1.

Give an account on:

- Ulcers of the tongue.
1. Dental ulcers: They are longitudinal ulcers occurring on the
sides of the tongue, against a sharp tooth.
2. Aphthous ulcers: They are tiny, whitish ulcers, surrounded
by a hyperemic zone. They are extremely painful and their cause
is unknown.
3. Syphilitic ulcers:
a. Chancre occurs in the first stage on the tip of the tongue and
is associated with submental lymph node enlargement.
b. In the second stage, multiple shallow mucous ulcers with
irregular margins are seen on the sides and undersurface of the
tongue.
c. In the third stage, gummas ulcerate and form typical
syphilitic ulcers with serpiginous outline and punched out edges.
Gummatous ulcers are found in the midline of the dorsal surface
of the tongue
4. Tuberculous ulcers: They are extremely painful ulcers,
present at the tip( if the patient spits the infected sputum in
cases of open pulmonary TB and the base of the tongue, if the
patient swallows the infected sputum as well as the margins of
the tongue. They have undermined edges.
5. Malignant ulcer: It is present at the lateral borders or
ventral surface of the anterior two thirds of the tongue, rarely
on the posterior third. It starts as a painless ulcer, which later
becomes painful. It has raised everted edges, hard indurated
base, and necrotic floor. It might be associated with glossitis.

- Chronic peptic ulcer.

Definition:
Chronic remitting or relapsing, ulcer in any portion of the alimentary
tract exposed to the aggressive action of acid-peptic juices. 98 % of
ulcers are found in the gastric antrum and first portion of the
duodenum.
Epidemiology:
Age: middle aged to older adults (20-40 years). A family history
exists for duodenal ulcers, but not for gastric ulcers. Duodenal ulcers
are associated with blood group O.
Pathogenesis:
The imbalance between the gastro-duodenal mucosal defense
mechanisms and damaging forces that cause chronic gastritis are also
responsible for the PUD. Thus PUD always develops on top of chronic
gastritis. The reason why some people develop only chronic gastritis
while others develop PUD is poorly understood.
The clinical settings for development of peptic ulcers could
be summarized as follow:
A) Decreased mucosal resistance through:
1- NSAIDs and aspirin.
2- Alcohol as a direct irritant.
3- Cigarette smoking: suppresses prostaglandins and impairs blood
flow.
4- Corticosteroids (act in high doses).
B) H. pylori infection:
The organism is present in the gastric mucosa of nearly all patients
with chronic duodenal peptic ulcers and in 75% of those with chronic
gastric peptic ulcers. Bacterial urease and protease may damage the
mucosa, predisposing to inflammation, which perpetuates the mucosal
injury. Antibiotic treatment of H. pylori infection promotes
(accelerates) healing of the ulcers and tends to prevent their
recurrence.
C) Gastric hyperacidity:
Acidity is necessary for peptic ulcer formation. Ulcers do not occur in
achlorhydric states. A marked increase in acid secretion occurs in
patients with Zollinger-Ellison syndrome (gastrin producing neoplasms
of the pancreas). The high level of gastrin, stimulates continuous
maximal acid secretion by parietal cells. The patients thus develop
severe peptic ulcers in the stomach, duodenum, and jejunum.
D) Abnormal gastric motility includes:
1- Increased rate of gastric emptying so that entry of gastric
contents exceeds the capacity of the duodenum to neutralize the
acid.
2- Delayed emptying leading to gastric ulcer.
3- Regurgitation of bile in case of pyloric incompetence.
E) Environmental influences:
Genetic factors, personality type (type A personality), blood group O,
and psychological stresses may be additional factors for occurrence
of peptic ulcers.
Sites:
1- Duodenum: PUD is four times more common in duodenum than in
the stomach. Duodenal ulcers mostly occur in first part of anterior or
posterior wall.
2- Stomach: Mainly on the lesser curvature near the interface of the
body and antrum.
3- Lower oesophagus: Associated with acid reflux irritating
unprotected oesophageal mucosa (GERD) or due to presence of
ectopic gastric mucosa in this part of the oesophagus.
4- Stomal (marginal) ulcer: At the stoma of gastro-jejunostomy
operation.
5- Meckel’s diverticulum: When associated with ectopic gastric
mucosa.
6- Distal duodenum and jejunum: In patients with Zollinger Ellison
syndrome.
7- Ileum and colon: Very rare, and it is associated with ectopic
gastric mucosa.
Morphology:
Grossly, all peptic ulcers have identical appearances. By definition,
they are defects in the mucosa that penetrate at least into
submucosa and usually into muscularis mucosa or deeper. Most ulcers
are solitary, round, sharply punched out defect, 2-4 cm in diameter,
rarely exceeding 5 cm. Those found in the duodenum are smaller. The
mucosal margin may overhang the base slightly particularly on the
upstream side but is usually level with the surrounding mucosa, but
unlike malignant ulcers, no significant elevation or beading of the
edges is seen The mucosal folds around the ulcer appear to radiate
outwards from the ulcer (an effect of fibrous contraction of the
base of the ulcer). The floor of the crater appears remarkably clean,
owing to peptic digestion of the inflammatory exudate and the
necrotic tissue.
Microscopically, the findings vary with the activity, chronicity, and
degree of healing.
In a chronic open ulcer, 4 zones can be distinguished:
a) The floor and margins are covered by a thin layer of fibrinoid
necrotic debris.
b) Beneath this layer, there is a zone of active acute nonspecific
inflammatory exudate with neutrophils predominating.
c) An underlying layer of granulation tissue.
d) An underlying deep layer of fibrous tissue scar that fans out
widely from the margins of the ulcer. Vessels trapped within the
scarred area are thickened, occasionally thrombosed. In some
instances these vessels are widely patent. With healing, the crater is
filled with granulation tissue, followed by reepithelialization from the
margins.
Clinical features:
It is a chronic ulcer, characterized by remissions and relapses of
symptoms associated with healing and activation of the ulcer
respectively. Relapses may be precipitated by emotional stress, drugs
(aspirin, ibuprofen, steroids) or by cigarette smoking. Few patients
die of their disease.
The patients may present clinically by:
1- Burning or gnawing (biting) pain in the epigastric region, related to
meals. It tends to be worse at night and occurs usually 1-3 hours
after meals during the day. Classically, the pain is relieved by alkalies
(which neutralize the acid) or food but there are many exceptions.
2- Nausea, vomiting, bloating, and weight loss.
3- Some patients come for the first time with manifestations of
complications e.g hemorrhage or perforation.
Diagnosis:
Best established by endoscopy, including biopsy to rule out malignancy
in gastric ulcers.
Complications:
1) Bleeding: Is the chief complication which may be life threatening.
It is the result of erosion of a blood vessel. It occurs in 30% of
cases. If the bleeding is slow and minimal in amount, it will lead to
occult blood loss in faeces. But when bleeding is rapid and in large
amounts (as occurs when a big artery is eroded), hematemesis or
melena will occur. Hemorrhage is responsible for 10% of deaths from
peptic ulcer disease.
2) Perforation: Occurs in 5% of patients, but accounts for 70% of
deaths from peptic ulcer disease. It is common with anterior duodenal
ulcers. The entry of gastric juice into the peritoneal cavity results in
chemical peritonitis, also entry of food may lead to septic peritonitis.
3) Penetration: The ulcerative process may extend through the full
thickness of the stomach wall into the adjacent organs e.g pancreas.
It occurs in posterior ulcers and may lead to constant backache.
4) Pyloric obstruction: Occurs if the fibrosis occurs in the pyloric
canal or first part of the duodenum but it is rare usually presenting
by vomiting.
5) Cicatrization in case of double ulcers leading to formation of
"hour-glass stomach". Here the severe fibrosis and contracture of
the fibrous tissue occurs in the lesser and greater curvatures
dividing the stomach into two chambers similar to an hour glass.
6) Malignant transformation: Very rare. It occurs in less than 1% of
gastric peptic ulcer.

- Dysphagia.
Definition: difficulty of swallowing
Causes: might be in the oral cavity, in the pharynx, or in the
oesophagus
I. Causes in the oral cavity:
Stomatitis
Carcinoma of the tongue
 Tonsillitis
Abscess of the tonsils
II. Causes in the pharynx
Foreign body
Infections
Malignancy
Plummer-Vinson syndrome
Retropharyngeal abscess
Enlarged cervical lymph nodes
III. Causes in the oesophagus: (functional or mechanical)
(A) Functional causes:
Achalasia
Psychosomatic muscle spasm
Neurologic diseases of the lower cranial nerves
Aging
(A) Mechanical causes:
Congenital
Atresia and/or stenosis
Acquired:
Foreign body
Stricture
Diverticulae
Neoplasms especially carcinoma.
Plummer Vinson sydnrome
Pressure from outside; by enlarged thyroid, bronchogenic
carcinoma, aortic aneurysm, and mediastinal tumours.

2. Enumerate types of cirrhosis and describe the pathology

of the most common one.
Classification of cirrhosis "Etiologic classification"
1. Post hepatitic cirrhosis mainly due to HBV & HCV infection
(the most common type in Egypt).
2. Alcoholic cirrhosis (Laennec's cirrhosis) (portal cirrhosis)
3. Biliary cirrhosis.
4. Metabolic diseases eg. Hemochromatosis, Wilson's disease
and α1 antitrypsin deficiency.
5. Cryptogenic cirrhosis (10%-15%).
6. Other causes as drugs, diffuse infiltrative cancer, syphilis
and severe cases of central hepatic necrosis.

3. Enumerate types of gall stones and discuss their

predisposing factors and complications.
Types:
• Cholesterol stone: they constitute more than 80% of gall
stones, they are either pure cholesterol stones (rare) or mixed
stones (most commonconstituting about 80% of gall stones).
• Pigment stones: They constitute about 20% of gallstones.
Risk factors:
I. Cholesterol stones: They result from either increased
cholesterol level or decreased bile salts in bile, risk factors
include:
Female
Above the age of 40 years.
Certain ethnic groups (75% in Native American Population)
where there is genetic biliary hypersecretion of cholesterol.
Persistent estrogenic stimulation as during pregnancy and
under the effect of oral contraceptives which leads to increase
hepatic cholesterol uptake & synthesis.
Obesity, rapid weight loss, & treatment with
hypocholesterolemic agents are associated with increased biliary
cholesterol secretion.
So, it is the disease of five "F" "fatty, fertile, female in
their forties or fifties"
II. Pigment stones: Presence of unconjugated bilirubin in the
biliary tree (as in chronic hemolytic anemias) increases the
likelihood of pigment stone formation.
 Complications:
1. Cholecystitis either acute or chronic.
2. Obstruction of the cystic duct at the bladder neck leading
to:
Mucocele: Gallbladder is transformed into a bag full of
bile. Bile is gradually absorbed and the gallbladder is
transformed into a bag full of mucus.
Empyema: The gallbladder is transformed into a bag full
of pus.
Acute cholecystitis (the most common cause of
emergency
cholecystectomy).
3. Obstruction of the common bile duct leading to:
Ascending cholangitis or obstructive cholestasis and
jaundice (in such cases
biliary colic is common).
Acute pancreatitis.
4. Very rarely stone may ulcerate through the gallbladder into
the intestine leading to fistula formation and may cause
intestinal obstruction {gall stone ileus).
5. Chronic irritation of the gallbladder wall by gallstones rarely
leads carcinoma of the gallbladder.

4. Discuss etiology and complications of peritonitis.

Definition: Inflammation of the peritoneum.
Types:
• Sterile peritonitis due to chemical irritation.
• Septic peritonitis due to bacterial invasion.
A. Sterile peritonitis
It is caused by chemical irritation by:
 1. Bile: Due to rupture of biliary system. At first the
peritonitis is sterile, then complicated by bacterial
infection and ends in septic peritonitis.
2. Pancreatic enzymes: Occurs in acute hemorrhagic
pancreatitis, where proteolytic and lipolytic enzymes evoke
peritoneal reaction and digest lipids.
The produced fatty acids precipitate calcium to produce
chalky-white precipitates. The peritonitis is at first sterile
then after 24-48 hours, bacterial permeation of the bowel
wall leads to frank suppurative exudate.
3. Surgically introduced foreign material, particularly
talc powder giving foreign body granuloma.
4. Gynecologic process as:
• Endometriosis which leads to introduction of blood into
the peritoneal cavity.
• Rupture dermoid cyst leading to intense granulomatous
reaction.
B. Septic or bacterial peritonitis
Causes:
• It is almost always secondary to extension of bacteria through
the wall of a hollow viscus or to rupture of a viscus, e.g.
appendicitis, cholecystitis, perforated peptic ulcer,
diverticulitis, strangulation of a bowel, acute salpingitis and
abdominal trauma.
Spontaneous bacterial peritonitis may occur in existing ascites,
e.g. nephrotic syndrome in children and adult cirrhotic patients.
Causative organisms: are E.coli, α & beta hemolytic
streptococci, staphylococcus aureus, enterococci, gram negative
rods, etc.
Fate and complications: Peritoneal infection may heal
spontaneously or with treatment (therapy). The net result may
be:
1. Resolution.
2. Chronic abscess formation
3. Intestinal obstruction due to organization of the exudates
and formation of adhesive bands.

5. Enumerate causes of portal hypertension and discuss its

clinical effects
Causes:
1. Prehepatic causes: Due to obstruction of the portal vein by
a thrombus,
neoplasm or inflammation.
2. Intrahepatic causes:
• Cirrhosis
• Bilharzial hepatic fibrosis
• Diffuse granulomatous diseases (miliary tuberculosis,
sarcoidosis)
• Massive fatty change.
• Diseases affecting the portal microcirculation.
3. Posthepatic causes:
• Severe right side heart failure.
• Constrictive pericarditis.
• Hepatic vein thrombosis (Budd Chiari syndrome).

Effects & manifestations of portal hypertension:

Portal hypertension induces four major clinical consequences
1. Fibrocongestive splenomegaly due to long standing
congestion.
2. Ascites: It is defined as collection of excess fluid in the
peritoneal cavity. In cirrhosis it is due to:
a) Hepatic sinusoidal hypertension drives fluid into the space of
Disse that will be removed by hepatic lymphatics,
b) Increased hepatic lymphatic outflow to a higher level than
the draining capacity of thoracic duct leading to percolation of
hepatic lymph into the peritoneal cavity,
c) Increased perfusion (hydrostatic) pressure within intestinal
capillaries,
d) Renal retention of sodium and water (due to secondary
hyperaldosteronism).
3. Portosystemic shunts: with rise in portal system pressure,
bypass develops wherever the systemic and portal circulation
share capillary
beds. Principal sites for portosystemic venous shunts are:
a) Cardioesophageal junction producing esophageal varices, their
rupture and bleeding cause massive hematemesis and death in
many cirrhotic patients.
b) Veins around and within the rectum manifested as piles.
c) Retroperitoneum
d) Falciform ligament and umbilicus where dilated subcutaneous
veins extend from the umbilicus toward the rib margins giving
what is called Caput medusae.
4. Hepatic encephalopathy. It is a metabolic disorder of
central nervous system and neuromuscular system. Its
pathogenesis is unclear, but it may be due to severe loss of
hepatocellular function with subsequent diminished
detoxification of toxic intestinal nitrogenous metabolites and
passage of these substances to the brain, due to porto-systemic
shunts. It is associated with increase in the level of ammonia in
the blood leading to impairment of neuronal functions and
causing generalized brain edema.
Clinically, disturbances in consciousness ranging from slight
behavioral abnormalities to marked confusion and stupor to deep
coma and death. "Flapping'
tremors are seen in the head and extremities.

6. Enumerate causes of acute intestinal obstruction.

I. Mechanical obstruction:
1. Hernias (internal and external)
 2. Adhesions
3. Intussusception
4. Volvulus
5. Tumors
6. Inflammatory strictures
7. Obstructive gall stones, faecolith, foreign body
8. Congenital stricture, atresia
9. Congenital bands
10. Meconium in cystic fibrosis
11. Imperforate anus
II. Pseudo obstruction:
1. Paralytic ileus (e.g. postoperative).
2. Vascular bowel infarction
3. Myopathies and neuropathies (Hirschsprung disease)

7. Give an account on:

- Pleomorphic adenoma of salivary gland.
Site:
It is the most common tumour of major and minor salivary
glands. However, the parotid gland is the most frequent site.
It is more common in females in the fourth to fifth decades
of life.
Morphology:
Grossly: The adenoma is usually round, 2-5cm in diameter,
encapsulated, with tongue-like protrusions into the surrounding
gland which makes enucleation of the tumor difficult. It is
lobulated, and firm in consistency. Its capsule is incomplete.
The cut surface is solid, grayish-white, with bluish
semitranslucent areas.
Microscopically, it is characterized by variable histologic
patterns.
 It is composed of epithelial and myoepithelial cells distributed
in sheets, strands, ducts and acini dispersed within an abundant
stroma of mucoid, myxoid, chondroid and bony tissues.
It has a deficient capsule causing difficulty in its complete
surgical removal, therefore it frequently recurs although it
remains totally benign.
It mesenchymal components are all derived from the
myoepithelial cells accounting for the currently accepted name
"pleomorphic adenoma".
Prognosis:
It is a benign tumour. However, incomplete removal of the
tumour may lead to recurrences in 25% of the cases
Malignant transformation may also occur leading to malignant
mixed salivary gland tumour.

- Ulcers of the large intestine.

1. Bilharzial ulcers
2. Amoebic ulcers Dysenteric ulcers
3. Bacillary dysentery ulcers
4. Ulcerative colitis
5. Crohn disease
6. Stercoral ulcers
7. Malignant ulcer
8. Uremic ulcers
9. Actinomycosis
10. Diverticulitis

- Ulcerative colitis (gross features and complications).

UC involves the rectum and extends proximally in a retrograde
fashion to involve the entire colon (pancolitis) in the more severe
cases. Three major pathologic features characterize UC and
help to differentiate it from other inflammatory conditions:
 1. Ulcerative colitis is a diffuse disease (skip lesions are
not found)
2. The inflammatory process is limited to the colon.
3. It is a disease of the mucosa only (mural thickness does
not occur and the serosal surface is normal).
I. Active disease, in this phase:
Mucosa is hyperemic, granular, and friable and bleeds easily on
touch.
Ulcerations may be extensive, are shallow and are seen mainly
in the distal colon but may involve the entire colon. They are
aligned along the axis of the colon.
Pseudopolyps: are raised isolated islands of regenerating
mucosa.
II. Chronic disease or healing of active disease, in this
phase, progressive mucosal
atrophy leads to flatten and thin mucosal surface.
Toxic megacolon: Occurs in most severe cases when toxic
damage to the muscularis propria and neural plexus leads to
complete shutdown of neuromuscular function. The colon
progressively dilates and may perforate.
Complications
1. Toxic megacolon: Cessation of bowel function with toxic
dilatation may occur with severe acute attacks.
2. Increased risk of cancer especially in:
- Long standing disease.
- Extensive disease (pancolitis).
- UC with epithelial dysplasia.

8. Mention complications of colonic diverticulosis.

1. Infection: it leads to diverticulitis, with fever, leukocytosis,
and left lower abdominal pain.
2. Pericolic abscess formation, due to extension of inflammation
and infection in the pericolic fat.
3. Intestinal obstruction, resulting from marked pericolic
fibrosis of healed diverticulitis.
4. Fistula may occur between the colon and urinary bladder.
5. Hemorrhage, due to erosion of a blood vessel in the wall of
the diverticulum.
6. Peritonitis, due to rupture of the diverticulae.

9. Discuss types and causes of bleeding per rectum.

Types:
1. Bright red blood, occurs with rapid bleeding or when the
source of bleeding is near the rectum.
2. Dark stool containing altered blood, occurs with bleeding in
the small intestine and proximal colon.
3. Tarry black stools (melena), occurs when bleeding is in the
stomach, or duodenum. Here the blood is altered by the action
of HCL.
4. Occult blood associated with stool: It is due to chronic slow
bleeding which may lead to iron deficiency anemia.
Causes:
1. Swallowed blood from esophageal varices.
2. Bleeding from peptic ulcer of stomach, duodenum or Meckel’s
diverticulum.
3. Intestinal bleeding due to: - Enterocolitis
- Dysentery (amoebic, bacillary and bilharzial)
- Inflammatory bowel disease (ulcerative colitis and Crohn
disease)
- Vascular bowel disease (ischemic bowel disease and
hemorrhoids)
- Anal fissure
- Tumors

10. Discuss the pathology of:

- Oesophageal carcinoma (predisposing factors and morphology).
Pathogenesis and predisposing factors:
Multi-factorial, with synergistic interaction of dietary and
environmental factors, perhaps modified by genetic factors.
1. Dietary factors:
• Fungal contamination of foodstuffs. (Aspergillus)
• High content of nitrites in food
• Vitamin deficiency (A, C, riboflavin, thiamine, pyridoxine)
• Deficiency of trace metals (zinc)
2. Lifestyle:
• Chronic alcoholism
• Tobacco smoking
3. Oesophageal disorders:
• Plummer-Vinson syndrome
• Achalasia
• Long standing oesophagitis (Barrett esophagus)
4. Genetic factors:
• Racial
• Alteration or loss of p53 and other tumour suppressor genes
Morphology:
Grossly, the carcinoma may appear in the form of:
1. Polypoid fungating mass (60% of cases).
2. Malignant ulcer (25% of cases).
3. Diffuse infiltrative form causing thickening, rigidity and
narrowing of the lumen (15% of cases).
Microscopically, squamous cell carcinoma is the usual type.
However, the incidence of adenocarcinoma is markedly increasing
and occurs on top of long standing GERD and Barrett esophagus.

- Non-neoplastic polypi of the large intestine.

Non Neoplastic Polyps:
They represent about 90% of epithelial polyps in the colon and it
is found in about 50% of all persons aged 60 years or older.
• Hyperplastic polyps
• Hamartomatous polyps
Juvenile polyps
Peutz-Jegher polyps
• Inflammatory polyps
1. Hyperplastic polyps: They arise at any age, but are usually
discovered in the sixth and seventh decades of life. These
polyps are small, less than 5 mm in diameter, nipple-like,
hemispheric, smooth protrusions of the mucosa, may be single or
multiple, more than 50% of these hyperplastic polyps are in the
sigmoid.
Microscopically, they are composed of well-formed mature
glands and scant lamina propria. They have no malignant
potential.
2. Hamartomatous polyps: They are of two types,
a. Juvenile polyps: They are hamartomatous malformations of
the mucosal elements. They are single, occur mostly in the
rectum. They occur in children younger than 5 years old, may be
found in adults at any age (retention polyps).
Grossly, the polyps are larger in children than adults. They are
rounded, smooth, slightly lobulated, 1-3 cm in diameter, and have
a stalk up to 2 cm in length.
Microscopically, these polyps are formed of dilated and cystic
glands embedded within abundant inflamed lamina propria.
Clinical features: May be the source of rectal bleeding. They
may become twisted on their stalks leading to painful infarction.
They have no malignant potential.
b. Peutz-Jegher polyps (P-J polyp):
Are uncommon hamartomatous polyps, scattered throughout the
gastrointestinal tract. They occur as a part of the rare
autosomal dominant Peutz-Jegher Syndrome. This syndrome has
in addition, melanotic mucosal and cutaneous pigmentation. It is
associated with intestinal and extra intestinal malignancies.
3. Inflammatory polyps (Pseudopolyps):
They represent islands of inflamed regenerating mucosa
surrounded by ulceration. They are seen in association with long
standing inflammatory bowel disease (ulcerative colitis, and
Crohn disease).

- Hepatic failure (causes and manifestations).

precipitating factors
 gastrointestinal bleeding,
 systemic infection,
 electrolyte disturbance
 severe stress as major surgery
 heart failure.
Clinical features:
Regardless of the cause, the clinical features are the same
which include:
1. Jaundice: Mainly in the form of conjugated
hyperbilirubinemia.
2. Hypoalbuminemia: Predisposes to peripheral edema and
ascites.
3. Hyperammonemia: Due to defective hepatic urea cycle
function.
4. Fetor hepaticus due to formation of mercaptans in the
gut.
5. Gynecomastia, testicular atrophy, palmar erythema and
spider angiomas of the skin. They are related to impaired
estrogen metabolism and hyperesterinism.
6. Coagulopathy: Due to impaired synthesis of blood
clotting factors leading to increased tendency for bleeding,
e.g. massive gastrointestinal hemorrhage.
 7. Hepatic encephalopathy
8. Hepatorenal syndrome
9. Respiratory failure with pneumonia and sepsis.
10. Coma: usually follows encephalopathy and precedes
death.

- Chronic cholecystitis as regards types, morphology and

complications.
It is either:
a. Chronic calcular
b. Or chronic acalcular cholecystitis.
It may occur either as a sequel of repeated bouts of acute
cholecystitis, or occur de novo.
Although most of the cases are associated with gallstones, yet
gallstones do not seem to play a direct role in the initiation of
inflammation or the development of pain. The cause of chronic
cholecystitis is super saturation of the bile.
Morphology:
Gross picture:
The gallbladder may be contracted, normal in size, or enlarged
(especially
when associated with of stones).
Microscopically:
The submucosa and subserosa are often thickened by fibrosis &
infiltrated by chronic inflammatory cells.
Clinical picture:
• Recurrent attacks of either steady or colicky epigastric, or
right upper quadrant pain.
• Nausea, vomiting,
• Intolerance to fatty meal.
Complications of cholecystitis
• Empyema, cholangitis and sepsis
• Perforation of gallbladder due to gangrenous necrosis leading
to local abscess formation or diffuse peritonitis.
• Intestinal fistula.
• Aggravation of pre-existing medical illness.

11. Discuss the etiology and morphology of HCC.

Etiology:
Major etiologic associations have been established
1. Liver cirrhosis. Over 80% of patients who develop HCC have
liver cirrhosis. This is due to increased liver cell turnover in
regenerating nodules which is associated with genetic
abnormalities.
2. HBV infection. Chronic carrier state may confer a 200-fold
increased risk for HCC by adulthood.
3. HCV infection
4. Aflatoxins; a hepatocarcinogen derived from the fungus
Aspergillus flavus which grows on improperly stored grains and
nuts including peanuts.
Morphology:
Gross picture: Soft mass which is either unifocal, multifocal, or
diffusely
infiltrating involving the entire liver.
Microscopic picture:
1. Conventional type: Ranging from well differentiated with
intracytoplasmic bile globules to poorly differentiated with
multinucleated anaplastic giant cells.
2. Fibrolamellar carcinoma. A rare distinctive variant of HCC
characterized by fibrosis. It occurs in young males & females
(20-40 years). It has no association with cirrhosis or other risk
factors & has a distinctly better prognosis.
12. Give a short account on the clinical settings for the
development of peptic ulcer.
Pathogenesis Q no.1

13. List the complications of:

- Colonic diverticulosis.
1. Infection: it leads to diverticulitis, with fever, leukocytosis, and
left lower abdominal pain.
2. Pericolic abscess formation, due to extension of inflammation and
infection in the pericolic fat.
3. Intestinal obstruction, resulting from marked pericolic fibrosis of
healed diverticulitis.
4. Fistula may occur between the colon and urinary bladder.
5. Hemorrhage, due to erosion of a blood vessel in the wall of the
diverticulum.
6. Peritonitis, due to rupture of the diverticulae.

- H. pylori type of chronic gastritis.

1. This is a precancerous condition causing Intestinal type
adenocarcinoma of the stomach
2. Also, reactive lymphoid hyperplasia may lead to gastric lymphoma.
3. Patients with type B-chronic gastritis have an increased incidence
of gastric peptic ulceration.
4. Delayed healing of peptic ulcers.

14. Give a short account on:

- The gross and microscopic picture of ulcerative colitis.
Grossly:
Site: UC involves the rectum and extends proximally in a retrograde
fashion to involve the entire colon (pancolitis) in the more severe
cases. Three major pathologic features characterize UC and help to
differentiate it from other inflammatory conditions:
1. Ulcerative colitis is a diffuse disease (skip lesions are not found)
2. The inflammatory process is limited to the colon.
3. It is a disease of the mucosa only (mural thickness does not occur
and the serosal surface is normal).
I. Active disease, in this phase:
Mucosa is hyperemic, granular, and friable and bleeds easily on
touch.
Ulcerations may be extensive, are shallow and are seen mainly in
the dista colon but may involve the entire colon. They are aligned
along the axis of the colon.
Pseudopolyps: are raised isolated islands of regenerating mucosa.
II. Chronic disease or healing of active disease, in this phase,
progressive mucosal atrophy leads to flatten and thin mucosal
surface.
Toxic megacolon: Occurs in most severe cases when toxic damage
to the muscularis propria and neural plexus leads to complete
shutdown of neuromuscular function. The colon progressively dilates
and may perforate.
Microscopic appearance is characterized by:
I. Active Disease
Diffuse predominantly mononuclear inflammatory infiltrate in the
lamina propria. Neutrophils are seen infiltrating surface epithelium
and crypt lumina (crypt abscess). Ulcerations may extend into the
submucosa.
II. With remission of active disease
1. Granulation tissue fills in the ulcer craters.
2. Regeneration of the mucosal epithelium.
III. In Healed disease there is:
1. Diffuse mucosal atrophy.
2. Distortion of mucosal architecture.
3. Submucosal fibrosis.
4. Epithelial dysplasia progressing to frank carcinoma may occur.

- Peptic ulcer as regards: (pathogenesis, most common locations

and morphology)
Q no.1
- Spread of gastric carcinoma
1. Direct Spread: to the submucosa, the muscle wall and the omental
fat.
2. Transcoelomic spread: Involvement of the serosa leads to spread
of tumour cells in the peritoneal fluid. Such metastases involve the
ovaries in females leading to bilateral ovarian deposits known as
"Krukenberg tumour". The tumour also may invade the rectovesical
and rectovaginal pouches.
3. Submucosal lymphatics: It results in satellite nodules present
some distance from the main mass.
4. Metastases to lymph nodes: reaching the lymph nodes around the
stomach. Later, the tumour extends up the thoracic duct to the left
supraclavicular lymph node (Virchow's node).
5. Blood spread: reaching the liver, the lungs and bones. It occurs
early in the disease.

15. Enumerate the different etiologies of cirrhosis

Classification of cirrhosis "Etiologic classification"
1. Post hepatitic cirrhosis mainly due to HBV & HCV infection (the
most common type in Egypt).
2. Alcoholic cirrhosis (Laennec's cirrhosis) (portal cirrhosis)
3. Biliary cirrhosis.
4. Metabolic diseases eg. Hemochromatosis, Wilson's disease and α1
antitrypsin deficiency.
5. Cryptogenic cirrhosis (10%-15%).
6. Other causes as drugs, diffuse infiltrative cancer, syphilis and
severe cases of central hepatic necrosis.

16. Mention the causes of acute pancreatitis.

Etiology and pathogenesis:
Approximately 80% of cases of acute pancreatitis are associated
with one of 2 conditions: gall stones or alcoholism.
• The anatomic changes of acute pancreatitis suggest auto digestion
of the pancreatic substance by inappropriately activated pancreatic
enzymes. They result from destructive effect of pancreatic enzymes
released from acinar cells.
• As is well known, pancreatic enzymes are present in the acini in a
proenzyme form and have to be activated to fulfill their enzymatic
potential. A major role of activation is attributed to trypsin which
itself is synthesized as the proenzyme trypsinogen.
• Once trypsin is formed, it can activate other pro-enzymes such as
prophospholipase and pro-elastase into lipase and elastase
respectively, these activated enzymes cause autodigestion of fat cells
and elastic fibers of blood vessels leading to fat necrosis and rupture
of blood vessels with hemorrhage.
• Trypsin also indirectly activates clotting and complement systems
leading to local inflammation and thrombosis, and systemic clotting
disorders. The mechanisms by which pancreatic enzymes are
activated are not entirely clear.
Three possibilities have been proposed:
1. Pancreatic duct obstruction by gallstones impacted in the ampulla
of Vater.
2 . Primary acinar cell injury (most probably by direct toxicity from
alcohol,
viruses, endotoxins, drugs, ischemia and trauma.
3. Defective intracellular transport of proenzymes within acinar
cells
(caused by pancreatic duct obstruction and alcohol exposure).
17. Compare between:
- Crohn’s disease and ulcerative colitis.
- Type A and B chronic gastritis
- Acute and chronic viral hepatitis regarding etiology, serology,
microscopic features and fate.

Acute viral hepatitis Chronic viral hepatitis

Can be caused by any type of Mainly HCV and HDV (80% of
Etiology
hepatotropic viruses superinfection) and some cases of HBC
1. Inflammation
In the mild cases, confined within the
portal tracts.
In severe cases inflammatory cells
spill over the adjacent liver
1. Infiltration of the portal
parenchyma (interface hepatitis)
tract by a mixture of
2. Degeneration (hydropic and fatty
inflammatory cells with
changes)
hypertrophy and
3. Necrosis
hyperplasia of kupffer cells
- Apoptosis
Microscopic 2. Degenerative changes in
- Drop out necrosis
features the form of ballooning
- Piece meal necrosis
degeneration and fatty
- Bridging necrosis
change (Especially in HCV)
4. Fibrosis
3. Liver cell necrosis
First fibrosis is limited to the
- Drop out necrosis
portal tracts. With time fibrotic
- Interface hepatitis
septa emerge from the portal
tracts, extend into parenchyma
and form fibrotic bridges
(bridging fibrosis)

HAV: Most of the cases undergoes

complete recovery within 4-6
weeks

HBV: Most of the cases (More than The clinical course is highly variable. It
90%) presenting with acute depends mainly on the underlying
hepatitis or subclinical develop a causative virus and the degree of fibrosis,
vigorous immune reaction resulting it either in the form of:
in elimination of the virus with - Spontaneous remission
Fate complete recovery. - Indolent disease without
About 1-2% develops chronic progression
hepatitis. Rare cases develop - Progressive disease with
fulminant hepatitis. development of liver
cirrhosis and hepatocellular
HCV: More than 70% progress to carcinoma
chronic hepatitis.
Less than 30% undergoes recovery.
Few cases develop fulminant
hepatitis
 HDV: it’s a defective virus and can
cause hepatitis only in the presence
of HBV (Coinfection)
- 90% of the cases undergoes
recovery
- 3-4% develop fulminant hepatitis
- rare cases progress to chronic
hepatitis

HDV Superinfection (Usually in HBV

carriers)
- 10-15% undergoes recovery
- 80% progress to chronic hepatitis
- 7-10% develop fulminant
hepatitis

HEV: Most of the cases undergoes

complete recovery
Rare cases develop fulminant
hepatitis EXCEPT if infection occurs
among pregnant females;
fulminant hepatitis occur in about
20% of cases (pregnant) and No
chronic hepatitis or carrier state
HBV: Persistence of HBsAg for more than
6 months (detected by ELISA technique)
Serology
HCV: Persistence of HCV RNA (Detected
by PCR)

- Peptic ulcer and malignant ulcer regarding sites, gross and

microscopic features, etiology and complications.
18. Enumerate the causes of hematemesis and describe the
pathology of the most common one.
1. Oesophageal causes:
a. Oesophageal varices in portal hypertension. It is the
most frequent cause in the oesophagus
b. Carcinoma of the oesophagus
c. Reflux oesophagitis with ulceration
d. Oesophageal perforation (traumatic or post endoscopic)
e. Leiomyosarcoma & lymphoma
2. Gastric causes:
a. Chronic gastric peptic ulcer. It is the most frequent
cause in the stomach.
b. Postgastrectomy marginal ulcer
c. Acute erosive gastropathy
d. Tumours of the stomach especially gastric carcinoma
3. Duodenal Causes:
a. Chronic duodenal peptic ulcer
b. Stress ulcers
c. Duodenal neoplasms
4. Generalized Diseases:
a. Hereditary hemorrhagic telangiectasia
b. Scurvy
c. Henoch Schoenlein purpura
d. Polyarteritis nodosa
e. Amyloidosis
f. Kaposi's-Sarcoma

ESOPHAGEAL VARICES
varix: refers to dilated, elongated tortuous congested veins in the
wall of cardiac end of the oesophagus (at its junction with the
stomach).
Pathogenesis:
Portal hypertension resulting from long standing obstruction of portal
blood flow to the liver. As a consequence, the normal blood flow from
the coronary veins of the stomach to the portal vein is reversed. So
the portal blood flow is thus diverted through the coronary veins into
the plexus of oesophageal subepithelial and submucosal veins, thence
to the azygos veins and the superior vena cava.
This porto-systemic shunt will lead to increased pressure in the
oesophagealplexus of veins producing the dilated, tourtuous veins
(varices).
Oesophageal varices occur in two thirds of all cirrhotic patients, and
are most often associated with alcoholic cirrhosis. In Egypt, the most
common cause is bilharzial hepatic fibrosis (BHF).
Effects:
1. Rupture leading to massive hemorrhage (hematemesis) which may
be fatal.
2. Hepatic coma, triggered by hemorrhage.

19. Enumerate ulcers of the small intestine and give the

pathology of the commonest one.
1. Peptic ulcer
2. Tuberculous ulcers
3. Typhoid ulcers
4. Crohn disease
5. Malignant ulcer

20. Discuss colonic carcinoma regarding etiology, gross and

microscopic features, grading, staging and prognosis.
Colorectal Carcinoma
Adenocarcinoma of the colon is the most common malignancy of the
GI tract and is a major cause of morbidity and mortality worldwide.
About 98% of all cancers in the large intestine are adenocarcinoma;
the peak incidence is 60 to 70 years age, except for young adults with
polyposis syndromes. Males are similarly affected as females except
for the rectum where males are more affected. The highest incidence
is in the developed countries.
Etiology and Pathogenesis:
Environmental factors particularly the dietary habits as well as
precancerous lesions in the colon are important factors in the
causation of colorectal carcinoma.
A. Environmental factors:
Low content of unabsorbable vegetable fibers; will lead to a decrease
in stool bulk and increased fecal retention in the bowel (constipation).
1. High content of refined carbohydrates will lead to decreased stool
bulk. At the same time carbohydrates are degraded by the bacteria
into toxic oxidative byproducts which are present in high
concentration in the small stool and are held in contact with the
colonic mucosa for a long time.
2. High fat content, this will increase the formation of cholesterol
and bile acids by the liver and in turn may be converted into
carcinogens by the intestinal bacteria.
3. Decreased intake of vitamin A, C and E which may act as oxygen
radical scavengers.
B. Precancerous lesions in the colon:
1. Inflammatory bowel disease especially ulcerative colitis.
2. Adenomatous polyps especially large villous adenomas.
3. Familial polyposis syndromes.

Morphology:
Colorectal carcinomas most often occur singly.
■ 25% of cases are present in the caecum or ascending colon.
■ 25% are present in descending colon and proximal sigmoid.
■ 25% are present in the rectum and distal sigmoid.
■ The remainder are scattered elsewhere.
Grossly: colonic carcinoma may be in the form of:
1. Polypoid fungating masses: Especially noticed in the capacious
caecum and ascending colon.
2. Annular, encircling masses, with "napkin ring" obstruction in the
distal colorectum.
3. Malignant ulcer: uncommon.
Microscopically, all colorectal carcinomas are adenocarcinoma ranging
from well differentiated to poorly differentiated or anaplastic
carcinoma. Some adenocarcinomas are mucin producing (mucoid
carcinoma). Cancers of the anal zone are mostly squamous cell
carcinoma.
Methods of spread:
1. Direct extension into adjacent structures.
2. Lymphatic spread to regional lymph nodes.
3. Hematogenous spread to liver, lungs, and bones.
4. Transcoelomic spread to serosal membranes of the peritoneal
cavity and to the ovaries leading to krukenberg tumour.

Clinical features:
Colorectal carcinomas remain asymptomatic for years, left-sided
carcinomas cause occult bleeding, fresh blood in stools, change in the
bowel habit (obstructive symptoms), and left lower quadrant
discomfort. Caecal and right colonic cancers cause iron-deficiency
anemia due to bleeding (occult blood in the stool). So iron-deficiency
anemia in an older male means gastrointestinal cancer until proved
otherwise.

Prognosis:
Although poorly differentiated and mucinous histologies are
associated with poor prognosis, the two most important prognostic
factors are depth of invasion and the presence or absence of lymph
node metastases. These factors form the core of the TNM (tumor-
nodes-metastasis) classification and staging system from the
American Joint Committee on Cancer.
‫دى زيادة مجاتش في امتحان بس اعرفوها برده ^_^‬