PAPER Ⅴ

GASTROINTESTINAL and HEPATOBILIARY

SYSTEM

2018/19 KU
PROBLEM- Ⅰ:
A 40 years old bus driver with history of regular consumption of spicy food with
alcohol intake arrived to medicine to medicine OPD with complaints of vague epigastric
discomfort, two episodes of vomiting: once blood stained with 3-4 ml of blood. Vomitus
was coffee color. After thorough examination, he has been diagnosed with peptic ulcer.
a. Describe the etiopathogenesis of peptic ulcer. (3)
b. What could be consequences of vagotomy in this case? Illustrate the role of vagus
nerve in HCL Secretion in stomach? (1+2=3)
c. Write down the pharmacological management of this case and justify. (4)
Ⅴ
SOLUTION:
a.
Etiology

Acute Peptic (Stress) Ulcers Chronic Peptic Ulcers

i. Psychological stress i. Helicobacter pylori gastritis
ii. Physiological stress ii. NSAIDs-induced mucosal injury
Shock iii. Genetic factors
Septicemia More in blood group ‘O’
Extensive burns (Curling’s ulcers) iv. Hormonal factors
Intracranial lesions (Cushing’s ulcers) Zollinger-Ellison syndrome

Local irritants (e.g. alcohol, smoking, coffee, heavily spiced foods etc.)

Pathogenesis

Peptic ulcers result from imbalances between mucosal defense mechanisms and
damaging factors.

Catalyst NEPAL 1
 Fig: Mechanism of gastric injury and protection Ⅴ
b.
Consequences of vagotomy in above case are as follows:

i. Diminished gastric acid secretin.

Due to elimination of interdigestive cephalic phase of gastric secretion
And reduced hormonal stimulation to parietal cell.
ii. Reduced gut motility and peristalsis.

Vagus Stimulation

Fig: Vagal regulation of HCl secretion

Catalyst NEPAL 2
 Parasympathetic innervation via the vagus nerve is the strongest stimulant of gastric
HCL secretion.
c.
Goal of therapy for peptic ulcers disease is to reduce gastric acid production, to
neutralize gastric H+ or to protect the walls of the stomach from the acid and pepsin.
Pharmacological management of peptic ulcer:
1. Reduction of gastric acid secretion
(a) H2 antihistamines: Cimetidine, Ranitidine, Famotidine, Roxatidine
(b) Proton pump inhibitors: Omeprazole, Lansoprazole, Pantoprazole
(c) Anticholinergic drugs: Pirenzepine, Oxyphenonium
(d) Prostaglandin analogue: Misoprostol
2. Neutralization of gastric acid (Antacids)
(a) Systemic: Sodium bicarbonate, Sod. citrate
(b) Nonsystemic: Magnesium hydroxide, Aluminium hydroxide, Magaldrate,
3. Ulcer protectives:
Sucralfate, Colloidal bismuth sub citrate (CBS) Ⅴ
4. Anti-H. pylori drugs:
Amoxicillin, Clarithromycin, Metronidazole, Tinidazole, Tetracycline

PROBLEM- Ⅱ:
It was middle of summer seasons and holiday time for school children. Raghu ,121
years of age, along with his family was travelling on train to his grandparent’s house.
On the way he had to take lots of water and fruits as it was very hot. These were, as
usual sold, by vendors of train. After arrival and till one week later, he was ok, but
later throughout he had a mild malaise. His mother got worried and took him to the
doctor. On physical examination, physician found that there was generalizes yellow
color pigmentation of skin, including the sclera. The abdomen was tender in upper
right part and he was restless. The doctors asked some blood investigation to be
done and asked him to reduce fat intake.
Blood investigations revealed he was suffering from jaundice, as his serum bilirubin
was very high and Vandenberg test was direct reacting. Further blood test reports
are awaited.
a. Draw a labeled normal histological diagram of affected organ in this case. [3]
b. What is mode of transmission of microorganism in the above case? Write its
laboratory diagnosis. [1+2=3]

Catalyst NEPAL 3
 c. Write down biochemical basis of differential diagnosis of jaundice. [4]

SOLUTION:
a.

Ⅴ
Fig: Histology of liver

Fig: Structure of hepatic lobules

b.

Catalyst NEPAL 4
 Mode of transmission of microorganism in given case is Feco-oral route.

Most probable microorganism is Hepatitis A/E virus.

Laboratory diagnosis:

1. Specimen
Feces or serum Maye be collected for demonstration of virus or its antibody
2. Direct demonstration
The virus can be visualized by IEM in fecal extract during late incubation
period and preicteric phase, but seldom later. This is not commonly used
for diagnosis.
3. Serology
Method of choice
▪ IgM demonstration Indicates current or recent infection

▪ IgG demonstration Indicates recent or remote infection

Ⅴ

c.

Parameter Hemolytic jaundice Hepatic jaundice Obstructive

jaundice

S Total Bilirubin Elevated but not more Elevated Elevated

than 5mg/dl
E
Subtype
R unconjugated bilirubin Mixed bilirubin Conjugated bilirubin

U Prothrombin time
PT {not correctable PT {correctable with
M with vit K} vit K}

Vandenburgh Indirect positive Biphasic Direct positive

reaction

Catalyst NEPAL 5
 Urine Bilirubin Absent Present Present

Feces Urobilinogen Increased Decreased Almost absent

[dark] [pale] [clay]

Catalyst NEPAL 6