Peptic ulcers are erosions in the stomach or duodenum caused by an imbalance between gastric acids and mucosal defenses. Risk factors include H. pylori infection, NSAIDs, smoking, and stress. H. pylori infection is the leading cause and eradication treatment involves PPIs and antibiotics. Complications of peptic ulcers include bleeding, perforation, and obstruction. Endoscopy is the best diagnostic tool and allows for treatment of bleeding ulcers. Surgery may be needed for complications or intractable disease.
Annular pancreas is an uncommon condition in adults.
The ring formation generally originates from the failure of
normal clockwise rotation of ventral pancreas. First
described by Tiedmann in 1818, its incidence is
1:20,000 population. It has bimodal presentation i.e is seen
either in Infants or in 4th & 5th decade of life.
Annular pancreas is an uncommon condition in adults.
The ring formation generally originates from the failure of
normal clockwise rotation of ventral pancreas. First
described by Tiedmann in 1818, its incidence is
1:20,000 population. It has bimodal presentation i.e is seen
either in Infants or in 4th & 5th decade of life.
A circumscribed ulceration of the GI mucosa occurring in areas exposed to acid and pepsin with a defect in the mucosa that extends through the
Muscularis mucosa into the
Submucosa or deeper.
This presentation is about Peptic Ulcer Disease. I presented it in 2017 to my colleagues at Al Ain hospital. Information provided is up to date. I allow you to use it for educational purposes.
This topic helps you , how to approach a patient having peptic ulcer disease and how to diagnose finally how to end up with treatment. Peptic ulcer disease a chronic disease of stomach and duodenum where the protective layer of stomach and duodenum weakens by many factors most common is H Pylori infection. Infection of H Pylori cause ulcer over time.
A localized loss of gastric as well as duodenal mucosa leads to the formation of peptic ulcer.
A peptic ulcer is a sore on the lining of your stomach, small intestine or esophagus. A peptic ulcer in the stomach is called a gastric ulcer. A duodenal ulcer is a peptic ulcer that develops in the first part of the small intestine (duodenum). An esophageal ulcer occurs in the lower part of your esophagus.
Peptic ulcer arises when the normal mucosal defense mechanisms (mucus blood flow formation of HCO3- PGE2 ) are impaired or overpowered by damaging factors (acids pepsin pylori)
Ulcers occur 5 times more commonly in the duodenum and 95% of them are found in pyloric channel
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Title: Sense of Taste
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 structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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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Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
2. Definition
🠶 Peptic ulcers are defined as erosions in the gastric or duodenal mucosa that extend
through the muscularis mucosae.
🠶 Benign Gastric Ulcer
🠶 Duodenal Ulcer
5. Helicobacter pylori Infection
🠶 H. pylori is a spiral or helical gram-negative rod with four to six flagella that resides
in gastric-type epithelium within or beneath the mucous layer. This location
protects the bacteria from acid and antibiotics. Its shape and flagella aid its
movement through the mucous layer, and it produces enzymes that help it adapt
to this hostile environment.
🠶 Most notably, H. pylori is a potent producer of urease, which is capable of splitting
urea into ammonia and bicarbonate, creating an alkaline microenvironment in the
setting of an acidic gastric milieu.
🠶 H. pylori organisms are microaerophilic and can live only in gastric epithelium.
6. mechanisms responsible for H. pylori–
induced GI injury
🠶 Production of toxic products that cause local tissue injury - Infection with H. pylori
leads to the disruption of the gastric mucous barrier by the enzymes produced by
the organism.
🠶 Induction of a local mucosal immune response.
🠶 Increased gastrin levels with a resultant increase in acid secretion.
🠶 Gastric metaplasia occurring in the duodenum protective response to decreased
duodenal pH allows H. pylori to colonize these areas of the duodenum
🠶 Some strains of H. pylori produce cytotoxins, notably the Cag A and Vac A
products, and the production of cytotoxins seems to be associated with the ability
of the organism to cause gastritis, peptic ulceration and cancer.
7. 🠶 The causative role of H. pylori infection in the pathogenesis of gastritis and PUD
was first elucidated by Marshall and Warren in Australia in 1984.
🠶 To prove this connection, Marshall himself ingested inocula of H. pylori after first
confirming that he had normal gross and microscopic gastric mucosa. Within days,
he developed abdominal pain, nausea, and halitosis as well as histologically
confirmed presence of gastric H. pylori infection.
🠶 Warren and Marshall, received the Nobel Prize for Medicine and Physiology in
2005.
🠶 H. pylori is now classed by the World Health Organisation as a class 1 carcinogen
8. H. Pylori Eradication
🠶 PPI + Clarithromycin + Amoxicillin
🠶 PPI + Clarithromycin + Metronidazole
🠶 Duration – 14 days.
🠶 PPI to be continued.
🠶 Ulcer healing to be checked after 8-12 weeks with endoscopy. Then PPI can be
stopped.
🠶 The profound hypochlorhydria produced by proton pump inhibitors combined with
antibiotics is also effective in eradicating the organism.
9. NONSTEROIDAL ANTIINFLAMMATORY
DRUGS AND ULCER DISEASE
🠶 NSAIDs increase the risk of peptic ulcers.
🠶 NSAIDs are the most commonly identified risk factor for peptic ulcer bleeding,
especially in older adults; the risk is drug specific and dose dependent.
🠶 NSAIDs decrease the mucosal defense by suppression of prostaglandin synthesis in
gastric and duodenal mucosa
🠶 Acid suppression is the mainstay in the therapy of NSAID-associated ulcer disease.
10. LOW-DOSE ASPIRIN AND ULCER DISEASE
🠶 Even at very low doses (75 mg daily), aspirin decreases gastric mucosal
prostaglandin levels and can cause significant gastric lesions.
🠶 PPI given with low-dose aspirin, can significantly decrease the risk of developing
peptic ulceration
11. ACID HYPERSECRETORY STATES AND
ULCER DISEASE
🠶 Zollinger-Ellison (ZE) syndrome – gastrinoma
🠶 Anastomotic or Marginal Ulceration
12. SEVERE SYSTEMIC DISEASE (STRESS
ULCER)
🠶 A breakdown of the gastroduodenal
mucosal barrier, often a result of severe
physiologic stress and splanchnic
hypoperfusion, combined with gastric
acid may lead to ulceration and
bleeding.
🠶 It can develop within hours in critically
ill patients, typically starting in the
fundus and spreading distally.
🠶 Head Injury Cushing ulcer
🠶 Extensive burns Curling ulcer
14. Incidence
🠶 Incidence has come down drastically due to wide spread use of gastric
antisecretory agents and H. pylori eradication therapy
🠶 peak incidence is now in a much older age group than previously
🠶 more common in men
15. Pathology
🠶 Most occur in the first part of the duodenum
🠶 A chronic ulcer penetrates the mucosa and into the muscle coat, leading to fibrosis
pyloric stenosis
🠶 kissing ulcers - a posterior and an anterior duodenal ulcer
🠶 Anteriorly placed ulcers tend to perforate
🠶 posterior duodenal ulcers tend to bleed, sometimes by eroding into the
gastroduodenal artery.
16. Histopathology
🠶 destruction of the muscular coat is observed
🠶 base of the ulcer is covered with granulation tissue,
🠶 the arteries in this region showing the typical changes of endarteritis obliterans
17. Clinical Manifestations
🠶 midepigastric abdominal pain
🠶 relieved by food intake
🠶 When the pain becomes constant, this suggests that there is deeper penetration of
the ulcer.
🠶 Referral of pain to the back is usually a sign of penetration into the pancreas.
🠶 Diffuse peritoneal irritation is usually a sign of free perforation
18. Diagnosis
🠶 Routine laboratory studies include complete blood count; liver chemistries; and
serum creatinine, serum amylase, and calcium levels.
🠶 A serum gastrin level should also be obtained in patients with ulcers that are
refractory to medical therapy or require surgery.
🠶 An upright chest radiograph is usually performed when ruling out perforation.
19. Upper gastrointestinal radiography
🠶 demonstration of barium within the ulcer crater,
which is usually round or oval and may or may not
be surrounded by edema
🠶 with double-contrast studies, 80% to 90% of ulcer
craters can be detected
20. Flexible upper endoscopy
🠶 most reliable method for diagnosing gastric and
duodenal ulcers.
🠶 visual diagnosis
🠶 endoscopy provides the ability to sample tissue to
evaluate for malignancy and H. pylori infection
Duodenal Ulcer
Benign Healing Gastric Ulcer
21. H. Pylori – Non-invasive testing
🠶 Serology
🠶 used to test for the presence of IgG antibodies to H. pylori
🠶 Antibody titers can remain high for 1 year or longer; consequently, this test cannot
be used to assess eradication after therapy
🠶 Urea breath test
🠶 The carbon-labeled urea breath test is based on the ability of H. pylori to hydrolyze
urea as a result of its production of urease
🠶 Stool antigen
🠶 H. pylori bacteria are present in the stool of infected patients
22. Treatment
🠶 Medical management
🠶 Antiulcer drugs fall into three broad categories—
1. drugs targeted against H. pylori,
2. drugs that reduce acid levels by decreasing secretion or chemical neutralization,
and
3. drugs that increase the mucosal protective barrier.
23. Surgical Treatment Recommendations for
Complications Related to Peptic Duodenal Ulcer
Disease
🠶 Intractable: Parietal cell vagotomy ± antrectomy
🠶 Bleeding: Oversewing of bleeding vessel with treatment of H. pylori
🠶 Perforation: Patch closure with treatment of H. pylori
🠶 Obstruction: Rule out malignancy and gastrojejunostomy with treatment of H. pylori
27. Gastric Ulcers
🠶 Gastric ulcers can occur at any location in the stomach, although they usually
manifest on the lesser curvature, near the incisura.
🠶 Modified Johnson Classification
28.
29. 🠶 H. pylori and NSAIDs are the important aetiological factors.
🠶 Gastric ulceration is also associated with smoking
🠶 Chronic gastric ulcers are much more common on the lesser curve (especially at the
incisura angularis)
🠶 Large chronic ulcers may erode posteriorly into the pancreas and, on other
occasions, into major vessels such as the splenic artery. Less commonly, they may
erode into other organs such as the transverse colon
30. Malignancy in gastric ulcers
🠶 any gastric ulcer should be regarded as being malignant, no matter how classical
the features of a benign gastric ulcer. Multiple biopsies should always be taken
35. Bleeding Duodenal Ulcer
🠶 Upper GI bleeding
🠶 Most nonvariceal bleeding (70%) is attributable to peptic ulcers
🠶 The initial approach to an upper GI bleed is similar to the approach to a trauma
patient. Large-bore intravenous access, rapid restoration of intravascular volume
with fluid and blood products as the clinical situation dictates, and close
monitoring for signs of rebleeding all are essential to effective management of
these patients.
🠶 NG tube placement
🠶 all patients with a potentially substantial acute upper GI bleed should undergo
endoscopy within 24 hours
36. Bleeding
Duodenal Ulcer
• The most commonly
used system for
classifying the
endoscopic
appearance of
bleeding ulcers is the
Forrest classification
37. Bleeding Duodenal Ulcer
🠶 All patients undergoing endoscopic examination should be tested for H. pylori
status.
🠶 For high-risk patients requiring intervention, the best initial approach is endoscopic
control, which results in primary hemostasis in approximately 90% of patients. The
most common method of control is injection of a vasoconstrictor at the site of
bleeding.
🠶 Thermocoagulation, clipping
🠶 All high-risk patients should be placed in a monitored setting, preferably an
intensive care unit, until all bleeding has stopped for 24 hours.
🠶 all highrisk patients should be placed on a PPI administered intravenously, with an
initial bolus followed by continuous infusion or intermittent dosing for up to 72
hours.
🠶 catheter-directed angiography and endovascular embolization
38. Bleeding Duodenal Ulcer - Surgery
🠶 upper midline laparotomy
🠶 anterior wall of the duodenal bulb is opened
longitudinally, and the incision can be carried
across the pylorus.
🠶 The gastroduodenal artery is oversewn, with a
three-point U stitch technique, which effectively
ligates the main vessel (superior and inferior
stitches) and prevents back-bleeding from any
smaller branches (medial stitch), such as the
transverse pancreatic artery
🠶 duodenotomy is closed transversely to avoid
narrowing
39. Duodenal Ulcer Perforation
🠶 sudden-onset, severe epigastric pain
🠶 free air visible on the chest radiograph
🠶 diffuse peritonitis
🠶 first portion of the duodenum
40. Duodenal Ulcer Perforation - management
🠶 Resuscitation
🠶 NG tube placement
🠶 Laparotomy
🠶 The most important component of
the operation is a thorough
peritoneal toilet to remove all of the
fluid and food debris.
🠶 place an omental patch over the
perforation
🠶 For very large perforations (>3 cm) -
jejunal serosa (Thal patch), pyloric
exclusion procedure
41. Gastric outlet obstruction
🠶 Acute inflammation of the duodenum functional gastric outlet obstruction
delayed gastric emptying, anorexia, nausea, and vomiting patients may become
dehydrated and develop a hypochloremic hypokalemic metabolic alkalosis
secondary to the loss of gastric juice rich in hydrogen and chloride
🠶 Chronic inflammation of the duodenum fibrosis and stenosis of the duodenal
lumen painless vomiting of large volumes of gastric contents, with metabolic
abnormalities
🠶 Endoscopic dilation and H. pylori eradication are the mainstays of therapy
🠶 Patients with refractory obstruction are best managed with primary antrectomy and
reconstruction along with vagotomy.
42. Intractable peptic ulcer disease
🠶 failure of an ulcer to heal after an initial trial of 8 to 12 weeks of therapy or if
patients relapse after therapy has been discontinued.
🠶 rule out gastrinoma
🠶 truncal vagotomy, selective vagotomy, or highly selective vagotomy, with or
without an antrectomy.