PEPTIC ULCER (GASTRIC AND DUODENAL ULCER)

Ans is ‘c’ ie Plummer-Vinson syndrome 

• Conditions asso. with peptic ulcer have already been described.
• Plummer Vinson Paterson Kelly syndrome  consists of :‑

a)       Iron deficiency anemia

b)       Dysphagia [d/t fibrous esophageal web at its upper end *]

c)       atrophic oral mucosa, glossitis

d)       brittle spoon shaped finger nails.

• Typically pts are Woman over 40 yrs of age.
• Its a Pre-malignant condition* for both oral cavity & esophagus.

Ans. is ‘a’ i.e., 1^st part of Duodenum 

1. Duodenum, 1^st portion
2. Stomach, usually antrum
3. At the gastro – esophageal junction, in the setting of gastroesophageal reflux or Barrett’s esophagus
4. Within the margins of a gastrojejunostomy
5. In the duodenum, stomach or jejunum of patients with Zollinger-Ellison Syndrome
6. Within or adjacent to Meckels diverticulum that contains ectopic gastric mucosa

Ans. is ‘b’ i.e., Duodenum

• Bailey writes – “The term ‘pyloric stenosis’ is a misnomer. The stenosis is seldom at the pylorus. Commonly, when the condition is due to underlying peptic ulcer disease, the stenosis is found in the first part of the duodenum, the most common site for a peptic ulcer.”
• Also know
• There are 2 common causes of gastric outlet obstruction

–  pyloric stenosis secondary to peptic ulcer

–  gastric cancer

–  Earlier peptic ulcer was the most common cause, but now the most common cause of gastric outlet obstruction is —> gastric cancer.

Ans. is ‘d’ ie. Warthin starry stain

Most cases of chronic gastritis are one of the two types –

Type A – Autoimmune type associated with pernicious anemia, it primarily involves the body and fundus. Type B – associated with H. pylori infection, it primarily involves the antrum.

Mnemonic

Type A – Autoimmune

Type B – Bacteria i.e. H. pylori

• In this pt. having chronic antral gastritis (type B) we will use a dye which will help stain H. pylori.
• Dye used for H. pylori is Warthin starry stain (or Giemsa or genta silver stain)*

Some other imp stains

Zeil Nelson*             —> i i ()bacterium tuberculosis

Albert stain*             —> Corynebacterium diptheria Oil red 0 stain* –^p Fats

PAS*                          —> Glycogen

Prussian blue*          -> Iron

Congo red *              –> Amyloid

Von Kossa*          —> Calcium

Ans ‘a’ fluids; ‘c’ immediate surgery

Management of Peptic ulcer perforation

Nasogastric tube: whenever a perforated ulcer is suspected, the first step is to pass a nasogastric tube and empty the stomach to reduce further contamination of the peritoneal cavity.

Intravenous crystalloid: The patient is resuscitated aggressively by administration of intravenous crystalloid.

– Intravenous broad-spectrum antibiotics

Surgery:

Surgery is mostly indicated, although occasionally nonsurgical treatment can be used in stable patients without peritonitis, and in whom radiologic studies document a sealed perforation.

Surgery whether laparoscopy or laparotomy involves two components:

i)        Thorough peritoneal toilet

to remove all the fluid and food debris

drain is not indicated

ii)      Management of perforation

For duodenal ulcer perforation

The most frequently performed operation for a perforated duodenal ulcer is simple closure with an omental onlay reinforcement or patch.

This is combined with postoperative H. pylori eradication (antibiotics + antisecretory agents)

–  Insertion of a nasoenteric or jejunal feeding tube should be considered

[Note that this current practice is in marked contrast to the prior recommendation suggesting the addition of a concomitant acid-reduction procedure to ulcer closure.]

For gastric ulcer perforation

All perforated gastric ulcers are best treated by distal gastric resection with or without a truncal vagotomy (Truncal vagotomy can be added for type II & III gastric ulcers. Type I and IV gastric ulcers do not need acid reducing procedures as they are associated with hyposecretion). Ulcer is removed along with gastric resection as it carries a risk of malignancy (cf: duodenal ulcer has no risk of cancer). If ulcer is left behind, biopsy is always done.

Other procedures used for gastric ulcers are

–   patch closure with biopsy  – wedge excision and closure

Ans is ‘d’ (H. pylori is known to increase the incidence of gastric malignancy)

Surgery is almost always indicated for perforated ulcers, although occasionally nonsurgical treatment can be used in stable patients without peritonitis, and in whom radiologic studies document a sealed perforation.

Though increased acid production is associated with duodenal ulcers, its not so with gastric ulcers. Gastric ulcers type I and type IV are associated with decreased acid secretion. (Gastric type II and type III are associated with acid hypersecretion)

Anti-H.pylori drugs are included in those pts. of peptic ulcer ds. who test positive for H. pylori.

Ans. is ‘a’ i.eAnterior aspect of the first part of duodenum 

Ans. is ‘b’ i.e. 75%

Sutton writes – ”The demonstration of pneumoperitoneum on plain film following a perforated viscus is, however, not invariable, and most series show that in only 75-80% of perforations is free gas demonstrable. A number of reasons for this have been suggested, including sealing of the perforation, lack of gas at the site of perforation, or adhesions around the site of perforation. However, radiographic technique is also important : a pneumoperitoneum can be detected in 76% of cases using an erect film only, but when a left lateral decubitus projection is included, a pneumoperitoneum is demonstrated in nearly 90% of cases.”

Ans. is ‘c’ i.e., Truncal Vagotomy with gastrojejunostomy 

Gastric outlet obstruction due to peptic ulcer can develop either acutely or chronically.

Acute obstruction

Is due to edema and inflammation..

Acute gastric outlet obstruction is treated by nasogastric suction, rehydration, and intravenous

administration of antisecretory agents. Acute obstruction due to pyloric inflammation resolves with

supportive measures within 72 hours.

Chronic obstruction

Repeated episodes of ulceration can lead to pyloric scarring and a fixed stenosis with chronic gastric

outlet obstruction.

Surgery for duodenal ulcer:

– Truncal vagotomty with antrectomy (surgery of choice)

– Truncal vagotomy with gastrojejunostomy

–  Surgery for gastric ulcer

– Distal gastrectomy

Ans. is ‘b’ i.e., Hemorrhage 

Ans. is ‘b’ i.e., X-ray abdomen 

Ans. is ‘b’ i.e., FII a 

Forrest Classification

Peptic ulcer disease is the most common cause of upper gastrointestinal bleeding. The endoscopic finding can give valuable information about the risk of rebleeding after hospital admission. Endoscopic signs indicating risk of rebleeding were classified in 1974 by Forrest et al. The classification is as follows –

Ans. is ‘b’ i.e., Non cirrhotic portal fibrosis

Splenomegaly, variceal bleeding and absence of any abnormality in the liver in a young adult suggests the diagnosis of Non cirrhotic portal fibrosis (NCPF).

Remember extrahapatic portal venous obstruction also presents with similar features but the important features to distinguish b/w these two conditions is, age of the patient

Age of presentation: ‑

EHPVO —> Children (1^st to 2^nd decade) NCPF Young adult (2^nd to 3^rd decade)

Ans. is ‘d’ i.e. Serum gastrin value of 200 pg/ml with secretin stimulation 

Diagnosis of ZES is made by secretin provocative test when serum gastrin value increases 200 pg/mL within 15 minutes [ Look closely at the option (d). It says serum gastrin value of 200 pg/mL with secretin stimulation. It mentions the absolute serum gastrin level, not the increase in level]

Zollinger Ellison syndrome

• ZES is caused by gastrin secreting gut neuroendocrine tumors (gastrinomas), which result in hypergastrinemia and acid hypersecretion.
• Clinical situations that create suspicion for ZES are

– ulcers in unusual locations, ulcers in second part of duodenum & beyond (includes the option c) ulcers refractory to standard medical therapy

– ulcer recurrance after acid reducing surgery.

– ulcers presenting with frank complications (bleeding, perforation and obstruction)

– ulcers in the absence of H. pylori or NSAID ingestion.

– giant ulcers (> 2 cm)

– multiple duodenal ulcers

– ulcers associated with diarrhoea

– ulcer patient with hypercalcemia or family h/o ulcers.

– ulcers with severe esophagitis.

– ulcers associated with prominent gastric folds

– ulcers with findings s/o MEN-1 (endocrinopathy, family h/o ulcers or endocrinopathy, nephrolithiasis)

Diagnosis of ZES (gastrinoma)

1)  The first step in evaluation of a patient suspected of having ZES or gastrinoma is to obtain as fasting gastrin

level.

All gastrinoma patients have a fasting gastrin level > 150 pg/mL.

2)       The next step is to assess acid secretion by measuring basal acid output (BAO) which should be Z 15 meq/h (normal < 4 meq/h)

[This is done to rule out hypochlorhydria which is much more common cause of hypergastrinemia than

gastrinoma]

A gastric pH of > 3.0 implies hypochlorhydria and excludes gastrinoma.

3)       Gastrin Provocative tests

– In a pt. with pH < 2.0 or BAO . 15 meq/hr and fasting gastrin level > 1000 pg/mL, the diagnosis of ZES is confirmed.

– With pH < 2.0 or BAO 15 meq/L and lower gastrin levels (150-1000 pg/mL), a secretin stimulation test is perforfmed to distinguish ZES from other causes of hypergastrinemia. A rise of 200pg/mL of serum gastrin level within 15 min of secretin injection, confirms ZES.

Ans. is ‘b’ i.e., Fatty hernia of the linea alba 

Ans. is ‘d’ i.e., MEN 1 syndrome 

Answer is D (Pernicious anemia):

Pernicious anemia is characterized by autoimmune destruction of parietal cells leading to hypochondria (J, acid production). It is not associated with peptic ulcer disease.

Aetiological Factors in peptic ulceration

Primary Aetiologcial Factors (selected)

• H. pylori infection
• NSAID’s and other drugs eg. steroids
• Stress – Head injury / Burns
• Bile Reflux
• Smoking /Alcohol use
• Genetic Factors

Associated Factors / Conditions (selected)

• Endocrinal Disorders – MEN

– Primary Hyperparathyroidism

– Zollinger Ellison Syndrome

– Cushing’s syndrome

• Cirrhosise
• Chronic Renal Failure
• Chronic Pulmonary Disease
• Chronic Paracreatic Disease
• Alpha 1 Antitrypsin deficiency

The answer is C (Plummer Vinson Syndrome):

Common causes include:

Helicobacter pylori and non-steroidal anti-inflammatory drugs (NSAIDs).

 tobacco smoking

stress due to serious illness

Behcet disease

Zollinger-Ellison syndrome

Crohn disease

liver cirrhosis.

Older people are more sensitive to the ulcer-causing effects of NSAIDs.

Answer is B (The incidence of complications has remained unchanged)

• H. pylori eradication decreases the likelihood of occurrence of complications.
• The incidence of H.pylori is > 80% in most developing countries, and so the chances of reinfection are also high.
• H. pylori eradication reduced the chances of recurrence
• ‘After successful eradication of H.pylori with antibiotics, ulcer recurrence rates are reduced dramatically to 5-20% at 1 year – CMDT 2003/571
• Option ‘b’ ‘The incidence of complications has remained unchanged’ is thus the answer of exclusion !!

Answer is A (1^st part of Duodenum)

MC site: ₋₋ 1st part of duodenum (overall MC site for peptic ulcer)

Sites in order of decreasing frequency :

1. Duodenum, 1^st portion
2. Stomach, usually antrum 
3. At the gastro-esophageal junction, in the setting of gastroesophageal reflux 
4. Within the margins of a gastrojejunostomy 
5. In the duodenum, stomach or jejunum of patients with Zollinger- Ellison Syndrome 
6. Within or adjacent to a Meckel’s diverticulum that contains ectopic gastric mucosa 
   

Peptic ulcers are usually solitary lesions less than 4 cm in diameter

Answer is C (Vagotomy + Antrectomy)

Repeat Vagotomy with Antrectomy is associated with lowest recurrence rates.

Answer is B (Duodenum)

Gastric outlet obstruction in a patient with peptic ulcer disease is suggestive of pyloric stenosis. The term pyloric stenosis is normally a misnomer. The stenosis is seldom at the pylorus.

Commonly the stenosis is found in the first part of the duodenum, the most common site for a peptic ulcer.

The answer is B (Noncirrhotic portal fibrosis) :

Features of portal hypertension in an adult with large splenomegaly (8cm below costal margin) with no history of jaundice or liver decompensation suggests a diagnosis of Non-cirrhotic portal hypertension.

Non-cirrhotic portal hypertension encompasses two distinct pathological conditions that present with similar clinical features.

The distinction between the two conditions should ideally be made investigations are similar in presentation makes clinical criteria unreliable.

Nevertheless, if we do have to choose one single best option the following clues may be helpful.

NCPF

• NCPF presents in young adults most commonly during the third and fourth decade
• Mode of presentation
• The onset of symptoms is gradual
• Mass in left upper quadrant (splenomegaly) is about 4 times more common in NCPF than EHPH

Extrahepatic portal hypertension

• EPH may present in two age groups children (I^st & 2^nd decade) (congenital malformations) Adults (4^th & 5^th decade) (thrombotic event)
• The onset is gradual in children where the cause is a congenital malformation
• The onset is acute in adults where the cause is usually a thrombotic even
• Mass in left upper quadrant (splenomegaly) is four times less common in patients with EHPH

 Thus a young adult presenting with a gradually progressive cause and a moderate to massive splenomegaly suggests the diagnosis of noncirrhotic portal fibrosis.

Ans. C: Round to oval, sharply punched out defect

Peptic ulcer are four times more common in the proximal duodenum than in the stomach.

Peptic ulcers are solitary in more than 80% of the patients.

Peptic ulcers are sharply punched out with straight walls and a flat base which is smooth. The adjoining mucosa is flat and the rugal folds extend to the margin of the ulcer and some reddening of the adjoining mucosa may indicate an associated gastritis. The gastric mucosa is often flattened due to the presence of chronic gastritis with atrophy. Acute ulcers may show edema and chronic ulcers show varying degrees of underlying fibrosis. The depth of the ulcer is variable with some showing only mucosal involvement in which case they are called erosions in contrast to deeply penetrating ulcers which involve submucosa and deeper layers. Occasionally evidence of active bleeding may be seen, and deep ulcers may perforate. Benign gastric ulcers are most commonly found along the lesser curvature near the interface of the body and antrum.

Size and location of the ulcer do not differentiate benign and malignant ulcers. However the gross appearance of chronic peptic ulcer is virtually diagnostic.

Malignant transformation of the peptic ulcer is very rare.

Ans. C i.e. Ciprofloxacin

H. pylori

Its eradication drastically reduces ulcer recurrence in patients with duodenal or gastric ulcers.

• 7-day triple therapies with a proton pump inhibitor (PPI) + two antibiotics given BID are currently recommended first-line for H. pylori eradication e.g. lansoprazole (or alternate PPI) + clarithromycin + either metronidazole or amoxicillin
• A dose of clarithromycin 250mg p.o. BID is preferred when using in combination with a PPI and metronidazole; however, the 500mg p.o. BID dose is recommended in combination with a PPI + amoxicillin.
• Maintenance acid suppression therapy is not necessary following H. pylori eradication except in high-risk patients (e.g. severe GI bleed; refractory ulcer disease).
• Ranitidine Bismuth Citrate or RBC is a new agent useful in H. pylori eradication regimens.

Ans. A: Omeprazole, C: Misoprostol

Drugs for peptic ulcer and GERD with safety uncertain/unsafe profile in pregnancy include:

• Cimetidine
• Omeprazole, pantoprazole, lansoprazole
• Cisapride, mosapride

Safer drugs in pregnancy for peptic ulcer/GERD are:

• Ranitidine, famotidine

Ans. C. H.pylori

Helicobacter pylori is a Gram-negative, microaerophilic bacterium that can inhabit various areas of the stomach and duodenum.

It causes a chronic low-level inflammation of the stomach lining and is strongly linked to the development of duodenal and gastric ulcers and stomach cancer.

Over 80% of individuals infected with the bacterium are asymptomatic.

The most reliable method for detecting H. pylori infection is a biopsy check during endoscopy with a rapid urease test, histological examination, and microbial culture.

The standard first-line therapy is a one week “triple therapy”

Ans. A: Truncal vagotomy with gastrojejunostomy

The diagnosis is typically made by X-ray, which will show an absent air bubble in the stomach, or by CT scan.

Causes of gastric outlet obstruction include peptic ulcer disease; tumours of the stomach, including adenocarcinoma (and its linitis plastica variant), lymphoma, and gastrointestinal stromal tumours; infections, such as tuberculosis; and infiltrative diseases, such as amyloidosis.

Metabolic alkalosis may develop as a result of loss of acid.

Traditionally severe cases of Gastric outlet obstruction are treated usually by a gastroenterostomy rather than a pyloroplasty. Truncal vagotomy leads to reduction of the maximal acid output by 50% as vagus nerves are sectioned which critically controls the secretion of gastric acid.

Ans. D: Fatty hernia of the linea alba

Pain in the case of epigastric hernia, also known as a fatty hernia of the linea alba, may simulate peptic ulcer.

Epigastric hernia:

• Located between the xiphoid process and umbilicus, usually in the midline
• More common in males
• Pain due to the incarceration of the preperitoneal fat
• Pain simulates peptic ulcer
• No sac

Ans. is ‘d’ i.e., Propylthiouracil

Drug/Toxin causing peptic ulcer disease:

Bisphosphonates

Chemotherapy

Clopidogrel

Crack cocaine

Glucocorticoids (when combined with NSAIDs)

Mycophenolate mofetil

Potassium chloride

Organ shown in the picture above represents duodenum.

Peptic ulcer

o Ulcers are defined histologically as a breach in the mucosa of the alimentry tract that extends through the

mucularis mucasea into the submucosa or deep.

MC site: 1^stpart of Duodenum (overall me site for peptic

ulcer)

o Peptic ulcers are chronic , most often solitary lesions that occur in any protion of the gastrointestinal tract exposed

to the aggressive action of acid / peptic juice .

Peptic ulcers located in the following sits, in order of decreasing frequency :

1.  Duodenum, 1′ portion
2. Stomach ,usally antrum
3. At the gastro – esophageal junction in the setting of gastroesphageal reflux or Barrett’s esophagus.
4. Within the margins of a gastrojejunostomy.
5. In the duodenum, stomach or jeunum of patients with Zollinger -Ellison Syndrome.
6. Within or adiacent to Meckels diverticulum that contains ectopic gastric mucosa.

Ans. is ‘a’ i.e., l^st part 

Peptic ulcer

• Ulcers are defined histologically as a breach in the mucosa of the alimentry tract that extends through the mucularis mucasea into the submucosa or deep.
• Peptic ulcers are chronic , most often solitary lesions that occur in any protion of the gastrointestinal tract exposed to the aggressive action of acid / peptic juice .

Peptic ulcers located in the following sits, in order of decreasing frequency :

1. Duodenum, l^s`portion
2. Stomach ,usally antrum
3. At the gastro – esophageal junction in the setting of gastroesphageal reflux or Barrett’s esophagus.
4. Within the margins of a gastrojejunostomy.
5. In the duodenum, stomach or jeunum of patients with Zollinger -Ellison Syndrome.
6. Within or adiacent to Meckels diverticulum that contains ectopic gastric mucosa.