and sometimes constipation. Antacids are most effective when ingested 1 hour after a mealbecause they can be retained in the stomach and exert their buffering action for longer periods. If taken on an empty stomach,antacids are emptied rapidly and have only a transient bufferingeffect. Because of this transient efficacy, the use of buffering antacids has largely been replaced by antisecretory therapy (either H2receptor antagonists or PPIs) for the treatment of PUD
Although intractable disease no doubt exists,its definition is nebulous, and determining exactly when and whattype of surgical intervention are required is primarily a matter of judgment. In the current era of excellent treatment options for H.pylori infection and acid suppression, few patients who are trulycompliant with medical therapy develop intractable ulcer diseasein the absence of malignancy.
In a case with exposed vessel,mechanical hemostasis using a clip is useful to control thebleeding
which ranges from 0 to 23, with higher scores indicating higher risk
which ranges from 0 to 23, with higher scores indicating higher risk
Panel Bshows the Rockall score, with point values assigned for each of three clinical variables (age and the presence of shock and coexisting illnesses) and twoendoscopic variables (diagnosis and stigmata of recent hemorrhage). The complete Rockall score ranges from 0 to 11, with higher scores indicating higherrisk. Patients with a clinical Rockall score (Age + Shock + Coexisting illness) of 0 or a complete Rockall score of 2 or less are considered to be at low riskfor rebleeding or death.
Panel Bshows the Rockall score, with point values assigned for each of three clinical variables (age and the presence of shock and coexisting illnesses) and twoendoscopic variables (diagnosis and stigmata of recent hemorrhage). The complete Rockall score ranges from 0 to 11, with higher scores indicating higherrisk. Patients with a clinical Rockall score (Age + Shock + Coexisting illness) of 0 or a complete Rockall score of 2 or less are considered to be at low riskfor rebleeding or death.
Forrest classification (Table48-4), which stratifies the risk of rebleeding based on observed“stigmata of recent hemorrhage.” Lower risk ulcers are much morefrequently encountered than actively bleeding ones, even in thesetting of inpatients undergoing endoscopy for diagnosis of upperGI bleeding
When the mortality forreoperation for rebleeding is considered, the overall mortality is probably comparable for the two approaches. Patientswho are in shock or medically unstable should not have gastricresection.
Oversewing of the bleeder followed by long-term acidsuppression is a reasonable alternative in high-risk or unstablepatients.
The mortality rate for surgery for bleeding peptic ulcer is around 20%. An initial pyloromyotomy incision allows access to thebleeding posterior duodenal ulcer, and an expeditious Kochermaneuver allows the surgeon to control the hemorrhage with theleft hand if necessary. Heavy suture material on a stout needleis used to place figure-of-eight sutures or a U-stitch to securethe bleeding vessel at the base of the posterior duodenal ulcer.Multiple sutures are usually necessary
second ulcer or a GI cancer has to be consudered in a patient with perforated and bleeding at a time
perforation istheir first symptom of ulcer disease
Perforation has the highest mortalityrate of any complication of ulcer disease, approaching 15%
perforation is usuallyin the first portion of the duodenum and can easily be accessedthrough an upper midline incision
larger perforations or ulcers with fibrotic edges that cannot be brought together without tension, a Graham patch repair with a tongue of healthy omentum is performed.
Multiple stay sutures are placed that incorporate a biteof healthy tissue on the proximal and the distal side of the ulcer.
The omentum is placed underneath these sutures, and they aretied to secure it in place and seal the perforation
there is clearly a trend away from definitiveoperation for perforated duodenal ulcer, probably because ofthe ready availability of PPI, and surgeon unfamiliarity withdefinitive operation in this setting.
Vagotomy is usually added for type II and III gastriculcers. Patch closure with biopsy; or local excision and closure;or biopsy, closure, truncal vagotomy, and drainage are alternative operations in the unstable or high-risk patient, or in thepatient with a perforation in an inopportune location. All perforated gastric ulcers, even those in the prepyloric position, shouldbe biopsied if they are not removed at surgery
adequate duration oftherapy, H. pylori eradication, and elimination of NSAID usemust be confirmed. A serum gastrin level should also be determined to R/o gastrinoma
Classic truncal vagotomy, in combination with aHeineke-Mikulicz pyloroplasty, is shown in Figure 48-12. Whenthe duodenal bulb is scarred, a Finney pyloroplasty or Jaboulaygastroduodenostomy may be a useful alternative