MSC - F. Surgery Answers 2025
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o Narrow hernial orifice.
oMechanical trauma and micro-inflammation.
Leads to adhesions between hernial sac and its contents (bowel loops, omentum).
Long-term use of abdominal binders may contribute.
Can progress to coprostasis or even fecal strangulation.
Clinical Picture
Hernia remains permanently protruded; not reducible even with gentle manual pressure.
Soft, non-tender swelling, retains cough impulse.
No signs of bowel ischemia.
Mild constipation or bloating may occur.
Occasionally, urinary symptoms (if bladder is involved).
General condition is preserved.
Diagnosis
Clinical examination is key:
o Swelling is non-tender, irreducible, but not tense.
o Cough impulse is present.
oNo systemic toxicity or acute abdominal signs.
Imaging (e.g., ultrasound or CT) may assist in complex or deep hernias.
Treatment
Planned hernioplasty is indicated in absence of complications.
If coprostasis is present:
o Begin with high enemas, laxatives.
oSurgery is required if obstruction or strangulation develops.
No emergency unless clinical deterioration occurs.
Differential Diagnosis: Irreducible vs. Strangulated Hernia
Feature |
Irreducible Hernia |
Strangulated Hernia |
|
Onset |
Gradual |
Sudden |
|
Pain |
Absent or mild |
Sharp, severe |
|
Tenderness |
None |
Marked |
|
Tension of sac |
Soft or mildly firm |
Tense, hard |
|
Cough impulse |
Present |
Absent |
|
Bowel sounds |
Normal or slightly |
Absent or high-pitched |
|
decreased |
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|
|
||
Obstruction |
Absent or partial |
Present (vomiting, absolute |
|
symptoms |
(coprostasis) |
constipation) |
|
Systemic signs |
Absent or mild |
Present (fever, tachycardia, |
|
hypotension) |
|||
|
|
||
General condition |
Stable |
Often toxic or shocky |
Key Differential Diagnoses
Coprostasis (fecal retention in the hernial loop): Mimics obstruction but less severe, no peritonitis.
Inguinal lymphadenitis: Painful lymph nodes, no hernia signs.
Metastatic lymphadenopathy: Hard, fixed, painless nodes.
Femoral vs inguinal hernia: Location in relation to inguinal ligament is diagnostic.
False strangulation: Painful hernia due to unrelated abdominal pathology (renal colic, pancreatitis, etc.).
Peptic ulcer of the stomach and duodenum. Complications of peptic ulcer disease.
1. The concept of peptic ulcer, a modern theory of the etiopathogenesis of gastric ulcer and duodenal ulcer.
Definition
A peptic ulcer is a chronic, recurrent, multifactorial disease characterized by a mucosal defect in the stomach or duodenum, resulting from an imbalance between aggressive and protective factors affecting the gastroduodenal mucosa.
Epidemiology
More common in urban populations than rural.
Men are affected more than women (~4:1 ratio).
Most cases occur in adults aged 25–50 years.
Complications (e.g. bleeding, perforation) are a major cause of mortality.
Etiology
Peptic ulcer disease is polyetiological. Multiple factors contribute to its development:
Aggressive ("Aggression") Factors:
Hydrochloric acid (HCl) and pepsin (main corrosive agents).
Helicobacter pylori infection.
Bile acids (especially in duodenogastric reflux).
NSAIDs (non-steroidal anti-inflammatory drugs).
Smoking, alcohol.
Stress, both physiological and psychological.
Disorders of gastric motility.
Defensive ("Protection") Factors:
Mucosal mucin layer and bicarbonate secretion.
Adequate blood flow to mucosa.
Cell regeneration and prostaglandin synthesis.
Proper gastric motility.
Modern Theory of Pathogenesis
1. Imbalance of Aggression and Protection
Ulceration results when aggressive factors overpower protective mechanisms.
2.Role of Gastric Acid and Pepsin
Excess acid (especially in duodenal ulcers) damages mucosa.
Pepsin further digests exposed tissue.
3.H. pylori Infection
Found in 80–90% of duodenal ulcers and 60–70% of gastric ulcers.
Causes chronic inflammation, disrupts mucous barrier, and stimulates acid secretion.
Also produces cytotoxins (CagA, VacA).
4.Impairment of Mucosal Defense
Damage to the mucus-bicarbonate-phospholipid layer allows acid penetration.
Leads to epithelial injury, histamine release, and microvascular damage.
5.Histamine-Acetylcholine Cascade
Histamine and acetylcholine stimulate further acid and pepsin secretion.
Result: a self-perpetuating cycle of mucosal injury.
6.Microcirculatory Disturbance
Ischemia, edema, and microhemorrhages reduce tissue oxygenation.
Leads to hypoxia, cell death, and ulcer formation.
7.Duodenogastric Reflux Theory
Bile acids refluxing into the stomach damage mucosal cells.
Bile acids, activated by HCl, degrade mucin and epithelial tight junctions.
Morphology
Ulcers are typically round or oval mucosal defects.
Located in:
o Duodenum (most common): anterior wall of the first part. o Stomach: lesser curvature (antrum or prepyloric region).
Clinical Implications
Understanding the modern pathogenesis is crucial for:
Targeted therapy (e.g., H. pylori eradication).
Use of proton pump inhibitors (PPIs) and prostaglandin analogs.
Avoidance of NSAIDs in at-risk patients.
Stress management and dietary counseling.
2.Clinical picture of gastric ulcer and duodenal ulcer.
General Clinical Presentation
Main symptom: Pain in the upper abdomen.
Both gastric and duodenal ulcers share similarities but differ in pain characteristics, localization, and relation to food.
Other symptoms: pyrosis (heartburn), vomiting, nausea, and sometimes complications like pyloroduodenal stenosis.
Pain Characteristics
Feature
Location of pain
Relation to food
Diurnal pattern
Nature of pain
Exacerbation time
Gastric Ulcer
Epigastric region, radiating to left thorax, scapula, back
Occurs during or immediately after meals; food aggravates pain
Less night pain, pain is persistent and dull
Dull, persistent, boring or pricking
Often in autumn and spring
Duodenal Ulcer
Right hypochondrium, radiating to right shoulder, supraclavicular, right lumbar region
Occurs 1.5-3 hours after meals; food relieves pain
Night and hunger pains common; pain wakes patient at night
Spasmodic, severe, "hunger pain"
Periodicity more marked; attacks in spring and autumn
Other Symptoms
Pyrosis (heartburn): Burning sensation in epigastrium, caused by gastroesophageal reflux, more pronounced in duodenal ulcer.
Vomiting: Common in gastric ulcer during exacerbations, often relieves pain. Self-induced vomiting may occur.
oEvening vomiting with undigested food suggests pyloroduodenal stenosis (a complication).
Appetite:
oGastric ulcer: appetite reduced due to pain after eating.
oDuodenal ulcer: appetite often good; frequent eating relieves pain.
Weight changes:
oGastric ulcer: weight loss common.
o Duodenal ulcer: weight gain or maintenance due to frequent eating.
Comparison Table: Chronic Gastric Ulcer vs Chronic Duodenal Ulcer
Feature Chronic Gastric Ulcer Chronic Duodenal Ulcer
Age
Sex
Constitution
Periodicity
Pain
Relation to food
Vomiting
Appetite
Dietary habits
Weight
Hemorrhage
Middle-aged
More common in males
Thin, anemic, hypotonic J- shaped stomach
Less marked; attacks last weeks, with 2-6 months remission
Epigastric, boring/pricking, worse with food, no night pain
Food aggravates pain; pain not felt on empty stomach
Frequent, relieves pain, often self-induced
Reduced due to pain after eating
Avoid fried/spicy foods
Weight loss
Less common; hematemesis more frequent
Young to middle-aged adults (25– 40 years)
Males dominate but less than gastric ulcer
Healthy, "steer-horn" stomach, positioned high
Well marked; attacks last weeks, remissions 2-6 months, often spring/autumn
Transpyloric pain (~1 inch right of midline), spasmodic, hunger and night pain
Pain appears 2.5-3 hours after meal; relieved by food
Rare unless complicated by pyloric stenosis
Good; patient eats frequently to avoid pain
Usually no food avoidance unless patient is aware
Weight gain or stable due to frequent eating
More common; melena more frequent than hematemesis
Physical Tenderness in mid-epigastrium Tenderness at "duodenal point"
Feature |
Chronic Gastric Ulcer |
Chronic Duodenal Ulcer |
exam |
or slightly left |
(transpyloric plane, 1 inch right |
|
|
midline) |
Summary of Key Differences
Gastric ulcer pain: Immediate post-meal, aggravated by food, dull, and no hunger or night pains.
Duodenal ulcer pain: Delayed (2–3 hours post-meal), relieved by food, characterized by hunger and night pains.
Vomiting: Common and pain-relieving in gastric ulcers; rare in uncomplicated duodenal ulcers.
Appetite and weight: Gastric ulcer patients tend to avoid food leading to weight loss; duodenal ulcer patients eat more frequently to relieve pain and maintain or gain weight.
Complications: Pyloroduodenal stenosis more common in duodenal ulcer, presenting with vomiting of undigested food.
3.Diagnosis of gastric ulcer and duodenal ulcer.
Diagnosis of Gastric and Duodenal Ulcers
1.Clinical Evaluation
History:
oCollect detailed case history focusing on:
Predisposing factors: past GI diseases, family history, emotional stress, smoking, alcohol abuse, diet.
Pain characteristics: timing, location, relation to food (key to differentiate gastric vs duodenal ulcer).
o Pain periodicity typical for each ulcer type is crucial.
Physical Examination:
oTenderness on palpation:
Gastric ulcer: epigastric region.
Duodenal ulcer: right hypochondrium.
2.Laboratory Investigations
Blood tests:
oLow hemoglobin indicating chronic blood loss.
oRaised ESR (erythrocyte sedimentation rate) may suggest malignancy in gastric ulcer.
Stool tests:
oOccult blood test to detect hidden bleeding.
oMelena (black, tarry stools) indicates bleeding in GI tract.
3.Gastric Secretion Tests
Measure gastric acid secretion, both basal and stimulated.
Procedure:
oFasting overnight.
o Avoid antacids and anticholinergics 24 hours before test. o Nasogastric tube insertion to aspirate gastric juice.
oMeasure volume and acidity.
Findings:
oDuodenal ulcer: high basal and stimulated acidity.
o Gastric ulcer (body location): low acidity, possibly anacidic.
oHypersecretion suggests conditions like pyloric obstruction, pylorospasm.
Types of secretion tests:
oNight fasting secretion (Dragstedt test):
12-hour aspiration overnight.
Normal acid output: 10-20 mEq.
Duodenal ulcer: 40-80 mEq.
Gastric ulcer: 5-15 mEq.
Zollinger-Ellison syndrome: 100-300 mEq.
oBasal secretion:
Morning basal acid output.
Duodenal ulcer: ~5 mEq/hr.
Gastric ulcer: 1-2 mEq/hr.
oStimulated secretion tests:
Kay’s augmented histamine test (stimulates maximal acid output).
Pentagastrin test.
Hollander’s insulin test.
4.Radiological Investigations
Barium meal X-ray:
oVisualizes stomach and duodenum.
o Detects ulcer crater (“niche” or “recess”).
oShows gastric emptying and motility.
Gastric ulcer findings:
oUlcer crater projecting from smooth stomach outline.
o Localized muscle spasm causing a notch.