STOMACH Flashcards
(188 cards)
1
Q
Q: What percentage of people worldwide are infected with Helicobacter pylori?
A
A: Over 50%.
2
Q
Q: Is Helicobacter pylori infection a chronic disease?
A
A: Yes, it does not resolve spontaneously without specific treatment.
3
Q
Q: What percentage of gastritis is accounted for by H pylori–induced gastritis?
A
A: 80% to 90%.
4
Q
Q: What is the most important risk factor for peptic ulcer and gastric adenocarcinoma?
A
A: Chronic gastritis associated with H pylori.
5
Q
Q: What effect does successful H pylori treatment have on peptic ulcers?
A
A: It largely eliminates recurrent peptic ulcers in infected patients.
6
Q
Q: What would be the impact of eradicating H pylori worldwide?
A
A: It would eliminate most cases of gastric adenocarcinoma.
7
Q
Q: What other conditions are associated with Helicobacter pylori infection?
A
A: MALT lymphoma, dyspepsia, hyperplastic gastric polyps, and immune thrombocytopenic purpura.
8
Q
Q: What type of Helicobacter strains are nonpathogenic?
A
A: Strains that lack either flagella or urease.
9
Q
Q: What is the first step in the pathogenesis of Helicobacter infection?
A
A: Survival in the acidic gastric lumen.
10
Q
Q: How does Helicobacter move across the mucus layer?
A
A: Through flagellated movement.
11
Q
Q: What is the role of cytoplasmic urease in Helicobacter?
A
A: It converts periplasmic urea into CO2 and ammonia, buffering the surrounding acid.
12
Q
Q: Does H pylori invade the surface epithelial cell layer?
A
A: No, it triggers a host immune response by attaching to gastric epithelial cells.
13
Q
Q: What are important Helicobacter adhesins?
A
A: Neutrophil activating protein A, heat shock protein 60, and sialic acid–binding adhesin.
14
Q
Q: Name two toxins produced by Helicobacter.
A
A: Vacuolating cytotoxin A and cag A (cytotoxin-associated gene A).
15
Q
Q: What characterizes the initial inflammatory response to Helicobacter infection?
A
A: Recruitment of neutrophils, followed by T and B lymphocytes, plasma cells, and macrophages.
16
Q
Q: What cytokine-related changes occur in chronic gastric inflammation due to Helicobacter?
A
A: Enhanced mucosal expression of multiple cytokines and presence of reactive oxygen and nitrogen species.
17
Q
Q: What long-term effects are associated with Helicobacter infection?
A
A: Mucosal cell DNA damage, chromosomal instability, and increased apoptosis.
18
Q
Q: What is the net effect of Helicobacter infection on mucosal defenses?
A
A: Weakening of mucosal defenses.
19
Q
Q: What is a current research focus regarding Helicobacter?
A
A: The mechanism by which it avoids recognition and destruction by the mucosal immune system.
20
Q
Q: What is the major cause of peptic ulceration?
A
A: H pylori infection.
21
Q
Q: How much more likely are patients with H pylori infection and antral gastritis to develop PUD?
A
A: Three and one-half times more likely.
22
Q
Q: What percentage of patients with duodenal ulcers have H pylori infection?
A
A: Up to 90%.
23
Q
Q: What percentage of patients with gastric ulcers have H pylori infection?
A
A: At least 70%.
24
Q
Q: What effect does curing H pylori infection have on the natural history of PUD?
A
A: It dramatically decreases the recurrent ulcer rate.
25
Q: What is the recurrent ulcer rate for patients treated with acid-suppressive therapy alone?
A: More than 75%.
26
Q: What is the recurrent ulcer rate for patients treated with antibacterial therapy?
A: Less than 20%.
27
Q: What are the mechanisms related to decreased antral somatostatin synthesis and release?
A: (a) Antral alkalinization due to Helicobacter urease, (b) toxic cytokine effect on antral D cells, (c) Helicobacter production of N-α-methylhistamine.
28
Q: How does acid in the antrum affect somatostatin release?
A: Acid in the antrum releases somatostatin.
29
Q: What leads to hypergastrinemia in H pylori infection?
A: The gastritis does not involve the oxyntic mucosa, leading to parietal cell hyperplasia.
30
Q: What is thought to result from acid hypersecretion and antral gastritis?
A: Antral epithelial metaplasia in the postpyloric duodenum.
31
Q: How does duodenal metaplasia relate to H pylori?
A: It allows H pylori to colonize the duodenal mucosa, where duodenal ulcers occur.
32
Q: What is the increased risk of developing a duodenal ulcer in patients with gastric metaplasia of the duodenum?
A: 50-fold increase.
33
Q: What happens when H pylori colonizes the duodenum?
A: A significant decrease in acid-stimulated duodenal bicarbonate release.
34
Q: What tends to happen to acid secretory physiology after successful H pylori treatment?
A: It tends to normalize.
35
Q: What may relapse of duodenal ulcer after H pylori eradication signal?
A: Reinfection of the gastric mucosa by the organism.
36
Q: What are peptic ulcers?
A: Focal defects in the gastric or duodenal mucosa that extend into the submucosa or deeper.
37
Q: How can peptic ulcers be classified?
A: They may be acute or chronic.
38
Q: What ultimately causes peptic ulcers?
A: An imbalance between mucosal defenses and acid/peptic injury.
39
Q: What is important for optimal ulcer healing?
A: Elimination of H pylori infection or NSAID use.
40
Q: Why is eliminating H pylori or NSAID use important?
A: It is crucial for preventing ulcer recurrence and/or complications.
41
Q: What are some diseases known to cause peptic ulcers?
A: Zollinger-Ellison syndrome (gastrinoma), antral G-cell hyperfunction and/or hyperplasia, systemic mastocytosis, trauma, burns, and major physiologic stress.
42
Q: What drugs are known to cause peptic ulcers?
A: All NSAIDs, aspirin, and cocaine.
43
Q: What lifestyle factors contribute to peptic ulcers?
A: Smoking and psychological stress.
44
Q: What percentage of serious peptic ulcer complications in the U.S. can be attributed to H pylori, NSAID use, and smoking?
A: Probably more than 90%.
45
Q: How variable is acid secretion in patients with gastric ulcers?
A: Acid secretion is variable.
46
Q: How many types of gastric ulcers are currently described?
A: Five types.
47
Q: What is the location of Johnson type I gastric ulcer?
A: Near the angularis incisura on the lesser curvature, close to the border between antral and corpus mucosa.
48
Q: What is the acid secretion status in patients with type I gastric ulcer?
A: Usually normal or decreased.
49
Q: What is type II gastric ulcer associated with?
A: Active or quiescent duodenal ulcer disease.
50
Q: What is type III gastric ulcer known as?
A: Prepyloric ulcer disease.
51
Q: What is the acid secretion status in type II and type III gastric ulcers?
A: Normal or increased.
52
Q: How are type II and type III gastric ulcers treated surgically?
A: Similar to duodenal ulcers.
53
Q: Where do type IV gastric ulcers occur?
A: Near the gastroesophageal junction.
54
Q: What is the acid secretion status in type IV gastric ulcers?
A: Normal or below normal.
55
Q: What are type V gastric ulcers caused by?
A: Medication-induced, occurring anywhere in the stomach.
56
Q: How much does chronic use of NSAIDs increase the risk of peptic ulcer disease?
A: About fivefold.
57
Q: How much does chronic use of NSAIDs increase the risk of upper GI bleeding?
A: At least twofold.
58
Q: What factors increase the risk for NSAID-induced GI complications?
A: Age >60, prior GI event, high NSAID dose, concurrent steroid intake, and concurrent anticoagulant intake.
59
Q: How much more likely are smokers to develop peptic ulcer disease (PUD) compared to nonsmokers?
A: About twice as likely.
60
Q: How does smoking affect gastric acid secretion?
A: It increases gastric acid secretion.
61
Q: What effect does smoking have on duodenogastric reflux?
A: It increases duodenogastric reflux.
62
Q: What happens to gastroduodenal prostaglandin production due to smoking?
A: It decreases.
63
Q: How does smoking affect pancreaticoduodenal bicarbonate production?
A: It decreases.
64
Q: What could explain the association between smoking and PUD?
A: The effects of smoking on gastric acid secretion, duodenogastric reflux, and prostaglandin and bicarbonate production.
65
Q: What is the most common complaint of patients with peptic ulcer disease (PUD)?
A: Abdominal pain.
66
Q: Describe the typical characteristics of the pain in PUD.
A: Nonradiating, burning in quality, located in the epigastrium.
67
Q: When do patients with duodenal ulcers typically experience pain?
A: 2 to 3 hours after a meal and at night.
68
Q: What percentage of patients with duodenal ulcers experience pain that awakens them at night?
A: Two-thirds.
69
Q: How does the pain of gastric ulcers differ from that of duodenal ulcers?
A: Gastric ulcer pain more commonly occurs with eating and is less likely to awaken the patient at night.
70
Q: What history suggests a diagnosis of PUD?
A: A history of PUD, use of NSAIDs, over-the-counter antacids, or antisecretory drugs.
71
Q: What are other signs and symptoms of PUD?
A: Nausea, bloating, weight loss, stool positive for occult blood, and anemia.
72
Q: How does the prevalence of duodenal ulcers compare between men and women?
A: Duodenal ulcer is about twice as common in men compared to women.
73
Q: Is the incidence of gastric ulcer similar in men and women?
A: Yes, it is similar.
74
Q: On average, how do the ages of gastric ulcer patients compare to those of duodenal ulcer patients?
A: Gastric ulcer patients are older than duodenal ulcer patients.
75
Q: What trend is observed regarding the incidence of gastric ulcers in the elderly?
A: The incidence is increasing, possibly due to increasing NSAID and aspirin use.
76
Q: What are the three most common complications of peptic ulcer disease (PUD)?
A: Bleeding, perforation, and obstruction.
77
Q: In what order of frequency do these complications occur?
A: In decreasing order: bleeding, perforation, obstruction.
78
Q: What percentage of patients with bleeding peptic ulcer stop bleeding with acid suppression and nothing by mouth?
A: Three-fourths.
79
Q: What percentage of patients continue to bleed or rebleed after an initial quiescent period?
A: One fourth.
80
Q: What defines the high-risk group for rebleeding?
A: Shock, hematemesis, transfusion requirement exceeding four units in 24 hours, and certain endoscopic stigmata (active bleeding or visible vessel).
81
Q: What are the maximal scores for the Blatchford and Rockall scoring systems?
A: Maximal Blatchford score is 23; maximal Rockall score is 11.
82
Q: What Blatchford or Rockall scores indicate very low risk of life-threatening upper GI bleeding?
A: Blatchford score of 1 or less; Rockall score of 2 or less.
83
Q: What is the role of endoscopic therapy in high-risk patients?
A: It benefits high-risk patients to stop the bleeding.
84
Q: What are common endoscopic hemostatic modalities?
A: Injection with epinephrine and electrocautery.
85
Q: When should surgery be considered after endoscopic failures?
A: After two endoscopic failures.
86
Q: How does perforated peptic ulcer typically present?
A: As an acute abdomen with excruciating abdominal pain.
87
Q: What initial treatments are given for perforated peptic ulcer?
A: Analgesia, antibiotics, isotonic fluid resuscitation, and surgery.
88
Q: What is gastric outlet obstruction, and how common is it in PUD?
A: It occurs in no more than 5% of patients, usually due to duodenal or prepyloric ulcers.
89
Q: What are common symptoms of gastric outlet obstruction?
A: Nonbilious vomiting, pain, discomfort, weight loss, and possibly metabolic alkalosis.
90
Q: What initial treatments are given for gastric outlet obstruction?
A: Nasogastric suction, IV hydration, electrolyte repletion, and acid suppression.
91
Q: What is important to rule out when diagnosing gastric outlet obstruction?
A: Cancer, as most patients may have a malignancy.
92
Q: What are the four anatomic regions of the stomach?
A: Fundus, Cardia, Body, Antrum.
93
Q: How long is the duodenum?
A: 20-30 cm.
94
Q: What are the boundaries of the duodenum?
A: It extends from the pyloric sphincter to the ligament of Treitz.
95
Q: How is the duodenum divided?
A: Into 4 parts.
96
Q: Where does 90% of duodenal ulcers occur?
A: In the 1st part of the duodenum (duodenal bulb/cap).
97
Q: What are some gastric function tests?
A: Pentagastrin test, Hollander’s insulin test, radioisotope labelled gastric emptying study, 24-hour intragastric pH monitoring, gastrin level estimation, fractional test meal (FTM), Kay’s augmented histamine test.
98
Q: What are the indications for a barium meal study?
A: 1. Gastric ulcer (shows a niche or notch); 2. Chronic duodenal ulcer (absence or deformed duodenal cap); 3. Gastric outlet obstruction (features include enormous stomach dilatation, greater curvature below the iliac crest, absence of duodenal cap, no filling of dye in 2nd part of duodenum, mottled appearance of stomach, evidence of gastritis); 4. Carcinoma stomach (irregular filling defect); 5. Pseudocyst of pancreas (widened vertebro gastric angle); 6. Stomal ulcer in previous gastrojejunostomy; 7. Chronic duodenal ileus (Wilkie’s syndrome showing dilatation of stomach and parts of duodenum).
99
Q: What are the causes of gastric outlet obstruction?
A: Chronic duodenal ulcer with pyloric stenosis or carcinoma pylorus.
100
Q: What are the features of gastric outlet obstruction?
A: Enormous dilatation of stomach, greater curvature below the level of iliac crest, absence of duodenal cap, no filling of dye in 2nd part of duodenum, mottled appearance of stomach due to retained food particles, evidence of gastritis.
101
Q: Where are the three biopsies taken for H. pylori testing?
A: One each from the antrum, body, and fundus.
102
Q: What are the tests for H. pylori and their sensitivities and specificities?
A: 1. Rapid urease test (90% sensitivity, 98% specificity); 2. C13/C14 breath tests (95% sensitivity and specificity; C13 requires spectrometry and is costly, C14 uses radioactivity); 3. Serology to identify IgG antibody (ELISA test with 90% sensitivity and specificity); 4. Biopsy and culture (very costly).
103
Q: What are acute ulcers after cerebral trauma or neurosurgeries called?
A: Cushing’s ulcers.
104
Q: What are acute ulcers after major burns called?
A: Curling’s ulcers.
105
Q: How is the diagnosis of these ulcers made?
A: By gastroscopy.
106
Q: What are the types of gastritis?
A: 1. Type A gastritis; 2. Type B gastritis; 3. Reflux gastritis; 4. Erosive gastritis; 5. Others (stress gastritis, lymphocytic gastritis, granulomatous gastritis, phlegmonous gastritis).
107
Q: What characterizes Type A gastritis?
A: Auto-immune disease with antiparietal cell antibodies, parietal cell dysfunction causing achlorhydria and vitamin B12 deficiency, no antrum involvement, 'G' cell hyperplasia with raised serum gastrin, formation of microadenomas of ECL cells with a predisposition to gastric carcinoma.
108
Q: What characterizes Type B gastritis?
A: Caused by Helicobacter pylori infection, affects the antrum, common peptic ulcer, and may lead to Helicobacter-related pangastritis and gastric cancer.
109
Q: What is reflux gastritis?
A: Usually occurs after gastric surgeries; prokinetic drugs like metoclopramide, domperidone, cisapride, and mozapride are useful.
110
Q: What causes erosive gastritis?
A: Caused by disturbed gastric mucosal barrier, induced by NSAIDs/alcohol, due to inhibition of COX-1 resulting in decreased cytoprotective prostaglandin production; COX-2 mediated NSAIDs do not cause erosive gastritis.
111
Q: What are the factors involved in gastric ulcer formation?
A: 1. Duodeno gastric reflux (reflux containing bile salts and lysolecithin breaks the mucosal barrier, making it more vulnerable to injury from drugs and pepsin); 2. Gastric stasis; 3. Ischemia of the gastric mucosa.
112
Q: What are the types of gastric ulcers according to Daintree Johnson?
A: 1. Type I: In the antrum near the lesser curve (55% incidence, normal acid level); 2. Type II: Combined gastric ulcer (in the body) with duodenal ulcer or cardia (25% incidence, high acid level); 3. Type III: Prepyloric ulcer (15% incidence, high acid level); 4. Type IV: Gastric ulcer in the proximal stomach (5% incidence, normal acid level).
113
Q: What are the barium meal X-ray features of a benign gastric ulcer?
A: Niche on the lesser curve with a notch on the greater curvature.
114
Q: What are the complications of gastric ulcers?
A: 1. Hourglass contracture; 2. Tea-pot deformity; 3. Perforation; 4. Bleeding by erosion into left gastric vessels, rarely splenic vessels, or vessels in the wall of the ulcer; 5. Penetration posteriorly into the pancreas or anteriorly into the liver; 6. Malignant transformation, usually into adenocarcinoma of the stomach (2-5%).
115
Q: What are the key differences between benign and malignant gastric ulcers in terms of mucosal folds, site, margin, floor appearance, edge characteristics, surrounding area, and size and extent?
A: 1. Mucosal folds: Benign gastric ulcers have converging mucosal folds up to the margin, while malignant ulcers exhibit effacing mucosal folds. 2. Site: Benign ulcers are found 95% on the lesser curvature, whereas malignant ulcers are more common on the greater curvature. 3. Margin: The margin of benign ulcers is regular, while malignant ulcers have an irregular margin. 4. Floor: Benign ulcers typically have granulation tissue in the floor, in contrast to malignant ulcers, which have a necrotic slough. 5. Edge: The edges of benign ulcers are not everted and are either punched or sloping, while malignant ulcers have everted edges. 6. Surrounding area: The surrounding area of benign ulcers appears normal, whereas malignant ulcers show nodules, ulcers, and irregularities. 7. Size and extent: Benign ulcers are small and deep, extending up to part of the muscle layer, while malignant ulcers are large and deep.
116
Q: What are the causes of duodenal ulcers?
A: 1. Common in people with blood group O +ve; 2. Stress and anxiety ('hurry, worry, curry'); 3. Helicobacter pylori infection (90% of cases); 4. NSAIDs and steroids; 5. Endocrine causes such as Zollinger–Ellison syndrome, MEN syndrome, and hyperparathyroidism; 6. Other causes include alcohol, smoking, and vitamin deficiency.
117
Q: What are the characteristics of pain associated with duodenal ulcers?
A: Pain is more intense before food, in the early morning, and decreases after eating. This is classically referred to as 'hunger pain' as it is relieved by food. Night pains are also common.
118
Q: Who is more commonly affected by duodenal ulcers?
A: Duodenal ulcers are more common in males.
119
Q: What is the periodicity of duodenal ulcers compared to chronic gastric ulcers?
A: The periodicity of duodenal ulcers is more common and may show seasonal variation compared to chronic gastric ulcers.
120
Q: What symptoms may accompany duodenal ulcers?
A: Symptoms may include water-brash, heartburn, and vomiting. Melaena is more common, and haematemesis can also occur.
121
Q: How does appetite and weight change in patients with duodenal ulcers?
A: Appetite is usually good, and there may be a gain in weight, though this decreases once stenosis develops.
122
Q: How do patients typically manage their eating habits with duodenal ulcers?
A: Patients often eat more frequently without any restrictions.
123
Q: What are the types of chronic duodenal ulcers?
A: Chronic duodenal ulcers can be either uncomplicated or complicated.
124
Q: What is pyloric stenosis in the context of duodenal ulcers, and what causes it?
A: Pyloric stenosis is a complication resulting from scarring and cicatrization of the first part of the duodenum due to chronic inflammation and ulceration.
125
Q: How common is bleeding as a complication of duodenal ulcers, and what percentage of cases does it affect?
A: Bleeding occurs in about 10% of cases of duodenal ulcers.
126
Q: What is the incidence of perforation in duodenal ulcers, and which type of ulcers are most likely to perforate?
A: Perforation occurs in about 5% of cases of duodenal ulcers, with anterior ulcers being the most likely to perforate.
127
Q: What is a residual abscess, and how does it relate to chronic duodenal ulcers?
A: A residual abscess can develop as a complication of chronic duodenal ulcers, but it does not indicate malignancy.
128
Q: How can a duodenal ulcer penetrate nearby organs, and which organ is most commonly affected?
A: Duodenal ulcers may penetrate into the pancreas, which is a serious complication of the condition.
129
Q: Do chronic duodenal ulcers have the potential to turn into malignancy?
A: No, chronic duodenal ulcers do not turn into malignancy.
130
Q: What general measures should be taken to manage duodenal ulcers?
A: General measures include avoiding alcohol, NSAIDs, smoking, and spicy foods, as well as having more frequent meals.
131
Q: What is the role of H2 blockers in the treatment of duodenal ulcers, and how do they promote healing?
A: H2 blockers promote ulcer healing within 4-8 weeks by reducing acid secretion. Examples include cimetidine, ranitidine, famotidine, roxatidine, and nizatidine.
132
Q: What are the typical dosages and forms of ranitidine used in treating duodenal ulcers?
A: Ranitidine is typically dosed at 300 mg at bedtime (HS) or 150 mg twice daily (BID), with an IV preparation also available.
133
Q: How do proton pump inhibitors (PPIs) work in the treatment of duodenal ulcers?
A: PPIs inhibit the H+, K+ ATPase enzyme in parietal cells, completely stopping acid secretion. They are used for 6-12 weeks.
134
Q: Can you name some common proton pump inhibitors and their dosages?
A: Common PPIs include: Omeprazole (20 mg OD before food), Esomeprazole (40 mg), Lansoprazole (30 mg), Pantoprazole (40 mg, IV preparation available), and Rabeprazole (20 mg, IV preparation available).
135
Q: What is the function of antacids in the treatment of duodenal ulcers?
A: Antacids neutralize hydrochloric acid (HCl) to form water and salt, inhibiting peptic activity. Commonly used antacids include aluminum hydroxide and magnesium trisilicate.
136
Q: What is sucralfate, and how does it aid in healing duodenal ulcers?
A: Sucralfate is an aluminum salt of sulfated sucrose that provides a protective coat to the ulcer crater, promoting healing and inhibiting peptic activity. The typical dose is 1 g four times daily (qid) for 6 weeks before meals.
137
Q: What is the anti-Helicobacter pylori regimen, and how long is it typically administered?
A: The anti-Helicobacter pylori regimen is a useful treatment given for 7-14 days, after which proton pump inhibitors are continued.
138
Q: What is the role of colloid bismuth sulfate in ulcer treatment, and what is a notable side effect?
A: Colloid bismuth sulfate is effective for ulcers but can stain the oral cavity and mucosa.
139
Q: What is misoprostol, and why is it significant in the treatment of duodenal ulcers?
A: Misoprostol is the only accepted prostaglandin agonist used in the treatment of duodenal ulcers.
140
Q: Why is follow-up gastroscopy important in the management of duodenal ulcers?
A: Follow-up gastroscopy is essential to confirm that the ulcer has healed.
141
Q: What is highly selective vagotomy (HSV), and how is it performed in the treatment of uncomplicated duodenal ulcers?
A: Highly selective vagotomy involves cutting specific branches of the vagus nerve that innervate the stomach, reducing acid secretion while preserving gastric motility.
142
Q: What is selective vagotomy with pyloroplasty (SV + P), and when is it indicated?
A: Selective vagotomy with pyloroplasty involves cutting the vagus nerve to reduce acid secretion and performing pyloroplasty to facilitate gastric drainage. It is indicated when preserving gastric function is important.
143
Q: What does truncal vagotomy with gastrojejunostomy (TV + GJ) involve, and how does it differ from other surgical options?
A: Truncal vagotomy with gastrojejunostomy involves cutting the main trunk of the vagus nerve, which significantly reduces acid secretion, followed by creating a connection between the stomach and jejunum to bypass the pylorus. This method is used when other options are not suitable.
144
Q: What pathological changes occur in chronic duodenal ulcers that lead to pyloric stenosis?
A: Chronic duodenal ulcers can undergo scarring and cicatrization over many years, resulting in total obstruction of the pylorus and causing significant dilatation of the stomach.
145
Q: What are the common clinical features of pyloric stenosis due to chronic duodenal ulcer?
A: Common clinical features include severe, persistent pain in the epigastric region, a feeling of fullness, large quantities of foul-smelling vomitus containing partially digested or undigested food, loss of appetite and weight, visible gastric peristalsis (VGP), and a positive succussion splash.
146
Q: How is visible gastric peristalsis (VGP) assessed in patients with pyloric stenosis?
A: VGP can be elicited by having the patient drink a cup of water, which may reveal the peristaltic movements of the stomach.
147
Q: What does a positive succussion splash indicate, and how is it performed?
A: A positive succussion splash indicates gastric outlet obstruction. It is performed by placing a stethoscope over the epigastric region and shaking the patient after ensuring their stomach has been empty for 4 hours.
148
Q: How does the ausculto-percussion test help in diagnosing pyloric stenosis?
A: In pyloric stenosis, the ausculto-percussion test shows that the greater curvature of the stomach lies below the level of the umbilicus, indicating dilation due to obstruction.
149
Q: What electrolyte changes are associated with pyloric stenosis due to chronic duodenal ulcer?
A: Patients may experience hypochloraemic, hyponatraemic, hypokalaemic, hypocalcaemic, and hypomagnesaemic alkalosis, leading to paradoxical aciduria due to vomiting.
150
Q: What is the significance of not being able to palpate a mass in pyloric stenosis?
A: The absence of a palpable mass indicates that the obstruction is due to functional or structural narrowing rather than a tumor or other mass effect.
151
Q: What findings are expected in a barium meal study for pyloric stenosis?
A: Findings include the absence of the duodenal cap, a dilated stomach with the greater curvature below the iliac crest, mottling of the stomach, and barium failing to pass into the duodenum.
152
Q: Why is gastroscopy performed in cases of pyloric stenosis?
A: Gastroscopy is performed to rule out gastric carcinoma and to visualize the stenosed area.
153
Q: What is the purpose of conducting electrolyte studies and ECG in patients with pyloric stenosis?
A: Electrolyte studies are done to correct imbalances caused by vomiting, while an ECG checks for changes related to hypokalaemia.
154
Q: What is meant by a perforated peptic ulcer?
A: It refers to the perforation of a duodenal ulcer, gastric ulcer, or stomal ulcer, with similar clinical features and management.
155
Q: What percentage of perforated peptic ulcers are due to duodenal ulcers?
A: 75% of perforated peptic ulcers are due to duodenal ulcers.
156
Q: Which type of ulcer has higher mortality when perforated?
A: Gastric ulcer perforation has higher mortality, especially in the elderly.
157
Q: In which demographic is perforated duodenal ulcer most common?
A: It is most common in males aged 35-45 years, with a male-to-female ratio of 8:1.
158
Q: Which type of perforation is most common in duodenal ulcers?
A: Anterior ulcer perforation is the most common.
159
Q: What percentage of cases have a history of chronic duodenal ulcers prior to perforation?
A: In 80% of cases, there is a history of chronic duodenal ulcer.
160
Q: What characterizes silent perforation in duodenal ulcers?
A: In 20% of cases, the perforation may occur without prior symptoms.
161
Q: What factors can precipitate perforation of a duodenal ulcer?
A: Perforation can be precipitated by steroids, analgesics (NSAIDs), alcohol, and antimalarials.
162
Q: What is the overall incidence of perforated duodenal ulcers?
A: The overall incidence is about 5%.
163
Q: Which ulcers are more likely to perforate?
A: Active ulcers are more likely to perforate.
164
Q: What occurs in the stage of chemical peritonitis?
A: Stomach contents escape into the peritoneal cavity, causing severe pain, vomiting, and signs of peritonitis.
165
Q: How does the stage of reaction (illusion) affect the patient?
A: The peritoneum secretes fluid to neutralize the escaped contents, temporarily reducing pain and making the patient feel better for about 6 hours.
166
Q: What happens in the stage of diffuse bacterial peritonitis?
A: After about six hours, bacteria from the gastrointestinal tract migrate from the perforation site, causing diffuse peritonitis.
167
Q: What is the initial presentation of pain in perforation?
A: Severe persistent pain in the epigastrium, later shifting to the right side of the abdomen.
168
Q: What is the cause of the sudden onset of pain in perforation?
A: The pain is due to contact of expelled gastric contents with the parietal peritoneum.
169
Q: What are the signs of tenderness in abdominal examination?
A: Tenderness and rebound tenderness (Blumberg sign) are present all over the abdomen.
170
Q: What systemic signs are observed in perforation?
A: Fever, vomiting, dehydration, oliguria, tachycardia, hypotension, and tachypnoea.
171
Q: What abdominal changes occur in perforation?
A: Abdominal distension, guarding, rigidity, and dullness over the flank due to fluid.
172
Q: What happens to liver dullness in perforation?
A: Obliteration of liver dullness occurs due to the collection of escaped gas under the diaphragm.
173
Q: What is observed in the abdomen during auscultation?
A: A silent abdomen with an absence of bowel sounds.
174
Q: What can mimic appendicitis in perforation cases?
A: Fluid trickling down along the right paracolic gutter can collect in the right iliac region, causing pain and tenderness.
175
Q: How do slow, small perforations typically present?
A: They may present with subacute features, but diffuse peritonitis sets in within 24-48 hours.
176
Q: What are the signs of terminal stage perforation?
A: Oliguria, septicaemia, shock, Hippocratic facies, and multi-organ dysfunction syndrome (MODS).
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3 stages of perforation
chemical peritonitis illusion then bacterial peritonitis
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Q: What does a plain X-ray of the abdomen in erect posture show in perforation cases?
A: It shows gas under the diaphragm in 70% of cases.
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Q: Why might gas not be visible under the diaphragm in some cases?
A: Gas may be less than 1 ml, there may be adhesions from previous surgery, or a sealed peptic ulcer.
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Q: What does an ultrasound of the abdomen reveal in perforation?
A: It shows free fluid and often gas.
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Q: What blood tests are helpful in the investigation of perforated peptic ulcer?
A: Blood urea, serum creatinine, total count, and electrolytes.
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Q: Where do perforated gastric ulcers commonly occur?
A: They commonly occur in the lesser curve near the antrum.
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Q: How does the amount of escaped gas compare between gastric and duodenal ulcers?
A: The amount of gas escaped is more in gastric ulcer perforation than in perforated duodenal ulcers.
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Q: Why should malignancy be suspected in gastric ulcer perforation?
A: Because of the high mortality rate (20%) and the need for biopsy from the edge of the ulcer.
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Q: What is the common position of gastric ulcers that perforate?
A: They are commonly prepyloric in position.
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Q: What is the typical surgical procedure for perforated gastric ulcers?
A: Primary closure with an edge biopsy is commonly used.
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Q: What is a better surgical option if the patient's condition is favorable?
A: Distal gastrectomy including the ulcer area is a better option.
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Q: Why is posterior gastric ulcer perforation challenging to diagnose?
A: It is often difficult to diagnose both clinically and radiologically.
