1. UOG, CMHS, School of Nursing,
Department of Surgical Nursing
Seminar presentation on:
PUD & Gastric Ca
By: Alamirew Enyew
January 27 /2022
2/9/2024 1
3. Learning objective
At the end of this presentation you will be able to:
ī Define PUD and gastric ca
ī Explain the epidemiology of PUD and gastric ca
ī discus causes/risk factors &path-physiology of them
ī List clinical features of PUD and gastric ca
ī List DDx of PUD and gastric ca
ī Identify the dx methods of PUD and gastric ca
ī List nursing and medical mgt of PUD and gastric ca
ī Complications PUD
2/9/2024 3
4. Anatomy of stomach
īIt is greatly expanded & most proximal abdominal
organ of GIT
īIt occupies part of the epigastrium, umbilical,& Lt.
hypochondrium
īIt is J-shaped &has two curvatures-lesser & greater
īhas 5 parts-cardia, fundus, body, pyloric part&
pylorus ( Fig:1)
2/9/2024 4
8. Venous drainage
īąVenous drainage parallels the arterial supply
īLeft and right gastric veins drain into the portal vein
īRight gastroepiploic drains into the superior
mesentric vein
īLeft gastroepiploic and short gastric artery drains
into the splenic vein
Manipal manual of surgery
2/9/2024 8
9. Nerve supply
Manipal manual of surgery
Innervation:
īParasympathetic via vagus
īŧ Left-- anterior
īŧ right-- posterior.
īSympathetic via celiac
plexus.
īIntrinsic enteric neurons
2/9/2024 9
10. Lymphatic drainage
âĸ Lymphatic drainage is into four zones:
īSuperior gastric
īSuprapyloric
īPancreaticolienal
īInferior gastric/subpyloric
âĸ All four drain into the celiac group of nodes and into
the thoracic duct.
2/9/2024 10
11. Function
ī It stores & facilitates the digestion, absorption &
propulsed into SI.
īAntrum & pylorus allowing entry of food to
duodenum & returning to proximal stomach until
it is appropriate for delivery into the duodenum.
Schwartz's Principles of Surgery 8th edition
2/9/2024 11
12. Gastric Cell Types, Location, and Function
Sabiston Textbook of Surgery, 18th ed.
2/9/2024 12
15. Mechanism of HCL secretion contâĻ
Bailey and Love's Short Practice of Surgery
2/9/2024 15
16. Functions of gastric acid
īIt plays a critical role in digestion of a meal.
īConvert pepsinogen to pepsin used for hydrolysis of
proteins to polypeptide (pepsinogen HCL pepsin)
īElicits the release of secretin from the duodenum,
which results in pancreatic bicarbonate secretion.
īLimit colonization of the upper GI tract with bacteria.
Sabiston Textbook of Surgery, 18th ed.
2/9/2024 16
17. Other gastric secretary products
ī Gastric Juice: secreted by parietal, chief & mucus cells
ī Intrinsic Factor: mucoprotein secreted by parietal cell
w/c essential for absorption of vit B12 in terminal ileum
ī Pepsinogens: are proteolytic proenzymes secreted by the
glands of the gastroduodenal mucosa.
ī Mucus & bicarbonate combine to neutralize gastric acid
at the gastric mucosal surface.
Sabiston Textbook of Surgery, 18th ed.
2/9/2024 17
18. Peptic ulcer disease (PUD)
ī Are focal defects in the gastric or duodenal mucosa
which extend into the sub mucosa or deeper (muscle
to the peritoneum)
ī It is acid peptic digestion of alimentary mucosa
ī It may be gastric, duodenal, or esophageal ulcer
ī Are more common in duodenum than stomach
Brunner and Suddarthâs textbook of medical-surgical nursing
12th edition , Sabiston Textbook of Surgery, 18th ed
2/9/2024 18
19. PUD contâĻ
ī Common sites for PUD are:
īŧ first part of the duodenum and
īŧ lesser curve of the stomach.
ī Also occur on stoma after gastric surgery, distal
esophagus, distal duodenum, jejunum and Meckelâs
diverticulum
Bailey and Love's Short Practice of Surgery
2/9/2024 19
20. Types of PUD
Based on site
ī DU
ī GU
ī Combined(zollinger Ellision
syndrome)
ī Esophageal
ī Anastomotic
Based on duration
ī Acute
ī Chronic
Manipal manual of
surgery
2/9/2024 20
23. Compression between GU &DU
Criteria Gastric ulcer Duodenal ulcer
Site Stomach duodenum
Common in age >50 years 30-60 years
Acid secretion Normal /hypo secretion Hyper secretion
weight loss Gain /normal
Duration of pain Immediately after meal
Rarely at night
2-4 hrs after meal &
usually night
Food Aggravate pain Relive pain
Vomiting and
bleeding
common rare
2/9/2024 23
24. Epidemiology of PUD
ī PUD is a global problem with a lifetime risk 5% to 10%.
ī DU are 4 times more common than GU and DU are more
common in men (Lanas A, Chan FKL. 2017)
ī A recent SR & MA of 21 studies revealed that the
prevalence of PUD in the world in age range of 17â
82 years was 8.4%(Salari,N., Darvishi,N., Shohaimi,S. et
al., 2021.)
ī Incidence rate of PUD in Nigeria was 6.7% and GU to DU
ratio was 1.4:1 (Ray-Offor E, Opusunju KA. 2020)
2/9/2024 24
25. Epidemiology contâĻ
ī At UoGH, prevalence of PUD among dyspepsic patients
was 35% in which 72% were DU, 19% gastritis/doudenitis,
6% gastric mass & 4% pyloric obstruction (Assefa B,
Tadesse A, Abay Z. etal, 2021)
ī A study done in TASH, ABO B/G distribution of PUD pts.
was 19.04% , 19.04% , 11.11% and 50.79% for B/G A, B,
AB, and O, respectively.
(Teshome Y, Mekonen W, Birhanu Y, Sisay T, 2019)
What could be the reason? b/g O More risk?
2/9/2024 25
26. Causes of PUD
ī H. pylori infection,
ī Ingestion of NSAIDs most common
ī Increase acid & pepsin
ī Food habits (spicy food, smoking and
alcohol, poor in vitamins)
2/9/2024 26
27. Causes contâĻ
ī Psychogenic âAnxiety, worry (stimulation of vagus---
increase acid secretion)
ī Genetic ( eg B/Group O more risk)
ī Endocrinal
īŧ (ZES)Tumor of pancreases with hypergastrinaemia
īŧ Hyperparathyroidism (increase ca---increase parietal
cell----acid secretion)
Manipal manual of surgery
2/9/2024 27
28. Cause cont..
1. H. pylori infection
ī 90% of DU and 75% of GU are associated with H. pylori infection
ī The mechanisms of H. pyloriâinduced GI injury
1.Production of toxic products to cause local tissue injury
2. Induction of a local mucosal immune response(cytokines.. )
3. Increased gastrin levels with a resultant increase in acid
secretion
Sabiston Textbook of Surgery, 18th ed
2/9/2024 28
29. Cause contâĻ
2. NSAID
ī Common for GU by altering mucosal defense
ī Ulcerations is proportional to the daily dosage
ī In addition, complications increases with:
īŧ age older than 60,
īŧpatients having a prior GI event, or
īŧconcurrent use of steroids or anticoagulants.
Sabiston Textbook of Surgery, 18th ed
2/9/2024 29
34. Investigation of PUD
ī Hx and P/E
ī Esophagogastroduodenoscopy (EGD)-(gold standard)
ī Ultrasonography-- (less sensitive)
ī CT scanning
ī Helicobacter pylori testing:
īŧSerologic testing, Urea breath test, stool antigen test and
endoscopic biopsy for culture.
ī CBCâĻ
Bailey and Love's Short Practice of Surgery
2/9/2024 34
35. Treatment of peptic ulceration
1. Medical treatment:
ī H2-receptor antagonists (eg Cimetidine)
ī Proton pump inhibitor (Omeprazole)+
ī Eradication therapy(Clarithromycin+Amoxacillin/Metronidazol)
2. Surgical Rx (vagotomy or partial gastrectomy)
ī For DU: Billroth II gastrectomy (Gastrojejunostomy),
Vagotomy &drainage
ī For GU: Billroth I gastrectomy (gastroduodenostomy )
Bailey and Love's Short Practice of Surgery
2/9/2024 35
37. Indication of surgery for PUD
ī Fail to heal after 12 to 16 wks medical Rx
ī Life-threatening hemorrhage,
ī Perforation, or
īObstruction (GOO)
Brunner and Suddarthâs textbook of medical-
surgical nursing 12th edition
2/9/2024 37
38. Surgical Rx contâĻ
What is truncal vagotomy?
What are other types of vagotomy??
Brunner and Suddarthâs textbook of
medical-surgical nursing 12th edition
2/9/2024 38
41. Nursing management
ī Monitoring and managing potential complications
ī Advice about:
īŧ stress reduction, rest & D/c NSAIDs
īŧ Improve hygiene to prevent infection
īŧ Smoking cessation (how it prevent ?)
īŧ Dietary modification(decrease consumption of meat
extracts, alcohol, coffee, milk and cream.. )
ī Diet compatibility is an individual matter;
īŧ eat foods that are tolerated
īŧ avoid those that produce pain.
2/9/2024 41
42. Possible Nursing Dx for Pts. with PUD
ī Acute pain related to the effect of gastric acid
secretion on damaged tissue
īAnxiety related to an acute illness
īImbalanced nutrition related to changes in diet
ī Deficient knowledge about prevention of
symptoms and management of the condition
2/9/2024 42
43. Planning and Goals
īRelief of pain
īReduced anxiety
īMaintenance of nutritional requirements
īImprove knowledge about the management
and prevention of ulcer recurrence
ī Absence of complications.
2/9/2024 43
44. Nursing Interventions
īRelive pain
īŧby prescribed medications, avoid aspirin, foods
and beverages that contain caffeine.
īŧ Eat at regular intervals & relaxed setting
īReducing Anxiety
īŧGive appropriate information regarding dx&Rx.
īŧInteracts with pt. in a relaxed manner
īŧ Encouraged pt. to participate in care
īŧ provide emotional support
ī Advise pt to comply with Rx & dietary
restrictions.
2/9/2024 44
45. Complications PUD
īUpper GI bleeding
īGastric outlet obstruction/GOO
īPerforation (most in DU) (Teshome H, Birega M,
Taddese M. 2020)
īPenetration
īGastric cancer
Brunner and Suddarthâs 12th edition
2/9/2024 45
46. Complication of peptic ulcer surgery
īRecurrent ulceration
īSmall stomach syndrome
ī Bilious vomiting
ī Early and late dumping (if vagotomy)
īDiarrhoea and Steatorrhea
īMalignant transformation
Bailey and Love's Short Practice of Surgery
2/9/2024 46
47. Brain storming with real case senario
A 60 yrs female admitted in UGCSH after she present with:
īŧ Epigastric discomfort & burning sensation 3 months duration.
īŧ But no Hx of vomiting, loss of appitite, Wt loss, diarrhea
īŧ Had similar symptoms 2 yrs back & took different medications.
P/E:
īŧ G/A---well looking, V/S stable
īŧ HEENT---PC&NIS
īŧ LGS----1x1cm palpable, non-tender mobile supraclavicular LN
īŧ Abdomen---distended abdomen move with respiration
---tender epigastric area on palpation
2/9/2024 47
48. Investigations done:
1. Endoscopic insisional biopsy
īŧ Gross----------multiple grey white matter tissue 1.5 cmx 4
īŧ Microscopy---gastric surface epithelium with underlying
submucosal proliferation, no necrosis
2. OFT ( Cr-----0.5, Urea --29 , GOT---23, GPT----20)
3. Electrolyte---(Kâ3.83 , Naâ136.9, Clâ105.6 )
4. Serum albumin---4.4
5. CBC (WBCâ6.5, RBC---4.5, HCT---41.7, Plt ---305)
6. BG---B +ve
Discus 1. The Possible medical dx
2. Medical/surgical Rx 5 minute
3. Nursing dx and intervention
2/9/2024 48
49. Gastric neoplasm
Benign
ī Rare
ī Polyps
ī Leiomyoma
Malignant
ī >90%
ī Adenocarcinoma (>95%)
ī Lyhphoma(4%)
ī Leiomyosarcoma(1%)
ī Others
49
It is cells in the stomach grow out of control.
(GIST)
2/9/2024
50. Types of stomach adenocarcinomas:
Intestinal Diffused
Environmental Familial (Blood type A more)
Gastric atrophy, intestinal
metaplasia
Does not arise in gastritis
More common in men More Common women
Higher incidence with age Younger age group
Gland formation present Poorly differentiated, no gland
formation
Haematogenous spread Transmural extension &lymphatic
Better prognosis poor prognosis
Spread less slowly spread more quickly
More common less common
2/9/2024 50
51. Epidemiology
ī Gastric ca was the 4th most common & the 2nd cause of
death of all malignancies worldwide (Jemal A, Bray F,
Center MM. etal 2011)
ī The American Cancer Society estimated 26,560 cases of
stomach ca in 2021 (ACS, 2021)
ī Gastric ca is the 15th most common ca in US, > 11,000
death/year & higher incidence in men ( American Cancer
Institute 2021)
2/9/2024 51
52. Epidemiology contâĻ
ī Over 60% of the new gastric cancer cases are observed in
eastern Asia (most in Japan)
ī Currently, there is gastric ca screening in Japan, and Korea
for >=50 & >=40 years respectively.
(Sekiguchi M. Oda I. Matsuda T. etal , 2022)
ī In 2020, gastric ca was the 5th most common ca & the 4th
highest mortality rate ( table below) (Globocan, 2020)
ī Study in Black lion hospital showed gastric ca was most
prevalent in male. Of 96 patients 68 were males(with ratio of
M:F 2.4:1) (Johnson, Olivier, Ersumo, T. Ali, A. 2000)
2/9/2024 52
54. Risk factors gastric ca
ī Diet
īŧ high in smoked, salted, or
pickled foods
īŧ low in fruits & vegetables
(defi of antioxidants(Vit C.)
īŧLack of refrigeration
ī Achlorhydria/decre acid
ī Genetics( more B/G A)
ī Smoking
Bailey and Love's Short Practice of Surgery
2/9/2024 54
55. Risk factors cont..
ī Medical
īŧChronic
inflammation
īŧ H. pylori infection
īŧSubtotal gastrectomy
2nd PUD
īŧ GU, Gastric atrophy& gastritis
īŧ Adenomatous polyps
īŧ Pernicious anemia
ī Male gender
Bailey and Love's Short Practice of Surgery
2/9/2024 55
57. Clinical features and P/E
ī Features are obvious in advanced ca (muscular
mucosa & or serosa involvement +- L/node)
īŧEarly satiety, bloating, distension & vomiting
īŧ Bleeding (lead IDA)
īŧDysphagia, epigastric fullness
2/9/2024 57
58. Clinical features and P/E
On P/E
ī Palpable metastatic
L/nodes
ī Palpable mass
ī Epigastric tenderness
ī Heart burn
ī Loss of appetite
ī Weight loss
ī Feeling tired
ī Vomiting blood
Bailey and Love's Short Practice
of Surgery
2/9/2024 58
59. Diagnosis/Investigations
ī Imaging
īŧUS
īŧCT scan (check metastasis)
īŧ MRI
īŧEndoscopy to take biopsy
īŧEndoscopic ultrasound -stage
the tumor
ī Biopsy
ī Laboratory
īŧCBC (to identify anemia)
īŧElectrolyte
īŧLiver function tests
īŧTumor markers
2/9/2024 59
64. TNM staging contâĻ
Manipal manual of surgery
AJCC Cancer staging manual 6th edition
Other staging methods:
Reading assignment
2/9/2024 64
65. Treatment
ī Surgery (only curative option)
īŧEndoscopic sub-mucosal dissection( ESD)
īŧGastrectomy (partial or total) (resection)
īRadiation therapy
īChemotherapy
īThese treatments are generally combined.
What is the difference b/n
Neoadjuvant & adjuvant Therapy (2mi)
2/9/2024 65
66. Prevention gastric ca
īEating a healthy diet
īŧ high in fruits and vegetables
īŧ low in red meats, smoked, salted, pickled
foods
īMaintain a healthy weight
īAvoid smoking
2/9/2024 66
67. Possible nursing dx for gastric ca
ī Anxiety related to the disease and anticipated Rx
ī Imbalanced nutrition, less than body requirements,
related to early satiety or anorexia
ī Pain related to tumor mass
ī Anticipatory grieving related to the diagnosis of ca
ī Deficient knowledge regarding self-care activities
2/9/2024 67
68. Planning and Goals
ī Reduced anxiety
ī Optimal nutrition
ī Relief of pain
ī Anticipated lifestyle changes
2/9/2024 68
69. Nursing Interventions
Reducing Anxiety
īŧ Make relaxed atmosphere
īŧ Encourages the family to
support the patient.
īŧ Advises the pt about any
procedures & Rx
Promoting optimal nutrition
īŧ Small, frequent nonirritating
foods
īŧ high in calories, vit A & C &
Fe to repair tissue
īŧ Vit B12 if total gastrectomy
īŧ Note metabolic
abnormalities (Na, K,
glucose,BUN)
īŧ Antiemetics if prescribed
2/9/2024 69
70. Nursing Interventions contâĻ
Relieving Pain
ī Administers analgesic.
ī Assesses frequency,
intensity &duration pain
ī position changes,
imagery, distraction &
relaxation exercises
Providing psychosocial support
īŧ Encourage to express fears,
concerns, and grief about dx.
īŧ Answer the ptâs questions
honestly
īŧ Encourage pt. to participate in
Rx decisions.
īŧ Offers emotional support and
involve family
2/9/2024 70
71. Reference
Salari, N., Darvishi, N., Shohaimi, S. et al. The Global
Prevalence of Peptic Ulcer in the World: a Systematic
Review and Meta-analysis. Indian J Surg (2021).
Ray-Offor E, Opusunju KA. Current status of peptic ulcer
disease in Port Harcourt metropolis, Nigeria. African Health
Sciences. 2020 Oct 7;20(3):1446-51.
Assefa B, Tadesse A, Abay Z, Abebe A, Tesfaye T, Tadesse M,
Lakew AM. Prevalence of Peptic Ulcer Disease and
Associated Factors Among Dyspeptic Patients At Endoscopy
Unit, University of Gondar Hospital, Northwest Ethiopia.
Teshome Y, Mekonen W, Birhanu Y, Sisay T. The association
between ABO blood group distribution and peptic ulcer
disease: a cross-sectional study from Ethiopia. Journal of
blood medicine. 2019;10:193.
2/9/2024 71
72. Reference contâĻ
Bailey and Love's Short Practice of Surgery
Manipal manual of surgery
Sabiston Textbook of Surgery, 18th ed.
Brunner and Suddarthâs textbook of medical-surgical nursing 12th
edition
Schwartz's Principles of Surgery 8th edition
Jemal A, Bray F, Center MM, Ferlay J, Ward E, Forman D. Global
cancer statistics. CA Cancer J Clin. 2011;61(2):69â90.
2/9/2024 72
73. Reference contâĻ
Teshome H, Birega M, Taddese M. Perforated Peptic Ulcer
Disease in a Tertiary Hospital, Addis Ababa, Ethiopia:
Five Year Retrospective Study. Ethiop J Health Sci. 2020
May;30(3):363-370.
American Cancer Society. Key statistics about stomach
cancer. American Cancer Society. January 22, 2021;
Surveillance, Epidemiology, and End Results Program.
SEER Stat Fact Sheets: Stomach Cancer. National Cancer
Institute. Available
at http://seer.cancer.gov/statfacts/html/stomach.html
Sekiguchi M. Oda I. Matsuda T. etal epidemiological trends
and future perspectives of gastric cancer in Eastern Asia,
2022, Vol.103
2/9/2024 73
The first 3 parts make up the proximal stomach:
Cardia:Â the first part, which is closest to the esophagus
Fundus:Â the upper part of the stomach next to the cardia
Body (corpus):Â the main part of the stomach, between the upper and lower parts
The lower 2 parts make up the distal stomach:
Antrum:Â the lower portion (near the small intestine), where the food mixes with gastric juice
Pylorus:Â the last part of the stomach, which acts as a valve to control the emptying of the stomach contents into the small intestine
2 openings
Gastroesophageal- to esophagus
Pyloroduodenal - to the duodenum
Sphincters
Cardiac
Pyloric
B/supply of stomach is by coeliac trunk and its branches.
What is coeliac trunk?
Celiac Artery
The celiac artery, also called the celiac trunk orceliac axis, is the first major visceral branch of the abdominal aorta.
It arises from the anterior aortic surface, between the diaphragmatic crura. It then bifurcates about 1 to 3â¯cm from its origin into the common hepatic and splenic arteries. The celiac artery also gives rise to the left gastric artery.
1.Lt gastric @----Direct branch of coeliac trunk and supplies (anterior &posterior wall of stomach)
2.Rt gastric @----Branch of hepatic artery and supplies lessure curvature and body of stomach.
3. Lt Gastric epipolic @----arise from splenic artery and supply greater curvature
4. Rt gastric epioplic @----branch of gastrododunal a w/h is branch of hepatic artery
5. Short gastric @--------branch of spleenic a and supply fundus
Innervation:
Parasympathetic via the vagus.
Left anterior and right posterior.
Sympathetic via the celiac plexus.
Intrinsic enteric neurons and by extrinsic projections, including sympathetic and parasympathetic efferents as well as visceral afferents, all of which are compromised by age to different degrees.
Gastric innervation :
parasympathetic via the vagus (motor and secretory) and
sympathetic via Meissner's and Auerbach's plexus.
Gastric cancers drain into any of these groups regardless of location of the tumor.
Thoracic duct ---drain lymph from:
lower limbs
abdomen
left upper limb
lt hemithorax
left side of face and neck
Somatostatin is able to
1. directly inhibit parietal cell acid secretion but
2. indirectly inhibit acid secretion through inhibition of gastrin release and down-regulation of histamine release from ECL cells. The principal stimulus for somatostatin release is antral acidification, whereas acetylcholine from vagal fibers inhibits its release.
H. pylori causes a decrease in antral D cells with a resultant decrease in somatostatin levels. The reduction in somatostatin causes disinhibition of antral G cells, leading to increased gastrin release which in turn leads to an increase in gastric acid secretion
Histamine plays a prominent role in parietal cell stimulation. Administration of H2-receptor antagonists almost completely abolishes gastric acid secretion in response to both gastrin and acetylcholine.
Ghrelin:
appears to be under endocrine and metabolic control, has a diurnal rhythm, likely plays a major role in the neuroendocrine and metabolic response to changes in nutritional status, and may be a major anabolic hormone. Ghrelin displays a strong growth hormoneâreleasing action that is mediated by the activation of growth hormone secretagogue receptor type 1a
may contribute to the physiologic control of insulin and glucagon release
Intrinsic factor is a mucoprotein secreted by the parietal cell that is essential for the absorption of vitamin B12 in the terminal ileum
Intrinsic factor deficiency lead pernicious anemia or in patients undergoing total gastrectomy, and both groups of patients require vitamin B12 supplementation.
Gastrin is the major hormonal regulator of the gastric phase of acid secretion following a meal
(ECL) cellâ entero chromaffin-like Cell
ingestion of a meal stimulates vagal fibers to release acetylcholine (cephalic phase).
Binding of acetylcholine to M3 receptors located on the ECL cell, parietal cell, and G cell results in the release of histamine, hydrochloric acid, and gastrin, respectively.
Binding of acetylcholine to M3 receptors on D cells results in the inhibition of somatostatin release.
Following a meal, G cells are also stimulated to release gastrin, which interacts with receptors located on ECL cells and parietal cells to cause the release of histamine and hydrochloric acid (gastric phase).
Release of somatostatin from D cells decreases histamine release and gastrin release from ECL cells and G cells, respectively. In addition, somatostatin inhibits parietal cell acid secretion (not shown). The principal stimulus for activation of D cells is antral luminal acidification (not shown).
Three phases of the acid secretory response to a meal have been described: cephalic, gastric, and intestinal. These three phases are interrelated and occur concurrently not consecutively.
The cephalic phase originates with the sight, smell, thought, or taste of food, which stimulates neural centers in the cortex and hypothalamus
The gastric phase of acid secretion begins when food enters the gastric lumen. Digestion products of ingested food interact with microvilli of antral G cells to stimulate gastrin release. Food also stimulates acid secretion by causing mechanical distention of the stomach
The intestinal phase of gastric secretion remains poorly understood but appears to be initiated by entry of chyme into the small intestine. It occurs after gastric emptying and lasts as long as partially digested food components remain within th1/27/2022proximal small bowel.
H ion exported from parietal cells via proton pump when histamine act on H2 receptors(most).
So, PPIs abolish HCL secretion.
Gastric acid secretion
The secretion of gastric acid and pepsin tends to run in parallel, although the understanding of the mechanisms of gastric acid
secretion is considerably greater than that of pepsin. Numerous factors are involved in gastric acid production. These include
neurotransmitters, neuropeptides and peptide hormones, and several other factors.
Maximal acid output (MAO) is obtained by averaging the output of the two final 15-minute periods. Peak acid output is the highest rate of secretion obtained during a 15-minute period following secretogogue stimulation. Basal acid output (BAO) is generally about 2 to 3 mEq/hour, and MAO is in the range of 10 to 15 mEq/hour.
acid and pepsin (a digestive enzyme), which combine to make the gastric juice that helps digest food
What part of stomach is the most common for :
Gasritis, Ulcer and ca===Pyloric antrum( manipal manual of surgery)
It is one of the most prevalent and costly GI diseases
The term âpepticâ comes from the hormone pepsin which plays an important role in causing mucosal break.
Peptic ulcer (PU) bleeding is the most common cause of upper gastrointestinal bleeding in the western world [2] and results in significant morbidity, mortality, and healthcare costs [3].
PUD is a benign condition, is easily treatable by medical therapy, and rarely requires surgery.
PUD is a benign condition, is easily treatable by medical therapy, and rarely requires surgery
Gastric Ulcer Pathophysiology
Gastric ulcers can occur anywhere in the stomach, although they usually present on the lesser curvature near the incisura, as shown in Figure 47-10 .
About 60% of ulcers are located in this location and are classified as type I gastric ulcers. These ulcers generally are not associated with excessive acid secretion and may in fact have low to normal acid output. Most occur within 1.5 cm of the histologic transition zone between the fundic and antral mucosa and are not associated with duodenal, pyloric, or prepyloric mucosal abnormalities.
In contrast, type II gastric ulcers (âŧ15%) are located in the body of the stomach in combination with a duodenal ulcer. These types of ulcers usually are associated with excess acid secretion.
Type III gastric ulcers are prepyloric ulcers and account for about 20% of the lesions. These ulcers also behave like duodenal ulcers and are associated with hypersecretion of gastric acid.
Type IV gastric ulcers occur high on the lesser curvature near the gastroesophageal junction. The incidence of type IV gastric ulcers is less than 10%, and they are not associated with excessive acid secretion.
Finally, some ulcers may appear on the greater curvature of the stomach, but the incidence is less than 5%.
PUD have decreased with the universal use of acid suppressant therapy and decrease in prevalence of Helicobacter pylori infection due to improved socioeconomic status and eradication of H. pylori infection after detection .
prevalence of PUD in the world in age range of 17â82Â years was 8.4% (95% CI 5â13.7)
The findings of this study revealed a higher prevalence of PUD among patient with O blood group than other group types.
It can be explained that this is because of the carbohydrate antigens that contributed to the susceptibility or resistance to infectious diseases.
Especially, the H antigen of blood group O expressed in the gastric mucous membrane is suitable to the attachment of Helicobacter pylori bacillus which is identified to be the major cause of PUD.
Pepsin is a stomach enzyme that serves to digest proteins found in ingested food.
Gastric chief cells secrete pepsin as an inactive zymogen called pepsinogen.
Parietal cells within the stomach lining secrete hydrochloric acid that lowers the pH of the stomach
A gastrinÂproducing endocrine tumor causes ZollingerÂEllison syndrome.
It usually arises from the pancreas or duodenum. It results in multiple ulcers in the duodenum and jejunum. It can be diagnosed by measuring serum gastrin levels.
H. pylori is known to cause a local inflammatory reaction in the gastric mucosa and to produce chemotactic factors that attract neutrophils and monocytes.
Activated monocytes and neutrophils, in turn, produce a number of proinflammatory cytokines and reactive oxygen metabolites.
It is now recognized that most cases of histologic gastritis are due to H. pylori infection. Even 25% of the patients with an NSAID-associated ulcer have evidence of a histologic antral gastritis, as opposed to 95% of those with nonâNSAID-associated ulcers. In most cases, the infection tends to be confined initially to the antrum and results in antral inflammation
it is noteworthy that rapid healing follows antacid therapy, antisecretory therapy, or vagotomy, even when the lesion-bearing portion of the stomach is left intact because, in the presence of gastric mucosal damage, acid is ulcerogenic even when present in normal or less than normal amounts.
In comparison to
H. pylori ulcers, which are more frequently found in the duodenum,
NSAID-induced ulcers are more frequently found in the stomach.
H. pylori ulcers are also nearly always associated with chronic active gastritis,
whereas gastritis is not frequently found with an NSAID-induced ulcer, occurring about 25% of the time.
In addition, when NSAID use is discontinued, the ulcers usually do not recur, whereas with H. pyloriârelated ulcers, there is a 50% to 80% recurrence rate in 1 year unless the organism is eradicated.
The mechanism of occurrence of PUD results from an imbalance between gastric mucosal protective and destructive factors
prostaglandins are lipid autacoids derived from arachidonic acid. They both sustain homeostatic functions and mediate pathogenic mechanisms, including the inflammatory response.
prostaglandins (inhibit gastric secresion, stimulate bicarbonate secresion and blood flow===defense pud)
When we think about the pathogenesis of PUD, we must consider two factors:
Mucosal protective factors: gastric mucus layer, prostaglandin, bicarbonate, and mucosal blood flow.
Mucosal damaging factors: gastric acidity, pepsin, H. pylori infection, and NSAIDs.
PU occurs when there is an imbalance between these factors
ABDOMENAL EXAM
Exposure of the abdomen from the xiphoid process to the mid thigh; covering the genitalia
Monitor your examination by watching the ptâs face for any sign of discomfort
ORDER =Inspection---Auscultation---percussion---palpation
Is it abdominal wall swelling or intra-abdominal swelling?
Feel the swelling while the pt lifts her/his head and shoulders off the pillow to tense the abdominal wall
Prominently protruded swelling with above maneuver indicates abdominal wall mass,
where as the swelling disappears in intra abdominal mass.
Size and shape
Determine length, width and depth of the abdominal swelling.
Characterize the surface, edge and consistency of the abdominal swelling.
. Hard, nodular, irregular in outline mass is more likely to be malignancy
. Solid, tender, ill-defined mass is more likely to be inflammatory
. Regular, round, smooth, tense swelling is more likely to be cystic.
Mobility and attachment
Swelling arising from the liver, spleen, kidneys, gall bladder and stomach moves down ward during inspiration
Swelling arising from the small bowel, transverse colon, mesentery and greater omentum are not usually influenced by respiratory movement
Gastroesophageal reflux disease (GERD) - patients usually describe a burning sensation in the epigastrium and lower retrosternal area, excessive salivation, or intermittent regurgitation of food material.
Gastric cancer -Â apart from abdominal pain, patients usually describe alarm symptoms like weight loss, melena, recurrent vomiting, or evidence of malignancy elsewhere in case of metastasis.
Pancreatitis - epigastric or right upper quadrant pain that is more persistent and severe, worse in the supine position, and patients usually have a history of alcoholism or gallstones.[10]Â Elevated serum amylase and lipase are useful in the diagnosis.
Biliary colic - intermittent, severe deep pain in the right upper quadrant or epigastrium precipitated by fatty meals.
Cholecystitis - right upper quadrant or epigastric pain that usually lasts for hours and is exacerbated by fatty meals and is associated with nausea and vomiting. Fever, tachycardia, positive Murphy sign, leukocytosis, and abnormal liver functions help further distinguish this from biliary colic.[
Diagnosis of PUD requires history taking, physical examination, and invasive/noninvasive medical tests.
A physical exam may reveal epigastric abdominal tenderness and signs of anemia
Prostaglandin analogs (misoprostol) are sometimes used as prophylaxis for NSAID-induced peptic ulcers
Vagotomy, with or without pyloroplasty (transecting nerves that stimulate acid secretion and opening the pylorus), and
antrectomy, which is removal of the pyloric (antrum) portion of the stomach with anastomosis (surgical connection) to either the duodenum (gastroduodenostomy or Billroth I) or jejunum (gastrojejunostomy or Billroth II)
AntiÂsecretory drugs used for PUD include H2Âreceptor antagonists and the proton pump inhibitor (PPIs).
PPIs have their superior healing and efficacy
PPIs block acid production in the stomach providing relief of symptoms and promote healing
Treatment may be incorporated with calcium supplements as longÂterm use of the PPIs can increase the risk of bone fractures.
NSAIDs induced PUD can be treated by stopping the use of NSAIDs or switching to a lower dose.
Corticosteroid, bisphosphonates, and anticoagulants should also be discontinued if possible.
Prostaglandin analogs (misoprostol) are sometimes used as prophylaxis for NSAIDÂinduced peptic ulcers.
Pantoprazole, clarithromycin, and metronidazole or amoxicillin are used for 7 to 14 days. [6]
Antibiotics and PPIs work synergistically to eradicate H. pylori.[7]
Misoprostol and sucralfate are mucosal cytoprotective agents. Misoprostol is a synthetic analogue of prostaglandin E which is trophic to gastroduodenal mucosa, stimulates mucus and bicarbonate secretion from the gastroduodenal mucosa, and can form hydrophobic surfactant-like phospholipids in the gastric epithelial cells [50]. Misoprostol can also inhibit gastric acid secretion by suppressing histamine-stimulated cyclic AMP production but does not induce hypergastrinemia [51]. Misoprostol can heal both gastric and duodenal ulcers. Misoprostol 200 microgram four times a day should be given for 12 weeks
. Misoprostol is contraindicated in pregnant patients.
Vagotomy---Severing of the vagus nerve.
Decreases gastric acid by diminishing cholinergic stimulation to the parietal cells, making them less responsive to gastrin. May be performed via open surgical approach, laparoscopy, or thoracoscopy
Truncal vagotomy--Severs the right and left vagus nerves as they enter the stomach at the distal part of the esophagus
Selective vagotomy---Severs vagal innervation to the stomach but maintains innervation to the rest of the abdominal organs
Proximal (parietal cell) gastric vagotomy without drainageâDenervates acid-secreting parietal cells but preserves vagal innervation to the gastric antrum and pylorus
Pyloroplasty----Longitudinal incision is made into the pylorus and transversely sutured closed to enlarge the outlet and relax the muscle
What is the indication for Billorth I and II?
Billorth II when ulcer is on lessure curvature while Billorth I isâĻ.?
Total gastrectomies are best served with a Roux-en-Y anastamosis.
Prognosis The prognosis of PUD is excellent after the underlying cause is successfully treated.
Recurrence of the ulcer may be prevented by maintaining good hygiene and avoiding alcohol, smoking, and NSAIDs.
Studies have shown that smoking decreases the secretion of bicarbonate from the pancreas into the duodenum, resulting in increased acidity of the duodenum.
Research indicates that continued smoking may significantly inhibit ulcer repair (Suzuki, et al., 2006). Therefore, the patient is strongly encouraged to stop smoking.
When the ulcer crater erodes through the gastric wall or intestinal wall into the surrounding structure but there is no free perforation or leakage of luminal contents into the peritoneal cavity, it is called penetration.
The pancreas is the commonest site of penetration. Others omentum, biliary tract, liver, colon, mesocolon, and blood vessels.
Patients may notice change in pattern of abdominal pain, i.e., pain not being relieved by taking food or medication.
Diagnosis is confirmed by CT with contrast which may show loss of fascial plane between the gastric wall or intestinal wall and the surrounding structure, band of soft tissue density between them, ulcer crater, sinus tract, and enlargement of head of the pancreas in case of penetration into the pancreas . Treatment is surgical intervention.
It occurs in less than 5% cases of PUD. Duodenal ulcer and pyloric channel ulcer are generally associated with GOO
Dumping syndrome is an unpleasant set of vasomotor and GI symptoms that sometimes occur in patients who have had gastric surgery or a form of vagotomy.
Early symptoms include a sensation of fullness, weakness, faintness, dizziness, palpitations, diaphoresis, cramping pains, and diarrhea. These symptoms resolve once the intestine has been evacuated.
Later, there is a rapid, followed by increased insulin secretion. This results in a reactive hypoglycemia, which also is unpleasant for the patient. Vasoelevation of blood glucosemotor symptoms that occur 10 to 90 minutes after eating are pallor, perspiration, palpitations, headache, and feelings of warmth, dizziness, and even drowsiness. Anorexia may also be a result of the dumping syndrome, because the person may be reluctant to eat
Leiomyosarcoma (LMS) is a rare cancer that starts in smooth muscles that line organs like your stomach, bladder, and intestines.
Leiomyoma-arises from smooth muscles of the stomach,difficult to distinguish from GIST,large protruding lesions with central ulcer,presents with bleeding,Treatment-local excision
What is adenocarcinoma?
Gastri intestinal stormal tumors (GIST)
The intestinal type tends to have a slightly better prognosis (outlook). The cancer cells are more likely to have certain gene changes that might allow for treatment with targeted drug therapy.
The diffuse type tends to grow spread more quickly. It is less common than the intestinal type, and it tends to be harder to treat.
Once the second most common cancer worldwide, stomach cancer has dropped to sixth place, after cancers of the lung, breast, prostate, colon and rectum, and skin
Pathophysiolgy of gastric ca
Palpable metastatic lymph nodes ( eg Lt supraclavicular fossa)
Early gastric ca---limited to mucosa and sub mucosa of stomach regardless of lymph not involvement
advanced ca (muscular mucosa & or serosa involvement +- L/node)
If CT scan is negative, then laparoscopy is recommended as the next step in evaluation.
Several different tests can be used to help diagnose stomach cancer.
Radiologic tests like a CT scan, barium swallow and MRI can help identify a problem in the stomach if the tumor is large enough.
An upper endoscopy is used to take a biopsy (sample) of the lesion to make the diagnosis or to detect early cancer before a mass is large enough to be seen on radiologic tests. An upper endoscopy is performed by inserting a thin tube with a tiny camera through the mouth and into the stomach, where biopsies are obtained from the tumor.
To find out how much of the stomach wall a tumor involves and to help assess the âstageâ of the cancer, a doctor will order an endoscopic ultrasound, which uses a special type of endoscope that has an ultrasound probe. The endoscope is placed in the stomach through the mouth. The ultrasound probe is able to look through the surface of the stomach lining to the stomach wall beyond and see how much of the stomach is involved by the tumor.
Diagnosis
Testing
The goal of obtaining laboratory studies is to assist in determining optimal therapy. Potentially useful tests in patients with suspected gastric cancer include the following:
CBC: May be helpful to identify anemia, which may be caused by bleeding, liver dysfunction, or poor nutrition; approximately 30% of patients have anemia
Electrolyte panels
Liver function tests
Tumor markers such as CEA and CA 19-9: Elevated CEA in 45-50% of cases; elevated CA 19-9 in about 20% of cases
Imaging studies
Imaging studies that aid in the diagnosis of gastric cancer in patients in whom the disease is suggested clinically include the following:
Esophagogastroduodenoscopy (EGD): To evaluate gastric wall and lymph node involvement
Double-contrast upper GI series and barium swallows: May be helpful in delineating the extent of disease when obstructive symptoms are present or when bulky proximal tumors prevent passage of the endoscope to examine the stomach distal to an obstruction
Chest radiography: To evaluate for metastatic lesions
CT scanning or MRI of the chest, abdomen, and pelvis: To assess the local disease process and evaluate potential areas of spread
Endoscopic ultrasonography (EUS): Staging tool for more precise preoperative assessment of the tumor stage
Biopsy
Biopsy of any ulcerated lesion should include at least six specimens taken from around the lesion because of variable malignant transformation. In selected cases, endoscopic ultrasonography may be helpful in assessing depth of penetration of the tumor or involvement of adjacent structures.
Carcinoma stomach with large ulcerative lesion with involvement of serosa
n the early stages when the cancer is limited to the superficial (uppermost) layers of the stomach, the cancer can be removed through an upper endoscopy performed by a gastroenterologist. In this procedure (endoscopic submucosal dissection, or ESD), the tumor is dissected from the rest of the gastric wall and removed through the mouth.
Once the tumor invades beyond the superficial layers of the stomach, surgery will be required to remove the stomach and connect the esophagus (the tube through which food passes) to the small intestines to allow for digestion.
Radiation therapy uses high-powered beams of energy to kill cancer cells. Chemotherapy uses chemicals to kill the cancer cells. These treatments are generally combined.
Neoadjuvant Therapy (before surgery) while adjuvant after surgery
Radiation alone
Chemotherapy alone
Combined chemoradiation therapy
Aggressive resection of gastric cancer is justified in the absence of distant metastatic spread.
The surgery is tailored mainly to the location of the tumor and known pattern of spread.
R0 resection should be achieved, with a minimum of 6cm margins from gross tumor.
R0 â tumor free margins
R1 â microscopic disease
R2 â gross tumor at margins
Minimum of 15 nodes should be removed.
Tumors in the cardia and proximal stomach account for 35-50% of gastric adenocarcinomas. For these tumors a total gastrectomy should be performed, as opposed to proximal gastric resection which is associated with higher morbidity and mortality rates. Distal tumors may be removed by distal gastrectomy as long as adequate margins are achieved.
Open gastrectomy with lymph node dissection â at least D1 â is the current operative standard.
Laparoscopic gastrectomy has been shown to be safe with similar survival for patients with distal cancer
Yearly endoscopy should be performed for subtotal gastrectomies