Complete Final Pathology

Lymph Notes in Pathology |
Table of Contents
Diseases of upper respiratory system 2
Diseases of lower respiratory system 9
Diseases of GIT 37
Diseases of the liver 75
Diseases of gall bladder, pancreas & peritonium 80
Disease of the urinary system 86
Male genital system 101
Diseases of the female genital system 107
Diseases of the breast 122
Diseases of bones and Joints 128
Diseases of lymphoid tissue 141
Haemopoeitic disorders 147
Diseases of the endocrine glands 150
Diseases of the nervous system 157
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Chapter Three |
Diseases of upper respiratory system
GIVE AN ACCOUNT ON EACH OF THE FOLLOWING:
1. Rhinitis.
Definition:
It is inflammation of the nasal mucosa, usually accompanied by sinusitis.
Types:
I. Acute rhinitis:
1. Acute catarrhal.
2. Acute allergic.
II. Chronic rhinitis:

1. Chronic non specific.
2. Chronic specific:
Bacterial: Rhinoscleroma, T.B.
Fungal: Rhinosporoidosis.
Parasitic: Leishmaniasis.
Sarcoidosis.
2. Acute catarrhal rhinitis.
Etiology:
1. Rhinoviruses, may be followed by 2ry bacterial infection. (Causative organism)
2. Exposure to cold.
Pathology:
I. Grossly:
Swollen, hyperemic mucosa. First dry then pours serous discharge mixed with
mucin.
II. Microscopically:
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1. Swollen epithelial cells.

2. Vacuolated epithelial cells; due to mucin “Mucoid degeneration”.
3. Dilated capillaries, PMNs, fibrin and macrophages in submucosa.
Complications:
1. Spread of infection:
Sinusitis, pharyngitis, adenoids, ..etc.
2. Chronicity.
3. Acute allergic rhinitis.
An atopic disease caused by inhalation of certain antigens as pollens → allergic

inflammation rich in eosinophils “Type 1 hypersensitivity”.
Repeated attacks cause nasal polyps.
4. Nasal polyps.
Etiology:
Repeated attacks of allergic rhinitis and sinusitis.
Pathology:
I. Grossly:
Multiple soft pink “Pearly” Polyps projecting from the mucosa of nose and sinuses.
II. Microscopically (The polyp consists of):

1. Pseudostratified columnar ciliated epithelium
2. Squamous metaplasia is common.
3. CT core showing congested capillaries, edema, many eosinophils, plasma cells
and proliferated mucus glands.
Complications:
1. Nasal obstruction.
2. Epistaxis.
3. Not precancerous.
5. Scleroma “rhinoscleroma”.
Definition and etiology:

A common disease in Egypt caused by klebsiella rhinoscleromatis. Nose is the most
common site, but it can also affect other sites as pharynx, larynx and upper trachea.
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Pathological features of rhinoscleroma:
I. Grossly:
Single or multiple hard nodular swelling filling nasal cavity and may extend to the
upper lip, sinuses, pharynx, larynx and upper trachea.
1. The covering mucosa may show squamous metaplasia.
2. The submucosa is densely infiltrated with inflammatory cells and shows
progressive fibrosis.
3. The inflammatory cells of scleroma are:
- Mikulicz cells: these are the pathognomonic cells. They are macrophages with
hydropic cytoplasm and small central or eccentric nuclei “foamy cytoplasm”.
- Plasma cells and Russel bodies: hyalinosed plasma cells.
- Lymphocytes.
Complications:
1. Nasal obstruction and deformity.
2. Ulceration, bleeding and 2ry bacterial infection.
6. Diphtheria.
Definition and etiology:

This is infection of URT with “Corynebacterium diphtheria” and rarely conjunctiva, nose,
ear, vulva, skin wound.
The disease mainly affects unimmunized children 2-5 years.
Pathology:
I. Grossly:
The original mucous membrane is replaced by another false membrane which
appears yellowish grey, thick and adherent. If forcibly removed, it leaves a bleeding
surface which is reformed rapidly.
a. The false membrane consists of necrotic patches, fibrin and acute inflammatory
cells.
b. The underlying submucosa shows dilated capillaries, fibrin, and acute
inflammatory cells “PMNs” and macrophages.
Complications:
I. Asphyxia.
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II. Severe toxaemia that may lead to:

1. Acute heart failure due to toxic myocarditis.
2. Paralysis of respiratory, laryngeal and extraocular muscles.
3. Acute adrenal insufficiency due to adrenal necrosis and hemorrhage.
4. Zenker’s degeneration (hyaline necrosis of SM as rectus abdominis).
7. Nasopharyngeal carcinoma.
Age:
More common in:
- Young individuals (15-25 years). - Old individuals (60-70 years).
Predisposing factors:
Upper RT infections with “EBV”
Pathology:
1. Squamous cell carcinoma.
2. Undifferentiated carcinoma, commonly associated with dense lymphocytic infiltrate,
therefore it is called “lymphoepithelioma”.
Prognosis:
I. Spread:
Direct, lymphatic& late spread through the blood.
II. Radiotherapy:
Treatment of choice, cures 50% of patients, particularly young individuals.
8. Epistaxis.
Definition
It is the bleeding from the nose.
Etiology:
I. Local causes:
1. Trauma.
2. Foreign body.
3. Tumors of nose and sinuses.
4. Nasal polyp.
5. Rhinoscleroma.
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6. Rhinitis.
7. Idiopathic.
II. General causes:

1. Hypertension.
2. Fever.
3. Hot climate.
4. Blood diseases as leukaemia and purpura.
5. Vitamin C or K deficiency.
9. Acute tonsillitis.
Definition:
Bacterial infection most commonly by streptococcus hemolyticus.
Pathology (3 Types):
I. Catarrhal:
Enlarged tonsils with hyperemic mucosa.
II. Follicular “Suppurative”:

Remarkably enlarged, lymphoid follicles show pus which appears at the tonsillar
crypts.
III. Membranous:
In severe cases → mucosal necrosis → Exudate forming membrane covering the
tonsils.
Complications:
I. Direct spread:
1. Peri-tonsillar abscess “Quinzy”.
2. Otitis media.
3. Pharyngitis, laryngitis, bronchitis.
II. Lymphatic spread:

Cervical lymphadenitis.
III. Blood spread:

Leads to bacteremia, toxaemia,…etc.
IV. Hypersensitivity reactions:
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As rheumatic fever and glomerulonephritis.
V. Chronic non-specific tonsillitis.

10. Complications of acute suppurative otitis media.
I. Spread of infection:
1. Mastoiditis.
2. Intracranial infections as lateral sinus.
3. Thrombophlebitis, meningitis and brain abscess.
II. Aural polyp:

Mass of granulation tissue.
III. Chronic suppurative otitis media, this may lead to:
1. Tympanosclerosis.
2. Cholesteatoma:
Ingrowth of abundant keratinizing squamous epithelium from the tympanic
membrane into the lumen of middle ear.
11. Laryngeal nodule.
Definition:
It is a common lesion that occurs in the middle 1/3 of the vocal cords.
Etiology:
Related to excessive use of the voice and occurs in singers, teachers due to trauma of the
vocal cords.
Pathology:
I. Grossly:
It is a firm rounded nodule covered by mucosa.
Dilated vascular spaces, fibrosis and myxomatous changes.
Clinically:
The patient complains of hoarseness of voice.
12. Tumors of the larynx.
I. Squamous cell papilloma of larynx:
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May be induced by human papilloma virus and may occur in children or in adults.
I.I. Papilloma of adults:

1. More common in solitary arising in a vocal cord rarely multiplies.
2. Malignant change is rare.
3. Curable by excision, with no tendency for recurrence.
I.II. Papilloma of children:

1. More commonly multiple “papillomatosis” arising in and outside vocal cords.
2. Malignant change is extremely occasional.
3. Recurrence after excision is common.
II. Squamous cell carcinoma of larynx: (category A)

-Cancer larynx is not uncommon, usually occurs above the age of 40.
- Males are more common than females (7:1).
-Invasive stage is commonly preceded by in situ stage (75%).
- Predisposing factors include smoking and papilloma.
Pathology:
Anatomical site:
1. Glottic (65%):
- The tumor arises from vocal cords (anterior third). The tumor present
clinically with hoarseness of voice (can be detected and treated early.
- Microscopically, Most of these tumors are well differentiated, so they grow
relatively slowly; that’s why they have the best prognosis.
2. Supraglottic (35%) and infraglottic (<5%):

Less differentiated and usually have less favorable prognosis than the glottis
type.
Grossly:
Ulcerated mass, sometimes the tumor is very small and may be hardly visible
grossly.
Microscopically:
Squamous cell carcinoma ranging between well and poorly differentiated.
Spread:
Direct and by lymphatics to cervical lymph nodes. Blood spread is late.
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Chapter Four |
Diseases of lower respiratory system
E N U M E R AT E :
1. Four types of lung abscess.
1. Aspiration lung abscess.

2. Post-pneumonic lung abscess.
3. Pyemic lung abscess.
4. Post-bronchiectatic lung abscess.
2. Four different complications for each of the following:
A. Septic bronchopneumonia.
1. Bronchiectasis.
2. Post-pneumonic lung abscess & gangrene.
3. Fibrosis.
4. Toxemia → toxic myocarditis.
B. Emphysema.
1. Chest wall deformity (Barrel-shaped chest).

2. Rt. sided heart failure (Cor-pulmonale due to pulmonary hypertension).
3. Respiratory failure → Acidosis & cyanosis.
4. Rupture of widened air spaces → pneumothorax or mediastinal emphysema.
C. Bronchiectasis. (ASH ASH)
1. Lung Abscess may complicated by lung gangrene.

2. Secondary Amyloidosis.
3. Hemoptysis (due to damage of blood vessels in the bronchial walls).
4. Right-sided Heart failure due to lung fibrosis.
5. Squamous cell carcinoma on top of squamous metaplasia.
6. S pread:
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- Direct spread → empyema, pericarditis, and mediastinitis.

- Blood spread → septic thrombophlebitis & pyaemia.
WRITE A NOTE ON:
1. Pathological features of lobar pneumonia-gray hepatization.
I. Grossly:
The affected lobes appear:
1. Enlarged.
2. Gray.
3. Consolidated (hepatized).
4. Cut section → dry.
5. Pleurisy.
6. Enlarged hilar lymph nodes.
II. Microscopy:
1. Alveolar capillary congestion is reduced.
2. Alveolar walls are thinned; due to marked distension of alveoli → alveolar wall
compression.
3. Alveolar spaces show:
- Dead bacteria.
- Fibrin shrinks.
- Hemolysed RBCs.
- Much neutrophils.
- Macrophages.
2. Pathological features of septic bronchopneumonia.
I. Gross:
Both lungs are affected, particularly lower lobes show:
1. Multiple consolidated yellowish patches exuding pus on pressure.
2. Several patches may coalesce (confluent bronchopneumonia).
3. Fibrinous pleurisy & enlarged hilar lymph nodes.
II. Microscopy:
1. Walls of affected bronchioles show congested capillaries, neutrophils & pus cells.
Some of these inflammatory cells appear in the lumen.
2. Adjacent alveoli show 3 successive zones:
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- Alveolar inflammation (congested capillaries, neutrophils, pus cells & fibrin).

- Alveolar collapse.
- Alveolar dilation (compensatory emphysema).
3. Etiology of emphysema.
I. Excessive elastase (protease) activity.

II. Cigarette smoking.
III. Chronic bronchiectasis.
I. Excessive elastase (protease) activity:

1. Excessive protease activity → destruction of elastic tissue in the walls of alveoli →
diminished elastic recoil → progressive distension of air spaces.
2. The main sources of protease are neutrophils & macrophages.
3. Excess protease activity occurs in the following conditions:
- Congenital deficiency of protease inhibitor (α1 anti-trypsin deficiency) →
unopposed action of protease.
- Cigarette smoking.
II.Cigarette smoking:
1. Smokers have greater numbers of neutrophils & macrophages in their bronchi (as
cigarette smoke is irritant → stimulates inflammation).
2. Smoking stimulates release of elastase from neutrophils.
3. Smoking enhances elastase activity in macrophages.
4. Oxidants in cigarette smoke inhibit α1 anti-trypsin.
5. Smoking leads to chronic bronchitis.
III. Chronic bronchitis, helping factor due to:

1. Swelling of inflamed bronchial mucosa → partial bronchial obstruction.
2. Exaggerated obstruction during expiration → trapping of much air.
4. Pathological features of emphysema.
Microscopy:
I. Distention affects:
1. The respiratory bronchioles (in case of centrilobular emphysema).
2. The respiratory bronchioles, alveolar ducts and alveoli (in case of pan-acinar
emphysema).
II. The pulmonary capillaries are compressed.
III. Elastic tissue stains show reduced elastic tissue.
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IV. Walls of the affected spaces are thinned. In advanced cases, adjacent alveoli become
confluent creating large air spaces.
Gross features:
I. Both lungs:
1. Are voluminous.
2. They cover the heart and press the diaphragm.
3. They don't collapse on opening the chest.
4. They are dry, pale & light.
5. The surface shows indentations at the sites of ribs.
6. Bullae (measuring few centimeters) may develop.
II. The chest wall:

1. Barrel-shaped chest (exaggerated inspiratory position) due to over distention of
lungs.
2. Ribs become horizontal and sub costal angel is widened.
5. Aetiology of bronchiectasis.
I. Septic bronchopneumonia:
The mechanism:
1. The inflamed bronchial walls are week → easily pulled by the negative thoracic
pressure.
2. Interference with the cough reflex → retention of the exudate within the
bronchial lumens.
3. The adjacent inflamed alveoli may become fibrotic → more pull on the bronchial
lumens.
II. Bronchial obstruction:
Long standing obstruction by foreign body, tumor,... etc, leads to:

1. Greater predisposition to infections (which may cause bronchopneumonia : the
mechanism is mentioned before).
2. Obstruction → collapse of alveoli → exaggeration of the negative intra-thoracic
pressure → exaggerated pull on the bronchial walls.
III. Congenital lesions:
1. Kartegener's syndrome:
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Consists of situs inversus, sinusitis, and bronchiectasis. The latter is due to defective
ciliary motility → defective clearance of bacteria and secretions (which are good
media for bacterial growth) → infection → bronchiectasis.
2. Mucoviscidosis:
A congenital disease characterized by thick mucous secretions → bronchial
obstruction & infection → bronchiectasis.
6. Gross features and complications of bronchiectasis.
I. Grossly:
1. Usually bilateral and more common in lower lobes.
2. It has a patchy distribution.
3. Bronchial dilatation may be cylindrical, fusiform or saccular.
4. An important diagnostic feature is the finding of enlarged dilated bronchi near the
pleura (due to their exaggerated dimensions).
5. Lumens contain pus, mucous, and blood.
6. Mucosa shows ulcerations.
7. Surrounding alveoli are fibrotic.
8. Covering pleura shows pleurisy then fibrosis.
9. The draining lymph nodes are enlarged.
II. Complications:
6. Spread:
- Direct spread → empyema, pericarditis, and mediastinitis.
- Blood spread → septic thrombophlebitis & pyaemia.
7. Complications of lung abscess.
I. Rupture: leads to:

1. Hemoptysis.
2. Broncho-pleural fistula & pneumothorax.
II. Lung gangrene.
III. Spread:
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1. Direct → empyema, pericarditis & mediastinitis.

2. Blood → septicemia, pyaemia, meningitis, brain abscess.
IV. Chronic abscess:

May be complicated by 2ry amyloidosis.
8. The microscopic picture of lobar pneumonia.
Lobar pneumonia is an acute diffuse fibrinous inflammation affecting one or more lung
lobes. It passes in four stages:
I. Stage of congestion:
1. Alveolar capillaries are congested.
2. Alveolar walls are thickened.
3. Alveolar spaces contain bacteria & fluid exudate.
II. Stage of red hepatization:

3. Alveolar spaces contain bacteria, fibrin, neutrophils, and RBCs.
III. Stage of gray hepatization:

1. Alveolar capillaries congestion is reduced.
2. Alveolar walls are thinned; due to marked distention of the alveoli.
3. Alveolar spaces show: dead bacteria, much neutrophils, macrophages, hemolysed
RBCs, and fibrin shrinks.
IV. Stage of resolution:

1. Fibrin is liquefied by proteolytic enzymes of dead neutrophils & is phagocytosed by
macrophages.
2. Drainage of all these inflammatory products occurs. So, almost nothing is present in
the alveoli.
9. Pathological features & complications of bronchopneumonia.
Definition:
It's a patchy inflammation of bronchioles and adjacent alveoli.
Gross: both lungs particularly lower lobes show:

1. Multiple consolidated yellowish patches exuding pus on pressure. Several patches
may coalesce (confluent bronchopneumonia).
2. Fibrinous pleurisy and enlarged lymph nodes.
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Microscopy:
1. Wall of the affected bronchioles shows congested capillaries, neutrophils & pus cells.
Some of these inflammatory cells appear in the lumen.
2. The adjacent alveoli show three successive zones:
-Alveolar inflammation (capillary congestion, neutrophils, pus cells, and fibrin).
- Alveolar collapse.
- Alveolar dilatation.
IV. Complications:
1. Post-pneumonic lung abscess and gangrene.
2. Bronchiectasis.
3. Fibrosis.
4. Spread:
a. Direct: empyema, pericarditis, mediastinitis.
b. Blood: thrombophlebitis, septicaemia, pyaemia, and meningitis.
5. Toxaemia: Toxic myocarditis.
10. Pneumoconiosis.
Definition:
Pneumoconiosis is a group of chronic lung disease caused by inhalation of dust particles
as carbon, silica, cotton fibers, bagasse, asbestos, cement…etc
Types:
I. Silicosis:
Is due to inhalation of silica particles (as in miners), leading to granulomas.
Grossly:
Both lungs show numerous hard small grayish nodules.
Microscopy:
Multiple foreign body granulomas composed of silica particles surrounded by
macrophages, foreign body giant cells, lymphocytes & fibrosis.
Complications:
1. Lung fibrosis, which may lead to rt. sided heart failure (cor-pulmonale).
2. Bronchogenic carcinoma.
3. Pulmonary TB is common due to lower lung resistance.
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II. Byssinosis:
Inhalation of cotton fibers → lung fibrosis.
III. Bagassosis:
Inhalation of cane sugar fibers → lung fibrosis.
IV. Asbestosis:
Inhalation of asbestos leads to:
1. lung fibrosis.
2. Pleural mesothelioma.
V. Anthracosis:
Inhalation of carbon particles (mildest form of pneumoconiosis).
Grossly:
Both lungs show black patches.
Microscopy:
Macrophages engulf these particles and carry them to the draining lymph
nodes, which together with the affected lungs appear black.
Complications:
Rare. Fibrosis doesn't occur (except rarely in severe cases, e.g. in coal miners).
11. Bronchiectasis (definition, pathogenesis, microscopic picture, and

complications).
Definition:
Persistent dilatation of medium sized bronchi and bronchioles accompanied by chronic
suppurative inflammation of their walls.
Aetiology and pathogenesis:
I. Septic bronchopneumonia:
The mechanism of bronchiactesis:

1. The inflamed bronchial walls are weak → easily pulled on by the negative
intra-thoracic pressure.
2. Interference with cough reflex→ retention of the exudate within the
bronchial lumens.
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3. The adjacent inflamed alveoli may become fibrotic → more pull on the
bronchial walls.
II. Bronchial obstruction:

Long standing obstruction by foreign bodies, tumors…etc
Leads to:
1. Predisposition to infection → septic bronchopneumonia (see the mechanism
above).
2. Obstruction → collapse of the alveoli → exaggeration of the negative
thoracic pressure → exaggerated pull on the bronchial walls.
III. Congenital lesions:
1. Kartegener's syndrome:
It consists of situs inversus, sinusitis & bronchiectasis. The latter is due to
defective ciliary motility → defective clearance of bacteria → infection →
bronchiectasis.
2. Mucoviscidosis:
Congenital disease characterized by thick mucous secretions → bronchial
obstruction & infection V bronchiectasis.
Gross:
1. Usually bilateral & more common in lower lobes.
2. It has a patchy distribution.
3. Bronchial dilatation may be cylindrical, fusi-form, or saccular.
4. An important diagnostic feature is the finding of enlarged dilated bronchi near
the pleura (due to their exaggerated dimensions).
6. Lumen contains pus, mucus, and blood.
7. Covering pleura shows pleurisy then fibrosis.
8. The draining lymph nodes are enlarged.
Microscopy:
Bronchi are dilated and show:

1. Lumen: shed epithelial cells, inflammatory cells, and exudate.
2. Mucosa: ulceration and squamous metaplasia.
3. Rest of bronchial walls : destruction of mucoelastic tissue, fibrosis, and
inflammatory cells (neutrophils, macrophages, lymphocytes & plasma cells).
4. Adjacent lung and pleura: inflammation and fibrosis.
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Complications: (ASH ASH)

6. S pread:
a. Direct spread → empyema, pericarditis, and mediastinitis.
b. Blood spread → septic thrombophlebitis & pyaemia.
12. Lung abscess.
Definition:
A cavity containing pus due to localized suppurative inflammation of the lung.
Aetiology:
Causative bacteria:
Staphylococci, pneumococci, or other pyogenic bacteria.
Conditions leading to lung abscess:
1. Inhalation (aspiration) of septic material as:

- Blood clots during surgical operations of upper respiratory tract.
- Vomitus in persons under general anesthesia.
- Foreign bodies.
2. Bacterial pneumonia (lobar or bronchopneumonia) → post pneumonic abscess.
3. Septic emboli derived from septic thrombophlebitis → pyaemic abscess
4. Bronchiectasis.
5. Bronchial obstruction → accumulation of mucus → 2ry bacterial infection.
6. Secondary bacterial infection of hydatid cyst.
7. Direct spread of septic infection, e.g. Sub-phrenic abscess.
8. Bacterial infection following chest injuries.
Pathology:
I. Inhalation (aspiration) lung abscess:
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Definition:
Lung abscess caused by inhalation (aspiration) of septic material.
Pathology:
1. The right lung is more commonly affected.
2. The abscess is usually single.
3. It's related to peripheral bronchus.
4. It appears as variable-sized irregular cavity containing pus.
5. The covering pleura shows pleurisy
6. Hilar lymph nodes are enlarged.
7. Fibrosis replaces the abscess if small and surrounds it if large (chronic
abscess).
II. Post pneumococcal lung abscess:
Definition:
Lung abscess complicating bacterial pneumonia (lobar or septic
bronchopneumonia).
Pathology:
Single or multiple abscesses complicating pneumonia.
III. Pyaemic lung abscesses:
Definition:
Lung abscesses caused by septic emboli.
Pathology:
Multiple Bilateral small peripheral abscesses related to vessels.
Complications:
1. Lung gangrene.
2. Rupture, leads to:
- Hemoptysis.
- Bronchopleural fistula and pyopneumothorax.
3. Secondary amyloidosis complicating chronic abscess.
4. Spread:
- Direct → empyema, pericarditis, and mediastinitis.
- Blood → pyaemia, meningitis, brain abscess, … etc.
13. Describe the gross picture of chronic lung abscess.
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1. Small abscess is totally replaced by fibrosis.

2. Large abscess: oval or rounded with well-defined margins, smooth yellowish lining
with thick fibrous wall.
3. The covering pleura shows fibrosis & adhesions.
14. Discuss the pathology of lobar pneumonia (definition, aetiology, pathological
features, and complications).
Definition:
Acute diffuse suppurative inflammation of one or more lung lobes.
Aetiology:
I. Predisposing factors:
1. Age:
Young adults & middle aged persons.
2. Low resistance.
II Causative bacteria:
Pneumococci.
III. Route of infection:

Droplet infection.
Pathology: (Four stages)
I. Stage of congestion:
Duration:
1st day of illness.
Gross: The affected lobe appears:

1. Enlarged.
2. Red.
3. With wet sponge consistency.
4. Cut section exudes frothy blood.
Microscopy:
3. Alveolar spaces contain bacteria and fluid exudate.
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II. Stage of red hepatization:
Duration:
2nd- 4th day.

1. Enlarged.
2. Red.
3. Consolidated.
4. Cut section: dry pleurisy.
5. Enlarged hilar lymph nodes.
Microscopy:
3. Alveolar spaces contain: Bacteria, neutrophils, fibrin, and RBCs.
III. Stage of gray hepatization:
Duration:
5th- 8th day.

1. Enlarged.
2. Gray.
3. Consolidated.
4. Cut section: dry pleurisy and enlarged hilar L.Ns.
Microscopy:
1. Alveolar capillary congestion is reduced.
2. Alveolar walls are thinned due to marked distention of alveoli.
3. Alveolar spaces contain: dead bacteria, much neutrophils, macrophages, fibrin
shrinks, hemolysed RBCs.
IV. Stage of resolution:
Duration:
9th day till day 21.
If there is absence of necrosis → resolution is expected:
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1. Fibrin is liquefied by proteolytic enzymes of dead neutrophils.

2. Phagocytosis by macrophages.
3. Lymphatic drainage of the liquefied fibrin → gradually restore the normal
aeration of the alveoli.
4. The lung will return to normal, except that healing of pleurisy may lead to
some adhesions.
Complications: (Enumerate/Discuss)
1. Failure of resolution leading to fibrosis (carnification).
3. Spread:
- Direct → empyema, pericarditis, & mediastinitis.
- blood → pyaemia, septicaemia, meningitis.
4. Toxaemia: Toxic myocarditis; due to absorption of bacterial toxins on the 9th day.
14. What is the other name of lobular pneumonia and list its complications.
Septic bronchopneumonia, which is patchy inflammation of bronchioles and adjacent

alveoli.
Complications:
2. Bronchiectasis.
3. Fibrosis.
4. Spread:
- Direct → empyema, pericarditis, & mediastinitis.
- blood → pyaemia, septicaemia, meningitis.
5. Toxaemia: Toxic myocarditis.
15. What is meant by gray hepatization of the lung? Describe the microscopic
changes in this case.
It's the 3rd stage of lobar pneumonia in which the lung appears gray, consolidated, and
dry.
Microscopy:
(See above).
16. List types of pneumonia and describe the gross picture of the lung in the type of
pneumonia that is characterized by suppuration.
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I. Types of pneumonia:
1. Lobar pneumonia.
2. Lobular (broncho) pneumonia.
3. Interstitial pneumonia.
II. The type characterized by suppuration:

Septic bronchopneumonia.
III. Gross picture:
Both lungs, particularly lower lobes show:

1. Multiple consolidated yellowish patching exuding pus on pressure. Several
patches may coalesce (confluent bronchopneumonia).
2. Fibrinous pleurisy and enlarged Hilar lymph nodes.
17. What disease is characterized by permanent over-distension of air spaces distal
to terminal bronchioles with destruction of alveolar walls?
Describe the mechanism, the gross and microscopic pictures of the lung and the
complications of this disease.
Emphysema.
Grossly:
I. Both lungs:
1. Are voluminous.
2. They cover the heart and press the diaphragm.
3. They don't collapse on opening the chest.
4. They are dry, pale and light.
5. Their surface shows indentations at the sites of ribs.
6. Bullae may develop.
II. The chest wall:

1. Barrel shaped chest (exaggerated inspiratory position) due to overdistension of
the lungs.
2. Ribs become horizontal and subcostal angle is widened.
Microscopy:
I. Distention affects:
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1.The respiratory bronchioles (in case of centriacinar emphysema).

2. The respiratory bronchioles, alveolar ducts and alveoli (in case of panacinar
emphysema).
II. Pulmonary capillaries are compressed.
III. Elastic tissue stains show reduced elastic tissue.
IV. Walls of the affected spaces are thinned. In advanced cases, alveoli become confluent
creating large air spaces.
Causes of death in emphysema (Complications):

1. Right sided heart failure due to pulmonary hypertension.
2. Respiratory failure leading to cyanosis and acidosis.
3. Rupture of the widened air spaces leading to either pneumothorax which is fatal if
occurs bilaterally or interstitial emphysema, which is the presence of the air outside the
respiratory spaces → it may cause death in severe cases due to compression of the
vessels.
18. Brown induration of the lung.
It is an example chronic local venous congestion.
Aetiology:
Mitral stenosis, or left ventricular failure → blood stasis within the left side of the heart
→ chronic congestion of pulmonary veins.
Grossly:
1. Early the lungs are dark, moist, and heavy.
2. Later, they exhibit brown induration i.e. appear brownish (hemosiderin) and indurated
(firm) due to fibrosis.
Microscopy:
1. Early the inter-alveolar capillaries are congested, accompanied by oedema &
hemorrhage.
2. Heart failure cells ( macrophages engulfing hemosiderin) are seen.
3. Later hemosiderin is liberated from dead macrophages associated with some fibrosis.
Clinical effects:
- 24 -
1. Dyspnea and hemoptysis due to edema and hemorrhage.

2. Prolonged pulmonary congestion → pulmonary hypertension → right ventricular
failure (rt. Sided heart failure) → chronic generalized venous congestion.
DEFINE:
1. Bronchiectasis.
Persistent dilatation of medium-sized bronchi & bronchioles, accompanied by chronic

suppurative inflammation of their walls.
2. Bronchial asthma.
A type of COPD characterized by episodes of reversible broncho-spasm resulting from

increased responsiveness of the bronchial tree to various stimuli.
3. Emphysema.
Permanent over-distention of air spaces distal to terminal bronchioles accompanied by

destruction of their walls.
4. Bronchopneumonia.
Patchy inflammation of bronchioles and adjacent alveoli, also known as (lobular

pneumonia).
5. Interstitial pneumonia.
Lung inflammation in which inflammatory infiltrate is predominantly inter-alveolar

(interstitial). It may be viral or non-viral.
1. Pneumoconiosis
Group of chronic lung disease caused by inhalation of dust particles as Carbon,

cotton fibers, cement and silica
2. Silicosis
Chronic lung disease caused by inhalation of silica particles leading to granuloma

composed of silica surrounded by macrophages, foreign body giant cells,
lymphocytes and fibrosis
Complications
1. Pulmonary fibrosis → Rt. sided heart failure (cor pulmonale)
2. Bronchogenic carcinoma
3. Pulmonary T.B is common due to lowered lung resistance
- 25 -
3. Lung atelectasis
Inadequate expansion of air spaces of newborn.
4. Hemoptysis
Coughing blood which appears frothy (Mixed with air).

5. Hydrothorax
Accumulation of serous fluid (transudate)in pleural cavity
6. Mesothelioma
- Very aggressive malignant tumor arising from mesothelial cells of visceral or
parietal
pleura
- very poor prognosis
- very common in Egypt
- 26 -
E N U M E R AT E
1. Four predisposing factors of bronchogenic carcinoma

1.Tobacco smoking (aromatic hydrocarbons phenol derivatives)
2. Bronchiectasis
3. Lung scaring
4. Irradiation
5. Silicosis, asbestosis & industrial chemicals
6. Air pollution with exhaust fumes of diesel
7. Genetic factors
2. Causes of hemoptysis
1. Disease of bronchi, bronchitis, bronchiectasis carcinoma.

2. Lung disease: T.B, lung abscess, Actinomycosis, fungal infection, CVC, primary
and metastatic tumors.
3. General causes of bleeding
a) Hemorrhagic blood diseases (leukaemia- haemophilia-purpura)
b) Vitamin deficiency as scurvy
N.B T. B, lung cancer of CVC are the most common causes
3. Complications of Empyema
1. Blood spread, Toxemia, septicemia, pyemia

2. Chest sinuses (Empyema necessities)
3. Chest deformity due to dense pleural fibrosis
4. Chronic empyema leading to secondary amyloidosis
5. Direct spread: pericarditis, mediastinitis
GIVE A SHORT ACCOUNT ON
1. Pneumoconiosis
Definition
Group of chronic lung disease caused by inhalation of dust particles as silicosis,

carbon, cotton fibers bagasse, asbestos of cement
Types
I. Silicosis
due to inhalation of silica (in mines) leading to granulomas

Gross: Both lungs show multiple small hard nodules
Microscopy: Multiple foreign body granulomas formed of silica particles
- 27 -
surrounded by Macrophages, lymphocytes, foreign body giant cells of fibrosis.
Complications
1.Lung fibrosis → Rt sided heart failure

2. TB due to lowered lung resistance
3. Carcinoma
II. Byssinosis
Inhalation of cotton fibers lung fibrosis
III. Bagassosis
Inhalation of Cane sugar fibers→ lung fibrosis
IV. Asbestosis
Lung fibrosis and pleural mesothelioma, due to inhalation of asbestos
V. Anthracosis (mildest form)
Inhalation of carbon particles

Gross: Both lungs show black patches
Micro: Macrophages engulf carbon particles and carry them into draining
lymph nodes which together with the lung appear black
Complications:
Rare, fibrosis doesn't occur except in severe cases as in coal miners.
2. Lung atelectasis
Definition
Moderate expansion of airspaces in the newborn

Types
I. Complete (total) atelectasis

Non expansion of the lung may be due to cerebral birth injury or due to
intrauterine
hypoxia, baby is born dead
Gross: Lung is fleshy (doesn't crepitate under pressure as normal lung) -blue
(non oxygenated blood)
Micro: slit like alveoli
- 28 -
II. Incomplete (partial) atelectasis
Due to hyaline membrane disease, hyaline membrane disease is more common

in:
- premature infants (esp. These born by caesarean section)
- in case of maternal D.M
Gross: Lungs are fleshy and purple red

Micro: Bronchioles, alveolar ducts and random alveoli are lined by thick
eosinophilic
membrane lined by fibrin of necrotic cells
-the condition is fatal but 85-90% of cases treated with synthetic
surfactants
survive
3. Gross and microscopic picture of bronchogenic carcinoma
Gross:
1-Central (hilar) Type 85% 2- Peripheral Type 15%
- Arise from main bronchi - Arises from peripheral bronchi

- Forms a polypoid ulcerative or infiltrative - Appears as single or multiple nodular
growth patterns with necrosis of growth at the periphery of the lung
hemorrhage
- Bronchial destruction of lung invasion
occur
- 29 -
Microscopic picture
1. Squamous cell carcinoma 2. Adeno carcinoma 3. Anaplastic carcinoma

(small cell type)
- Commonest type - More common in females - Common type of 1ry lung
- At the main bronchus (50%of lung carcinoma) cancer
- Usual type of carcinoma - At lung periphery - Related to smoking
arising in smokers - Incidence has recently - Arises from neuroendocrine
- Usually it's poorly increased to the extent that cells
differentiated it becomes more common - Occurs in central portions
-Tumor cells are positive for than sq. cell carcinoma of the lung
ck5/6 (100% of cases) - +ve for ck7 and TTF1 - Consists of small rounded
(77% of cases) or oval cells with dark nuclei
showing high mitotic activity
of extensive necrosis
- Para neoplastic syndrome
(cushing and carcinoid
syndromes) may occur
- Tumor cells are +ve for
neuroendocrine markers
(synaptophysin) and TTF1 88%
-cell proliferation is 100% (as
assessed by Ki 67 proliferation
markers )
4- Anaplastic carcinoma, large cell type (or giant cell type )

-also it's neuroendocrine origin
5- Clear cell carcinoma:
I. squamous cell type
II. adenocarcinoma Type
III. Large cell neuroendocrine type
6-Uncommon tumors:
Adenosquamous carcinoma, sarcomatoid carcinoma, salivary gland tumor.
4. Lung secondaries (metastases)
Reach lung via

I. Blood
- 30 -
II. -Retrograde lymphatic spread in case of breast cancer

They are common and may be derived from
1. Carcinoma.
2. Sarcoma.
3. Melanoma.
4. Lymphoma.
Gross:
- Multiple round variable sized nodules
- These nodules may be very large as in case of renal carcinoma and seminoma
(cannon ball metastases)
Microscopy:
-like the primary (q 3)
Effects
1.Chest pain
2.Hemoptysis
3.Hemorrhagic pleural effusion
5. Empyema
Definition
Suppurative inflammation of the pleura (supp pleurisy).
Aetiology
Pyogenic bacteria (staph, strept, pneumococci)

1-Direct spread from lung infections (abscess, pneumonia…)
2-Direct spread from extra pulmonary infections as from osteomyelitis of the
ribs
3- penetrating chest injury
4- hematogenous spread in cases of septicemia
Pathology
I. The extent of empyema may be
1) Diffuse (total) empyema:

pus accumulated in pleural sac leading to total compression collapse of
the lung
2) Localized empyema, small amount of pus localized by fibrin leading to

partial
collapse of lung
II.. pleural fibrosis and adhesions are usually extensive
- 31 -
Complications
1.Chest sinuses (empyema necessitans)

2. Chest deformity due to dense pleural fibrosis
3. Direct spread, pericarditis, mediastinitis
4. Blood spread, toxaemia, septicemia and pyemia
5.Chronic empyema leading to 2ry amyloidosis
6. Pleural effusion
Definition:
Fluid accumulation in pleural sac may be mild or sever, may be uni or bilateral
Ty pes:
I. Transudative(hydrothorax):
occurs due to accumulation of transudate (serous fluid) in pleural sac
Aetiology
1.As part of generalized edema (cardiac, renal, nutritional)

2. meig’s syndrome (ascites, hydrothorax and ovarian fibroma)
Effects May lead to compression collapse
II. Exudative
1) Suppurative (empyema)
2) Tuberculosis
Spread of TB to pleura will lead to tuberculous pleurisy → exudative
reaction→ pleural effusion → later healing → fibrous adhesions
3) Other as:
-Viral infections
-uraemia
-malignant tumors
-Lung infarction
-bacterial infections
III.Chylous (Chy lothorax) :

due to lymphatic obstruction
Hemorrhagic pleural effusion
pleural effusion associated with He, it's most commonly exudative

most common causes
1. Primary lung carcinoma
- 32 -
2. Primary pleural malignancy

3. lung/pleural metastases
4- lung /pleural TB
7. Mesothelioma
Definition
Aggressive malignant tumors arising from mesothelial cells of visceral or parietal

layers of pleura.
very common in Egypt and very poor prognosis
Asbestos is a major predisposing factors
Gross
At first
Localized firm greyish white pleural mass
then: both layers are involved, thickened, become rigid → obliteration of pleural
sac
• hemorrhagic pleural effusion occurs
• the pleura becomes thickened, rigid, greyish, ensheathes the lung
Microscopy: one of 3 patterns
1. Monophasic epithelial: resembles papillary adenocarcinoma

2. Monophasic sarcomatoid : resembles fibrosarcoma
3.Biphasic : Mixed carcinoma and sarcoma
Spread
1) Direct → to lung, mediastinum, chest wall

2) Distant
Immunohistochemistr y:
Mesothelioma expresses most of the following markets:
• Mesothelin-calretinin-CK5/6 – WT1 –CK7- Vimentin

• Mesothelioma is negative for (TTF1, CK20, CDX 2)
Monophasic epithelial type can be easily mistaken for metastatic

adenocarcinoma.
N.B
• Hypertrophic chronic rhinitis  no end arteritis obliterans
- 33 -
• Atrophic chronic rhinitis End arteritis obliterans common in females

(estrogen dep.).
• klebsiella ozaenae atrophic rhinitis
• klebsiella rhinoscleromatis rhinoscleroma
• Mode of infection in tonsillitis ingestion and inhalation
• No broncheictasis in large (excess cartilage) or small bronchi (excess muscle)
• Complications of chronic bronchitisasthma...emphysema...spread(pneumonia)
• alpha 1 antitrypsin deficiency patientemphysema and cirrhosis
• Take carelobar pneumonia # lobular(bronchopneumonia)
• Lobar pneumoniaCornification
• Pulmonary oedema: Accumulation of fluid in interstitial and interalveolar spaces
I M P O R TA N T N A M E S :
• Mikulicz cells and Russel bodies Rhinoscleroma
• Zenker's degenerationcomplication of diphtheria
• Epstein-Barr virusNasopharyngeal carcinoma
• Kartegener's syndromeBroncheictasis(congenital)
• Curschmann's spiralsShed epithelium in Asthma
- 34 -
1 P.F of bronchial Carcinoma
BIG 5S
1-bronchectasis
2-irradiation
3-Gentic defect
4-SMOKING (IMP FACTOR)
5-smoker Air
6-scliosis
7-Scaring lung
8-substance (Nickel & Arsenic)
2- squamous cell papilloma of larynx
�‫ﻛﺎن ﻲﻓ أﻃﻔﺎل ﻛﺘ� زي اﻟﻌﻔﺎر�ﺖ ﻗﺎﻋﺪﻳﻦ ﻳﻠﻌﺒﻮا ﺟﻮة و ﺑﺮة اﻟﺒﻴﺖ و ﻛﻞ ﻣﺎ ﺣﺪ ﻳﻤﺸﻴﻬﻢ ﻳﺮﺟﻌﻮا ﺗﺎ‬
in children:
multiple �‫ﻛﺘ‬
malignant change ‫زي اﻟﻌﻔﺎر�ﺖ‬
in and outside vocal cords ‫ﺑﻴﻠﻌﺒﻮا ﺟﻮة و ﺑﺮة‬
recurrence after excision is common �‫ﻛﻞ ﻣﺎ ﺣﺪ ﻳﻤﺸﻴﻬﻢ ﻳﺮﺟﻌﻮا ﺗﺎ‬
in adults: ‫ﻋﻜﺲ اﻟ� ﻓﻮق ﺑﺎﻟﻈﺒﻂ‬
3- NASOPHARYNGEAL CARCINOMA
Remember it's 2 Syllables. Naso....pharyngeal ...so RAKAM EL SA3D (2)
• 2 WORDS: naso - pharyngeal
• 2 AGE GROUPS: Young (15-25) & Old (60-70)
• 2 Scientists discovered A VIRUS causing it: Epstein & Barr >> (EBV)
• 2 MAIN PATTERNS: Squamous cell carcinoma & Undifferentiated
lymphoepithelioma
• 2 MAIN FATES: either treatable by Radiotherapy (if undiff. Type) .... or Fatal
inoperable (if sq.c.c type)
Kollo kollo kollo 2 7atta el virus men kelmeteen
- 35 -
4- Predisposing factors of Lung Abscess:
‫ﺧﺒﻰ ﻋﺸﺎن ﺑﻮل زﻋﻼن‬

5B Pul SAD
• (2 Bronch= Bronchiectasis, Bronchial Obstruction, 3 Bacterial = Infection,
Secondary infection, Pneumonia)
• Pulmonary Actinomycosis
• Septic Emboli
• Aspiration
• Direct Spread of Septic infection
43 ‫ص‬
5- Predisposing Factors for Bronchiogenic
Carcinoma:
BIL GATES
• Bronchiectasis
• Irradiation
• Lung Scarring
•Genetic factors
• Air Pollution
• Tobacco Smoking
• Exhaust Fumes of Tar & Diesel
• Silicosis
6- Granulomatous lung diseases
" ‫ﻧﺠﻤﻌﻬﻢ ﻓﻰ ﻛﻠﻤﺔ " ﺑﺤﺐ ﺳﺖ اس‬
PAHB ST S
• PPneumoconiosis
• AActinomycosis
• HHistoplasmosis
• BBilharziasis
• SSarcoidosis
• T Tuberculosis
• S Syphilis
- 36 -
Chapter Five |
Diseases of GIT
WRITE A NOTE ON
1- ulcers of the tongue
I. Dental ulcer
shallow traumatic ulcer

Site: -
at age of the tongue, near a sharp tooth
II.Aphthous ulcers (dyspeptic ulcers-formerly-)
• multiple, small superficial painful ulcers
• more common in children and young adults
• unknown etiology (maybe autoimmune)
• resolve in few weeks, but may recur
III. Tuberculous ulcer
an ulcer with undermined edges and caseous floor

Site: -
at tip of tongue in case of cavitary pulmonary T.B. coughed sputum containing
T.B bacilli causing infection of the tongue
IV.Syphilitic ulcer
• primary stage of syphilis →ulcerated chancre

• secondary stage →ulcerated mucous patches
• tertiary stage → gummatous ulcer(precancerous)
V. malignant ulcer
with raised everted edges, rough necrotic floor and indurated base
Site: -
- 37 -
commonly in anterior 2/3of tongue, less common in posterior 1/3

2- pleomorphic adenoma of salivary gland
•it is benign mixed salivary tumor

•the commonest tumor of salivary gland mainly parotid
• more common in females
Gross: -
capsulated, lobulated firm mass at lower pole of parotid
2.5 cm in diameter
cut section show mucinous, solid and cystic foci
Microscopic
• proliferated epithelium cells forming acini and cords
• proliferated myoepithelial cells
• fibrous stroma with myxomatous and cartilaginous islands (pseudo cartilage)
Behaviour
-tiny prolongation of tumor tissue commonly perforate the capsule, so,
recurrence is
common after surgical excision
-true malignant transformation is evidenced by:
1.rapid increase in size with induration and fixation
2. facial nerve paralysis (due to invasion)
3. regional L.N enlargement (due to spread)
3- Carcinoma of the esophagus
predisposing factors : -
I- Ageusually above 40
II- Sex
more common in males
Except for post-cricoid type, more common in females
III- Diet
1). hot food and drinks
2). vit. deficiency (A, B. C)
IV- smoking and alcohol intake
- 38 -
V-achalasia of Les
VI- plummer-vinson syndrome (dysphagia, iron deficiency and sometimes post

cricoid carcinoma)
VII. Barrett esophagus
Site:
commonest in middle 1\3, then lower1\3, rarest in upper 1\3
Gross
1.polypoid fungating pattern
2.malignant ulcer (raised everted edge, rough floor and indurated base)
3.infiltrative pattern leading to annular stricture
Microscopy
1.95% of cases: squamous cell carcinoma
2.5% of case: adenocarcinoma (when it arises in lower 1\3)
Spread:
I. Direct
to trachea and mediastinal structures
II. lymphatic
supraclavicular, celiac and mediastinal L.N

III. blood(late)
to lungs, liver, …etc
Clinical manifestation
hemorrage→ ulcer ‫(ﻓﻮق‬ulcer ‫اﺳﻄﻤﺒﻪ)اى‬

Perforation→ ulcer‫ﺗﺤﺖ‬
Stricture→‫ﻋ� ﻣﺴﺘﻮاه‬
In oesophagus
1. hematemesis
2.tracheo_oesophagus fistula
3.oesophgeal obstruction
- 39 -
E N U M E R AT E : -
1- Three predisposing factors for esophageal carcinoma (see above)
2- Three predisposing factors for carcinoma of tongue
1.leukoplakia
2.tobacco use
3.human papilloma virus (type 11, 16, 18)
4.tertiay syphilis
3- Causes of hematemesis
1- Oesophageal causes: -
I. oesophageal varices
Def.
this is varicosity of oesophageal veins at submucosa of lower part of
oesophagus
The veins appear dilated, tortuous and engorged with blood
Aetiology:
due to portal HTN in case of
1. cirrhosis
2.bilharizal hepatic fibrosis
3.portal vein obstruction due to thrombosis or malignant invasion
II. oesophgeal carcinoma

III. 2soesophgatitis and oesophgeal ulcers
IV. Malignant mediastinal tumors infiltrating the oesophagus
V. Aortic aneurysms rupturing into the oesophagus
2- Gastric causes
I. Gastritis
II. Peptic ulcers
III. Acute ulcers
IV. Tumors
- 40 -
3- Duodenal cases
I. Doudenitis
II. Peptic ulcers
III. Acute ulcers
IV. Tumors
4- General causes (HHPL+2vit deficiency )
I. HTN
II. Haemophilia
III. purpura
IV. Leukaemia
V. vit c or k deficiency
4- Four predisposing factors of gastric carcinoma:
(P.S ABC)
1. Smoked & spicy food.
2. Chronic gastritis.
3. Peptic ulcer.
4. Adenomatous polyp.
5. Blood group A person.
5- Four complications of gastric peptic ulcer:
1. Hemorrhage → Hematemesis & melena.

2. Perforation (10%) → Peritonitis.
3. Fibrosis, leads to:
I. Pyloric stenosis.
II. Hour glass deformity of stomach; due to fibrosis of saddle ulcer.
4. Malignant change:
*In < 1% of gastric ulcers.
6- Four complications of amoebic liver abscess:
(SS CC R)
1. Chronicity: abscess wall becomes fibrotic & calcified.
2. Spread of amoebae through hepatic veins to lungs then systemic circulation.
- 41 -
3. Rupture:
* Upwards → lung abscess.
* Downwards → to peritoneum.
4. Compression of bile ducts → jaundice.
5. Secondary infection → pus formation & toxemia.
7- Three predisposing factors for duodenal peptic ulcer.
1. Habitual intake of spicy & irritant food.

2. Excessive cigarette smoking.
3. Excessive alcohol consumption.
4. Repeated use of drugs, as NSAIDs & corticosteroids.
5. Severe mental stress.
8- Chronic gastritis:
1. Chronic bacterial infection by Helicobacter pylori.

2. Chemicals & toxins: e.g.
I. Bile reflux (after gastro-jejunostomy).
II. Drugs (NSAIDs, …).
III. Alcoholism.
IV. Cigarette smoking.
3. Autoimmune disorder (maybe associated with pernicious anemia).
4. Granulomatous (as in Crohn's disease).
5. Others: as in irradiation & amyloidosis.
- 42 -
O T H E R C A T E G O R Y. A
1- Reflux oesophagitis(GERD)
Aeitology
Repeated reflux of gastric contents, prolonged exposure of oesophgeal mucosa
to the acidic contents of the stomach due to: -
1.incompetence of LES
2.hiatus hernia
Gross
Redness and superficial erosions of lower oesophageal mucosa
Microscopy
• mucosal epithelial hyperplasia
• intraepithelial neutrophils and eosinophils
• Barrett’s oesophagus which may be followed by dysplasia
Complication
1. Barrett’s oesophageal(define):
intestinal (goblet cell) metaplasia occurring within oesophageal mucosa,
may be followed by dysplasia, precancerous, adenocarcinoma
2. Peptic ulceration and fibrosis stricture
2- leukoplakia of tongue
Def.:
thick white mucosal patches, related to chronic irritation causing hyperplasia and
keratosis
Cases: Chronic irritation as in:

1. Smoking
2. Sharp tooth
3. Syphilis
Gross:
thick irregular white tongue mucosal patches
Microscopy:
1. Hyperplastic st. sq. mucosa showing → acanthosis (increase prickle cell)
- 43 -
→hyperkeratosis
2.the underlying submucosa show chronic inflammation
Effects:
precancerous→ squamous cell carcinoma
3- Squamous cell carcinoma of the tongue
Predisposing factors
1.leukoplakia
2.tobacco use
3.human papilloma virus infection (type 11, 16, 18)
4. Tertiary syphilis
Site:
Ant. 2\3 is more common than posterior 1\3 of tongue
Gross:
I. Exophytic pattern
• fungating polypoid pattern
• verrucal pattern: fungating papillary growth
II. Endophytic pattern

• ulcerative pattern (most common)
The malignant ulcer is irregular with everted edges, rough necrotic floor and
indurated base
• diffuse infiltrative pattern(uncommon)
Microscopy
I. squamous cell carcinoma

may be
•well differentiated
•moderately differentiated
•poorly differentiated
II. Verrucal carcinoma
- 44 -
•it is a form of squamous carcinoma formed of papillary groups of very well

differentiated squamous cells showing minimal atypia
• has limited tendency of invasion
Spread
I. Direct
Fixation of the tongue to the floor of the mouth
II. Lymphatic
to cervical L.N
N.B: - lymphatic spread is common due to: -
1.rich lymphatic of the tongue
2.tongue movement
III. Blood spread Late

prognosis
1.verrucous carcinoma has the best prognosis
2.carcinoma of ant.1\3 is better than post. 2\3
- 45 -
GIVE AN ACCOUNT ON:
1 Acute gastritis
Definition
Acute inflammation of gastric mucosa.
Etiology:
1. Irritant or spicy food.
4. Severe stress.
5. Drugs: as NSAIDs & cytotoxic drugs.
6. Uremia (chronic renal failure).
7. Chemical irritation by strong acids or alkalies (as in suicidal attempts).
8. Mechanical trauma: as during endoscopic examination.
9. Gastric irradiation.
10. Systemic infection: as in case of Salmonella.
Pathology
Mucosal erosions (erosive gastritis) associated with congestion , oedema and exudation
of neutrophils. In mild cases , it is acute catarrhal gastritis while in severe cases, it can
be acute hemorrhagic gastritis
2. Chronic gastritis:
Definition
Chronic inflammation of gastric mucosa.
Etiology
1. Chronic bacterial infection by Helicobacter pylori.
2. Chemicals & toxins: e.g.
a. Bile reflux (after gastro-jejunostomy).
b. Drugs (NSAIDs, ..).
c. Alcoholism.
d. Cigarette smoking.
3. Autoimmune disorder (maybe associated with pernicious anemia).
4. Granulomatous (as in Crohn's disease).
5. Others: as in irradiation & amyloidosis.
- 46 -
Pathogenesis:
I. In chronic helicobacter pylori infection:
Bacteria are present in gastric mucosa & stained by Giemsa.
- Bacteria secrete Urease enzyme → Ammonia production, which leads to:
a. Protection of bacteria from gastric HCl.
b. Toxic effect on gastric mucosa → Gastric peptic ulcer.
- Bacteria produce Protease enzyme → breaks gastric mucus → loss of protective
mucus layer → Gastric peptic ulcer.
- Both urease & protease lead to continuous destruction of gastric mucosa with
defective healing → Atrophic gastritis.
- Bacterial products affect parietal cells → They become less responsive to gastrin
→ -ve feed back → hypergastrinemia →↑ HCl secretion → Duodenal peptic ulcer.
II. In autoimmune gastritis:
There are autoantibodies against gastric parietal cells (which are located mainly in corpus
& fundus) → Atrophy parietal cells →↓ HCl & intrinsic factor → Hypoacidity & anemia.
Pathology:
I. Chronic superficial gastritis:
Mild (Early) form of chronic gastritis.
Not accompanied by mucosal atrophy.
Lamina propria shows chronic inflammatory cells (macrophages, lymphocytes & plasma
cells), sometimes neutrophils.
Lymphocytes may form lymphoid follicles (chronic follicular gastritis).
II. Chronic atrophic gastritis:
Advanced stage of chronic gastritis.
Accompanied by mucosal atrophy.
Lamina propria shows chronic inflammatory cells, end arteritis obliterans & fibrosis.
Grades: Mild, moderate & severe.
In severe cases, atrophy is seen without inflammatory cells.
Intestinal metaplasia may occur.
Dysplasia may occur → carcinoma in situ → invasive carcinoma (esp. in H. pylori gastritis).
Neoplasia complicating Pylori gastritis :
a. MALT lymphoma:
Chronic H.pylori gastritis is associated with lymphocytic infiltration and lymphoid
follicles formation. This is may be followed by MALT lymphoma (low grade indolent
small B cell lymphoma).
- 47 -
b. Adenocarcinoma.
3. Acute ulcers of stomach & duodenum
Etiology
Seen in cases of acute gastritis due to drugs, infection, severe stress (as in severe burns),
acute increase of gastric acidity & cerebrovascular accidents.
Shape
Multiple, small (< 1 cm), superficial & hemorrhagic.
4. Chronic peptic ulcer
Definition
A defect within the mucosa of any portion of GIT exposed to acid-pepsin secretion.
Site
1. Duodenum: 1st portion (80%).
2. Stomach: Mainly antral (18%).
3. Within a Barret's esophagus.
4. Margins of gastro-jejunostomy (stomal ulcer).
5. Within a Meckel's diverticulum containing ectopic gastric mucosa.
Etiology (Predisposing factors)
I. Sex
Male to female ratio is 3:1.
II. Age
Usually above 20 years.
III. Others
1. Habitual intake of spicy & irritant food.
4. Repeated use of drugs, as NSAIDs & corticosteroids.
5. Severe mental stress.
Pathogenesis
I. Duodenal ulcers are caused by:
I.I. Hyperacidity:
In case of H. pylori gastritis (most common cause).
In Zollinger-Ellison syndrome: pancreatic gastrin-secreting tumor (gastrinoma)
- 48 -
→hyperacidity → duodenal peptic ulcer.

In case of chronic stress with high vagal tone.
I.II Genetic predisposition:
Genetic defect → decrease of normal protective mechanisms (surface mucus & mucosal
prostaglandins).
Evidence of genetic predisposition:
Duodenal ulcers have familial tendency.
Duodenal ulcers are most commonly found in blood group O persons (30 times more
than other blood groups.
II. Gastric ulcers:
Not caused by hyperacidity (Gastric HCl is normal or low).
No genetic predisposition.
Causes of gastric ulcers:
a. Mucosal de-vitalization by:
H. pylori gastritis (by enzymatic effects & not hyperacidity).
Localized mucosal ischemia (microthrombi).
Duodenal gastric reflux → chemical mucosal injury by bile & pancreatic juice.
Delayed gastric emptying.
Impaired mucus-bicarbonate barrier.
b. Traumatic effect of irritant & spicy food.
Role of H. pylori infection in duodenal & gastric peptic ulcers:
Bacteria are present in gastric mucosa & stained by Giemsa.
- Bacteria secrete Urease enzyme → Ammonia production, which leads to:
1. Protection of bacteria from gastric HCl.
2. Toxic effect on gastric mucosa → Gastric peptic ulcer.
- Bacteria produce Protease enzyme → breaks gastric mucus → loss of protective
mucus layer → Gastric peptic ulcer.
- Both urease & protease lead to continuous destruction of gastric mucosa with
defective healing → Atrophic gastritis.
- Bacterial products affect parietal cells → They become less responsive to gastrin → -
ve feed back → hypergastrinemia →↑ HCl secretion → Duodenal peptic ulcer.
- 49 -
Pathology
I. Gross picture
Duodenal ulcer Gastric ulcer
Site: 1st inch of 1st part (anterior Pyloric antrum (at lesser
or posterior). curvature).
Size: 1-3 cm
Shape: Rounded or oval. Rounded or oval or saddle
shaped.
Edges: Sharp or sloping.
Floor: Smooth.
Base: Indurated, due to fibrosis.
II. Microscopy:
Superficial part of ulcer shows necrotic debris.
Deep part shows chronic inflammatory cells & fibrosis.
Complications:
I. Hemorrhage → Hematemesis & melena.
II. Perforation (10%):
• In gastric ulcer → Peritonitis.
• In duodenal ulcer → Acute hemorrhagic pancreatitis.
III. Fibrosis, leads to:
Duodenal or pyloric stenosis.
Hour glass deformity of stomach; due to fibrosis of saddle ulcer.
IV. Malignant change:
• In < 1% of gastric ulcers.
• Duodenal ulcers are not precancerous.
5. Carcinoma of stomach
Definition
Primary malignant neoplasm arising from gastric mucosa.
Etiology
Exact etiology is unknown, however the following are predisposing factors:
- 50 -
I. Age & Sex:

More common in males > 40 years.
II. Others:
• Smoked & spicy food.
• Chronic gastritis.
• Gastric peptic ulcer.
• Adenomatous polyp.
• Blood group A persons.
Pathology:
Site
Most common in pyloric antrum & cardia but anywhere in the stomach.
Gross picture
- Polypoid fungating projecting mass.
- Malignant ulcer: raised everted edges, rough necrotic floor & indurated base.
- Infiltrative pattern, maybe:
a. Deep infiltrative type → invades musculosa or deeper, either:
Localized: Affecting pyloric region which appears thickened & rigid, with dilatation of
rest of the stomach due to pyloric stenosis.
Diffuse: The whole stomach appears rigid & small (Leather bottle stomach or Linitis
plastica).
b. Superficial spreading type:
Limited to mucosa & submucosa which appear indurated, musculosa is free.
Microscopic types include:
- Adenocarcinoma (intestinal or diffuse type).
- Mucoid carcinoma.
- Signet ring cell carcinoma.
- Undifferentiated carcinoma.
Microscopic extent of invasion:
Superficial spreading type (early gastric carcinoma) → only mucosa & submucosa are
affected.
Advanced gastric carcinoma → deep invasion (musculosa or deeper).
- 51 -
Spread
1. Direct → Pancreas, colon, liver, spleen.
2. Lymphatic (early, either by embolization or permeation) → regional LNs (gastric, celiac,
para-aortic, ..).
3. Blood (late) → Liver mainly (portal), then lungs, bones, ...
4. Transcoelomic spread:
Peritoneal metastasis & hemorrhagic ascites.
Krukenberg tumors (bilateral ovarian metastasis).
Other effects:
1. Hematemesis & melena.
2. Pyloric obstruction.
3. Mucosal destruction → hypochlorhydria & intrinsic factor deficiency.
4. Anemia due to loss of blood & deficiency of intrinsic factor.
Immunohistochemistry & molecular genetics:
Tumor cells express cytokeratin, carcinoembryonic antigen & CDX2 (90% of cases).
Germline truncating mutations of E-cadherin (CDH1) gene found in families with
hereditary diffuse gastric cancer. Cancer susceptibility is so high that prophylactic
gastrectomy is advised in these patients.
6. Gastrointestinal stromal tumors (GIST)
Not uncommon.
Arise in any part of GIT, most commonly in stomach.
Consist of proliferated spindle cells (& sometimes epithelioid cells) that may exhibit
smooth muscle differentiation (express muscle markers as SMA & desmin), neural
differentiation (as S100), dual markers (both smooth muscle & neural markers).
They maybe undifferentiated.
Many tumors express CD117 (c-kit) & it is of therapeutic significance.
Unpredictable behavior (maybe benign or malignant).
Malignancy is more common in large-sized tumors with high mitotic activity.
7. Ulcerative colitis:
Definition
Chronic inflammatory disease of unknown etiology affecting mucosa of any part of
colon.
It's characterized by active phase of inflammation of colon, manifested by attacks of
abdominal pain, diarrhea & bleeding, separated by periods of remission.
Etiology:
Unknown, however maybe autoimmune, psychosomatic or genetic.
- 52 -
Pathology:
Site:
Starts in the rectum (ulcerative proctitis) & progresses to involve the whole colon
(ulcerative pancolitis).
Gross:
Congested friable mucosa, easily bleeding on touch.
During active phase, multiple superficial irregular ulcers are common.
In between attacks, mucosa between the ulcers show pseudopolyps.
Fibrosis occurs later on.
Microscopy:
1. Active phase is characterized by:
Mucosal ulcers.
Crypt abscesses (crypt lumen contains neutrophils, pus cells & necrotic debris).
Lamina propria shows congested capillaries & acute inflammatory cells (neutrophils &
macrophages).
Goblet cell depletion.
2. Chronic phase (in between attacks) is characterized by:
Crypt branching.
Pseudopolyps: Hyperplastic swollen edematous congested mucosa.
Mucosal dysplasia may occur.
Fibrosis.
Complications:
1. Hemorrhage (Bleeding per rectum).
2. Perforation → Septic peritonitis.
3. Fistula.
4. Fibrosis → Stricture of colon.
5. Precancerous → colonic carcinoma (30% of cases).
6. 2ry amyloidosis.
7. Liver damage of unknown mechanism → Steatosis & biliary cirrhosis.
8. Regional enteritis (Crohn's disease)
Definition:
Chronic inflammatory disease of unknown etiology affecting any part of the gut from
mouth to anus, but most commonly the terminal ileum.
Characterized by transmural inflammation of the affected part (whole wall is affected,
not only mucosa).
Manifested by attacks of abdominal pain, malabsorption & loss of weight.
- 53 -
Etiology:
Unknown, however maybe autoimmune, psychosomatic, genetic or infective factors.
Pathology:
Gross:
Mucosal fissure ulcers, mucosa in between is normal (skip areas).
Enlarged mesenteric LNs.
Rigid wall; due to fibrosis.
Congested mesentery.
Microscopy:
Chronic non-specific inflammation, with non caseating sarcoid-like granulomas
(epithelioid cells + giant cells) in 60% of cases.
Inflammation is transmural.
Fibrosis occurs later on.
Complications:
1. Hemorrhage (hematemesis, melena or bleeding per rectum according to affected
part).
2. Perforation.
3. Fistula.
4. Fibrosis & strictures.
5. 2ry amyloidosis.
6. Malabsorption.
7. Rarely carcinoma of small or large intestine.
9. Dysentery
Definition
Inflammation of mucosa of large intestine characterized by diarrhea & tenesmus, usually
accompanied by passage of blood & mucus with stools.
Types
1. Amoebic dysentery.
2. Bacillary dysentery.
3. Bilharzial dysentery.
Amoebic dysentery Bacillary dysentery
Etiology
Causative organism: Entamoeba histolytica Causative organism: Shigella bacilli.
cysts.
Mode of transmission: Ingestion of Mode of transmission: Ingestion of
- 54 -
contaminated food. contaminated food.

Pathogenesis
Cyst wall dissolves in small intestine Bacteria secrete exotoxins →
(alkaline pH) → 4 amoeba → proteolytic enz. pseudomembranous inflammation affecting
→ division & invasion of mucosa (mainly colon mainly.
colonic; due to fecal stagnation).
Gross picture
Colonic amoebic ulcers: Colonic pseudomembranous inflammation:
Multiple. Hyperemic swollen edematous mucosa,
Small or large. covered by firm greyish white necrotic
Undermined edges (flask shaped). pseudomembrane.
Yellowish necrotic floor. Parts of pseudomembrane detach → small
Base is formed of musculosa. superficial ulcers with sharp edges.
Mucosa between ulcers is normal. Intestinal lumen contains greenish exudate
Healing by fibrosis → stricture. & mesenteric LNs are enlarged.
Microscopy
Edges & floor of ulcers show amoebae The pseudomembrane consists of: necrotic
surrounded by clear zone (due to lysis of mucosa, PMNs, macrophages, bacteria &
surrounding tissue by their proteolytic fibrin.
enz.) Submucosa shows dilated capillaries, acute
Amoebae are rounded, 25 microns in inflammatory cells, acute inflammatory
diameter with eccentric nuclei. edema & fibrin.
Necrotic foci & inflammatory cells
surround amoebae.
Complications
1. Intestinal complications: 1. Intestinal complications:
Hemorrhage (bleeding per rectum). Hemorrhage (bleeding per rectum).
Perforation → Septic peritonitis & fistulae. Perforation → Septic peritonitis & fistulae.
Fibrosis → Stricture. Fibrosis → Stricture.
Straining → Rectal prolapse. Straining → Rectal prolapse.
Abnormal peristalsis → Intussusception. Abnormal peristalsis → Intussusception.
Amoeboma: Amoebic granuloma with Secondary infection.
secondary infection forming large mass. Chronic carrier.
Chronic carrier.
2. Spread: 2. Toxemia:
Direct → Perianal skin ulcer. Toxic myocarditis.
- 55 -
Blood → Amoebic liver abscess & Arthritis.

sometimes lung & brain abscesses. Peripheral neuritis.
Iritis.
10. Amoebic liver abscess:

Etiology:
Spread of amoeba from intestine to liver through portal vein.
Pathology:
Site:
Right lobe is more common.
Mechanism:
Foci of necrosis (Amoebic hepatitis) followed by putrefaction & formation of amoebic
abscess.
Gross:
Single or multiple.
Usually large.
Irregular shreddy wall.
Lumen contains chocolate-coloured fluid (amoebic pus).
Microscopy:
Amoebic pus: Necrotic liver tissue.
Wall of abscess contains amoebae & inflammatory cells.
Complications:
1. Chronicity: abscess wall becomes fibrotic & calcified.
2. Spread of amoebae through hepatic veins to lungs then systemic circulation.
3. Rupture:
Upwards → lung abscess.
Downwards → to peritoneum.
4. Compression of bile ducts → jaundice.
5. Secondary infection → pus formation & toxemia.
Typhoid ulcers:
Multiple & raised.
Undermined edges.
Rough necrotic floor.
In small intestine: Oval, with their longitudinal axis parallel to that of intestine.
In large intestine: Rounded.
- 56 -
CO MPAR E
1. Ulcerative colitis & Crohn's disease:

Ulcerative colitis Crohn's disease
Idiopathic inflammatory bowel disease, Idiopathic inflammatory bowel disease,
possibly autoimmune. possibly autoimmune.
Affects any part of colon. Affects any part of GIT; most commonly
terminal ileum.
Affected part shows superficial ulcers. Ulcers are usually fissuring.
Affected part may be dilated. Affected part is strictured.
Affected part shows no skip (free) areas. Affected part shows skip areas.
inflammation affects mucosa. Inflammation is transmural (full thickness).
Granulomas are uncommon. Granulomas are common.
Crypt abscesses are common. Crypt abscesses are rare.
Dysplasia & malignancy are uncommon.
Malabsorption doesn't occur. Dysplasia & malignancy are rare.
Malabsorption occurs.
2. Amoebic & bacillary dysentery:
Amoebic dysentery Bacillary dysentery

Etiology
Causative organism: Entamoeba histolytica Causative organism: Shigella bacilli.
cysts.
Mode of transmission: Ingestion of Mode of transmission: Ingestion of
contaminated food. contaminated food.
Pathogenesis
Cyst wall dissolves in small intestine Bacteria secrete exotoxins →
(alkaline pH) → 4 amoeba → proteolytic enz. pseudomembranous inflammation affecting
→ division & invasion of mucosa (mainly colon mainly.
colonic; due to fecal stagnation).
Gross picture
Colonic amoebic ulcers: Colonic pseudomembranous inflammation:
Multiple. Hyperemic swollen edematous mucosa,
- 57 -
Small or large. covered by firm greyish white necrotic

Undermined edges (flask shaped). pseudomembrane.
Yellowish necrotic floor. Parts of pseudomembrane detach → small
Base is formed of musculosa. superficial ulcers with sharp edges.
Mucosa between ulcers is normal. Intestinal lumen contains greenish exudate
Healing by fibrosis → stricture. & mesenteric LNs are enlarged.
Microscopy
Edges & floor of ulcers show amoebae The pseudomembrane consists of: necrotic
surrounded by clear zone (due to lysis of mucosa, PMNs, macrophages, bacteria &
surrounding tissue by their proteolytic fibrin.
enz.) Submucosa shows dilated capillaries, acute
Amoebae are rounded, 25 microns in inflammatory cells, acute inflammatory
diameter with eccentric nuclei. edema & fibrin.
Necrotic foci & inflammatory cells
surround amoebae.
Complications
1. Intestinal complications: 1. Intestinal complications:
Hemorrhage (bleeding per rectum). Hemorrhage (bleeding per rectum).
Perforation → Septic peritonitis & fistulae. Perforation → Septic peritonitis & fistulae.
Fibrosis → Stricture. Fibrosis → Stricture.
Straining → Rectal prolapse. Straining → Rectal prolapse.
Abnormal peristalsis → Intussusception. Abnormal peristalsis → Intussusception.
Amoeboma: Amoebic granuloma with Secondary infection.
secondary infection forming large mass. Chronic carrier.
Chronic carrier.
2. Spread: 2. Toxemia:
Direct → Perianal skin ulcer. Toxic myocarditis.
Blood → Amoebic liver abscess & Arthritis.
sometimes lung & brain abscesses. Peripheral neuritis.
Iritis.
- 58 -
DEFINE
1. Ulcerative colitis:
Chronic inflammatory disease of unknown etiology affecting mucosa of any part of
colon.
It's characterized by active phase of inflammation of colon, manifested by attacks of
abdominal pain, diarrhea & bleeding, separated by periods of remission.
2. Crohn's disease:
Chronic inflammatory disease of unknown etiology affecting any part of the gut from
mouth to anus, but most commonly the terminal ileum.
Characterized by transmural inflammation of the affected part (whole wall is affected,
not only mucosa).
Manifested by attacks of abdominal pain, malabsorption & loss of weight.
3. Dysentery:
Inflammation of mucosa of large intestine characterized by diarrhea & tenesmus, usually
accompanied by passage of blood & mucus with stools.
- 59 -
Diseases of large intestine
Give an account on
1. Complications of acute appendicitis

Acute gangrenous appendicitis
severe suppurative appendicitis may be followed by putrefaction → gangrene,
perforation, peritonitis → severe toxemia
Appendicular mass and abscess
in some cases of acute suppurative appendicitis, the appendix may become glued by
fibrinous exudate to the adjacent intestinal loops and the greater omentum (policeman
of the abdomen), producing appendicular mass
Inflammation may resolve or progress to appendicular abscess
Appendicular abscess may resolve or become complicated by:
a. Rupture
into peritoneal cavity (diffuse peritonitis) or into abdominal wall (sinus) or into loops of
intestine (fistula)
b. Healing
peritoneal adhesions → intestinal obstruction
Rupture & septic peritonitis
Portal pyaemia → due to thrombophlebitis of appendicular vein
Chronic appendicitis → fibrosis → stenosis of appendicular lumen (chronic obliterative
appendicitis) → repeated acute attacks
Mucocele → distention of appendix with mucous:
a) Rupture into peritoneal cavity >pseudomyxoma peritonii
b) 2ry infection > empyema of the appendix
- 60 -
2. Functional obstruction (paralytic ileus).

Definition
This is sudden loss of intestinal peristalsis
etiology
Sudden neuromuscular (autonomic) dysfunction by:
a. Sympathetic stimulation during abdominal operations
b. Parasympathetic inhibitors as by toxins in peritonitis
c. Spinal cord injuries
Effects
a. general effects → vomiting, dehydration, shock & electrolyte imbalance.
b. Local effects → intestinal dilatation due to loss of peristalsis.
1. Simple obstruction Vascular obstruction
(Mesenteric obstruction)
Definition Obstruction of the lumen of intestine Thrombosis or embolism of
&Aetiology without obstruction of vessels mesenteric vessels leads to
a. Mass of ascaris worms gangrene of the affected intestinal
b. swallowed foreign body segment with loss of peristalsis
c. Fecal concretion on top of chronic (intestinal obstruction)
intestinal obstruction a. Mesenteric artery thrombosis on
d. Gall stone ileus: it occurs when the top of atherosclerosis
inflamed gall bladder gets adherent to b. Embolism derived from cardiac
a loop of intestine accompanied by thrombi as vegetations
fistula formation through which a big
gall stone pass causing intestinal
obstruction.
General effects Vomiting, dehydration, shock and electrolyte imbalance
Local effects a. Bacteria my penetrate a. hemorrhagic infarction &
intestinal wall → peritonitis intestinal gangrene → toxemia,
rupture & peritonitis
b. intestinal collapse distal to obstruction
c. intestinal distention (fluids & gases) proximal to obstruction with strong
peristalsis
d. venous compression due to intestinal distention >> intestinal edema or
hemorrhage
- 61 -
3. Strangulated obstruction.
Intussusception Volvulus
definition Invagination of intestinal segment into a Twisting of a loop of intestine upon
distal segment. itself about the axis of its mesentery or
around on abnormal fibrous band.
The intussuscepted bowl may be palpable as
a sausage-shaped mass in abdomen.
Aetiology Most common in infants duo to irregular Volvulus of sigmoid (commonest):
peristalsis In patient with congenital long
mesocolon
- gastroenteritis
or loaded sigmoid due to constipation
- intestinal parasites
- volvulus of ileum (rarely)
- Meckel’s diverticulum In Meckel's diverticulum
- intestinal tumor or polyps
- irritant food and fasting
Types
- Ileo-cecal: commonest.
- Enteric (Ileo-ileal).
- Colonic (colo-colonic) is rare.
General Vomiting, dehydration, shock, electrolyte imbalance
effects
Local effects a. Hemorrhagic infarction & intestinal gangrene > toxemia, rupture & gangrene.
b. Intestinal collapse distal to obstruction.
c. Intestinal distention proximal to obstruction.
d. Venous compression due to intestinal distention > intestinal edema &
haemorrhage.
4. strangulated hernia.
Causes
a. Distention of the hernia intestinal loop by excess contents > constriction
(strangulation) of the loop against the edges of the defect
b. crowding of the hernia sac by herniation of a new loop of intestine or omentum
general effects
vomiting, dehydration, shock & electrolyte imbalance
- 62 -
local effects
1. Intestinal collapse distal to obstruction
2. Intestinal dilation proximal to obstruction
3. Compression of veins or intestinal wall > congestion & edema
4. Compression of arteries > intestinal infarction & moist gangrene
5. Leakage of intestinal contents through gangrenous loop > peritonitis & toxemia
5. Describe causes of melena.
Answer → see cause of hematemesis.
6. Chronic intestinal obstruction.
Definition
Gradual incomplete obstruction in large intestine
Aetiology
Fibrous stricture >crohn’s disease, dysentery, ulcerative colitis, diverticulosis, TB
a.Tumors
b. Peritoneal adhesions
c. Megacolon: congenital (Hirschsprung’s disease) or acquired (Idiopathic)
Pathological effects
1. Intestinal collapse distal to obstruction (some degree).
2. Intestinal hypertrophy and dilatation proximal to obstruction.
3. The mucosa shows stercoral ulcers caused by trauma of retained faeces.
4. The retained faeces may become hard (faecal concretion) & become impacted in the
narrow intestinal segment > acute intestinal obstruction.
5. Constipation & vomiting (less frequent than acute obstruction).
7. Carcinoma of large intestine.
Definition
This is a primary malignant neoplasm arising from large intestine mucosa
1. Hereditary: hereditary non polyposis colo-rectal cancer syndrome (HNPCC)
&familial polyposis colo-rectal cancer
2. Adenomas: villous, tubular, tubulovillous adenoma
3. Dysplasia of ulcerative colitis
- 63 -
4. Diet: increased dietary fat & decreased dietary fibers

Gross
- A polypoid mass fungating into the lumen
- An irregular malignant ulcer with >everted edges , necrotic floor, indurated base
- An infiltrative growth > stricture of a segment of intestine (annular type)
Site
a. 75% in rectum and sigmoid
b. 25% in the rest of colon
Microscopy
- Adenocarcinoma: see general pathology
- Mucoid carcinoma > this is an adeno-carcinoma with abundant extracellular mucin
secretion appear as pale mucinous pools around the malignant acini
- Signet ring cell carcinoma > the malignant cells show intracytoplasmic mucin that
pushed the nuclei eccentrically & no acinar differentiation
- Undifferentiated carcinoma > great cellular anaplasia& grow faster
Spread
1. Direct to urinary bladder, vagina & liver
2. Lymphatic to mesenteric paraortic lymph nodes
3. Blood to liver, lung & other sites
4. Trans-celomic → hemorrhagic ascites, peritoneal metastasis, Krukenberg tumors in
females
Effects
1. Bleeding per rectum
2. Piles
3. Intestinal obstruction → chronic
4. Intestinal perforation → septic peritonitis
5. Fistula between intestinal loops pf bladder an vagina
- 64 -
8. the benign tumors & describe the morphology of one of them.

I. Adenomas (polypoid adenomas)
Tubular Villous (papillary Tubulovillous Familial polyposis
(adenomatous adenoma)
polyp)
- Solitary or - Solitary, - Combined - Autosomal dominant disease.
multiple. Branching glands features of the - The entire colon shows
showing anaplasia two types
- Proliferated hundreds of small polyps of
tubular glands that - Highly precancerous. tubulovillous type.
show dysplasia - It’s highly precancerous and
- precancerous
malignant change occurs around
age of 30.
Polyposis syndrome:
- Gardner's syndrome → colonic
polyps, osteomas, exostosis.
- Turcot’s syndrome → colonic
polyps, brain tumors.
II. Hamartomatous polypi (Peutz-Jegher’s syndrome)

Autosomal dominant disease characterized by:
- Multiple gastro-intestinal polypi composed of mucous glands, fibrous cores, smooth
muscle bundles (hamartoma)
- Melanin pigmentation of face, lips, oral mucosa and digits
III. Others:
1. GIST ( Gastrointestinal stromal tumor)
2. Hemangioma
3. Lipoma
9. The colonic polypi and discuss the pathology of one of them.

a. Neoplastic polypi: (Q. 7)
- Adenomas (polypoid adenomas) > tubular, villous, tubulovillous, familial
- hamartomatous polypi
- 65 -
b. Non-neoplastic polypi:
1. Pseudopolypi:
Swollen, edematous, congested, inflamed& hyperplastic mucosa
2. Hyperplastic polypi:
Consists of hyperplastic mucosal glands showing excess mucin secretion and appear as
small sessile polyps
3. Juvenile polypi (retention polypi)
Hyperplastic colonic glands, some of them are cystically dilated with mucin
4. Bilharizial polyps:
Pathogenesis
Ova trapped in submucosa, surrounded by inflammation. Repeating of the process leads
to: mucosal elevation with mucosal hyperplasia & polyp formation
Gross
Single or multiple,
Sessile, pedunculated or complex branching polyps
Reddish & show granular cut section
2-20 cm in diameter
Microscopy
The polyp consists of core of CT derived from submucosa showing ova surrounded by
macrophages, lymphocytes, eosinophils, fibroblasts with cover hyperplastic mucosa
NBs
• Leukoplakia is differentiated from sq. cell papilloma by absence of hyperplastic
basal cells
• ّ
Tuberculous ulcer of tongue → in tip →mechanism of ‫ﺗﻔﻪ‬
• Lymphatic spread in sq. cell carcinoma of tongue due to motility and rich lymph
nodes
• Sq. cell carcinoma of lip → in lower → due to gravity (irritants)
• Pleomorphic adenoma is only benign tumor with recurrence after surgical
incision
• take care: Mikulicz disease → Sialadinitis
• But Mikulicz cells → Rhinoscleroma
- 66 -
• Complication of chronic gastritis: fibrosis-pyloric obstr.-dysplasia

• Autoimmune gastritis causes: micro and macrocytic anemia
• No spread in ch. Gastritis bec. H.pylori cannot live outside intestine
• Blood grp O → Duodenal ulcer
• Blood grp A →gastric carcinoma
Important names:
• Mikulicz disease: Sialadinitis

• Barrett's metaplasia: oesophagus (GERD)
• Plummer Vinson syndrome: oesophagus → female → carcinoma
• Menterier's disease: Hypertrophic gastropathy
• Zollinger-Ellison syndrome: gastrin s. Tumor → duodenal ulcer
• Krukenburg tumor: bilateral ovarian metastasis(transceolomic spread)
• Gardner's and turcot's syndromes: Colonic polypi (Adenomas)
• Peutz-jegher syndrome: Hamartomatous tumor of colon
.
1. Intussusception
Aetiology
Gas ‫ وﺟﻪ ﻟﻪ‬Polyp ‫ﻣﺎﻳﻜﻞ اﻛﻞ وﺣﺶ ﻓﻄﻠﻊ ﻟﻪ‬
Meckel's Diverticulum → ‫ﻣﺎﻳﻜﻞ‬

Irritant Food → ‫اﻛﻞ‬
Parasites → ‫وﺣﺶ‬
Polyp or tumor
Gas-troenteritis
85‫ص‬
Bleeding per Rectum ‫وﻟﺪ ﺻﻐ� ﻣﻦ ﻛﺮﺘ ﻣﺎﻫﻮ ﻛﺎن ﻣﺰﻧﻮق ﺟﻪ ﻟﻪ‬ .2
XD ‫ ﻋﻨﺪ ﺗﻴﺘﺎ‬XD ‫ﻓﺒﺎﺑﺎاه ﻗﺎل ﻟﻪ اﻋﻤﻞ ﺑﺒﻰ‬
TITA ‫ ﻋﻨﺪ‬PP
• Piles
- 67 -
• Polyps
• Tumors
• Idiopathic
• TB&Inflammation
• Anal Fissure
Page 91.
non neoplastic colonic polypi → ‫اﻟﺒﻠﻬﺎرﺳﻴﺎ ﻛﺪاﺑﺔ ﺑﺘﻘﻮل اﻧﻬﺎ ﻛﺒ�ة ﺑﺲ ﻫﻲ ﺻﻐ�ة‬ .3
‫ ﺑﻠﻬﺎرﺳﻴﺎ‬bilaharzial polyp
‫ ﻛﺪاﺑﺔ‬pseudopolyp
‫ ﻛﺒ�ة‬hyperplastic polyp
‫ ﺻﻐ�ة‬juvenile polyp
.
4. Aetiology of acute gastritis
(NSIAD & Chemical irritation) ‫ﻧﺎس ﻗﺎﻋﺪﻳﻦ ﻳﻀﺮﺑﻮا ﻓﻰ ﻛﻴﻤﻴﺎ‬
cigarette‫و‬
(spicy food ) ‫وﻣﻌﺎﻫﻢ اﳌ َﺰة ﺑﺘﺎﻋﺘﻬﻢ‬
irritation ‫ﺣﺼﻠﻬﻢ‬
(trauma ) ‫ﻗﺎﻣﻮا ﻋﻮروا ﺑﻌﺾ‬
(sever stress .ischemia and shock)‫ﻓﺪﺧﻠﻮا ﻓﻰ‬
uraemia &infection‫وﻧﺰود‬
p67
5. Aetiology of chronic gastritis. IIIIIA (5 i +A)
1. Infection with H.pylori.
2. Irritants. Drugs, bile reflux, spicy food, smoking & spirits.
3. Immunologic (autoimmune).
4. Inflammation.. granulomatous(Crohn's disease).
5. Irradiation
6. Amyloidosis ( I ‫)ﻣﻌﺮﻓﺘﺶ أﺟﻴﺒﻠﻬﺎ ﺣﺎﺟﺔ ﺗﺒﺪأ ﺑﺤﺮف اﻟـ‬
.
- 68 -
6. TYPHOID FEVER
Pathology
Intestinal lesions: SINUS
1st week → SI Swollen Intestine
2 nd week → N Necrotic mucosa
3 rd week → U Ulcer formation
4 th week → S Scar formation of healed ulcer
Complications
Intestinal
ulcer formation = ulcer complication stump.
hemorrhage.
perforation.
extraintestinal
3 systems
1. skeletal system -bone and joints-
2. circulatory system -heart and vessels-
3. nervous system
rest in a word - GTLK- ‫اﻫﻰ ﻃﺮ�ﻘﺔ ﺳﻬﻠﺔ "ﺟﺘﻠﻚ" ﻟﺤﺪ ﻋﻨﺪك‬
• Gall bladder
• Toxic lesion
• Lungs
• Kidneys
7. Causes of oesophageal hematemesis

it may be a serious case then “MOVE to ICU “
• M… Malignant
• OV … oesophageal varices
• E … Else:: Aortic aneurysm
• I… Inflammation (esophagitis)
• C … Carcinoma
• U… Ulcers
p 66.
- 69 -
8. Hematemesis
Esophageal, Gastric, Duodenal, General ‫ ﻣﻘﺴﻮم ﻷرﺑﻊ ﺣﺎﺟﺎت ﻛﺒﺎر‬Etiology ‫ﻫﻮ ﻣﻌﺮوف إن اﻟـ‬
causes
‫ﻓﻴﺼﻞ‬.‫ د‬Stamp ‫ ﻣﻌﺮوف ﻣﻦ‬General ‫ﺑﺎﻟﻨﺴﺒﺔ ﻟﻠـ‬
Hematemesis ‫ ﺣﺎﺟﺎت ﻟﻮ ﺟﻢ ﻫﻴﻌﻤﻠﻮا‬3 ‫ اﻟﺘﺎﻧ� ﻫﻤﺎ‬3 ‫ﺑﺎﻟﻨﺴﺒﺔ ﻟﻠـ‬
Inflammation or Ulcers or Tumors
Examples
1. Gastric cause:
Gastritis, Ulcers (acute / peptic), Tumors
2. Duodenal causes:
Duodenitis ..Ulcers(acute/peptic)..Tumors
3. Esophageal causes:
Oesophagitis... Oesophageal ulcers .. Tumors ( carcinoma of Oesophagus or mediastinal
Tumors infiltrating Oesophagus.
Artery & Vein �‫ﻟﻜﻦ ﺑﻤﺎ أن ده أﻫﻢ ﺳﺒﺐ ﻓﻬﻨﺰود ﻋﻠﻴﻪ ﺣﺎﺟﺘ‬
Artery → Aortic aneurysm
Vein → Oesophageal Varices
Page 66.
9. Etiology of acute gastritis (( 7S +2C+2 I))
• Smoking
• spicy food
• salmonellosis
• severe stress
• shock
• strong alkalies
• Cytotoxic drugs
• Consumption of alcohol
• Irradiation
• Ischemia
- 70 -
10. Chronic Gastritis Page 67

etiology
Ciara‫ﻣﺘﺠﻤﻌﺔ ﻲﻓ ﻛﻠﻤﺔ ﺳﻴﺎرة‬
C: Chemical irritation ex acids
I: infections (Specific → Crohn's disease .. Non specific → H.pylori)
A: Autoimmune disease
R: Radiation
A: Amyloidosis.
11. Causes of Bleeding Per Rectum

FRESH RED Blood ‫ﺑﻤﺎا إﻧﻪ‬
so
"‫"ﻳﺎ ﺣﺒﻴﺒﺘﻰ اﺷﺮﺑﻰ اﻟﻌﺼ� داا ﻓﻴﻪ ﻓﻴﺘﺎﻣﻴﻨﺎات‬
HAPIPTI + 2 Vitamins
• H ypertension & Hemophilia
• A nal fissure
• P iles
• I nflammation
• P olyps
• T umors
• I diopathic
• Vitamins C & K
12. Bleeding per rectum

General causes:
HHPLL w deficiency in 2 vitamins
Intestinal causes:
(2i +ATP)
- 71 -
• I → inflammation
• I → idiopathic
• A → anal fissure
• T → tumours
• P → polyps and piles
13. Ulcers of oral cavity

Common in Tongue (T +MDAS) ‫" َﻣﺪاس" ﻣﻌﻠﺶ ﻋ� اﻟﻜﻠﻤﺔ ﺑﺲ ﻣﻠﻘﺘﺶ ﻏ�ﻫﺎ‬
• T:tuberculous
• M:malignant
• D:Dental
• A:Aphthous
• S:Syphilitic
gross&site ‫ﻧﺼﻴﺤﺔ ﻟﻮ ﻋﺎﻳﺰ�ﻦ ﺗﺬاﻛﺮوﻫﻢ ﻳﺒﻘﻲ ﻲﻓ ﺟﺪول و ﺗﻘﺎرﻧﻮا ﻣﺎ ﺑﻴﻨﻬﻢ ﻲﻓ اﻟـ‬

�‫( و اﻟﺸﺒﺎب اﻟﻄﺎﻳﺶ و دول ﻛﺘ‬small) ‫ دﻳﻪ ﺑﺘﺎﻋﺔ اﻟﻌﻴﺎل اﻟﺼﻐ�ة‬Aphthous‫ﺑﺲ اﻟـ‬
‫ و اﻟﻜﻠﻤﺔ اﻟ� ﺑﻴﻘﻮﻟﻮﻫﺎ‬unknown aetiology ‫( و ﻣﺤﺪش ﺑﻴﺒﻘﻲ ﻓﺎﻫﻤﻠﻬﻢ ﺣﺎل‬multiple&common)
recurrence&remain for short time ‫اﻟﻨﻬﺎردة ﻳﺮﺟﻌﻮا ﻓﻴﻬﺎ ﺑﻜﺮه‬
.painful ‫و ﻣﺸﺎﻋﺮﻫﻢ ﺣﺴﺎﺳﺔ و ﺑﻴﺘﺄﳌﻮا ﺑﺴﺮﻋﺔ‬
14. Squamous cell carcinoma of tongue:
2 ‫رﻗﻢ اﻟﺴﻌﺪ ﺑﺘﺎﻋﻬﺎ‬

Etiology
�‫ ﺑﺲ ﻫﻨﺰود ﺣﺎﺟﺘ‬GIT‫ ﺑﺘﻮع اﻟـ‬5 S‫ و ﻫ�ص اﻟـ‬cancer ‫زي أي‬
Human papilloma virus, leukoplakia
Pathology
Site
‫ﻣﻔﻴﻬﻮش ﻣﺸﻜﻠﺔ‬
Gross
- 72 -
1. exophytic: fungating polypoid / papillary.

2. Endophytic: ulcerative / diffuse infiltrative growth.
Microscopic
1. sq. cell carcinoma
2. Verrucous carcinoma
Spread
‫ﻋﺎدي‬
Prognosis
1. Verrucous is the best
2. ant 2/3 is better than post 1/3
15. Sialadenitis
Sm ‫ ﻳﺎ‬VIP ‫اﻟﻐﺪة دﻳﻪ ﻓﻴﻬﺎ اﻳﻪ؟ ﻓﻴﻬﺎ ﺣﺎﺟﺎت‬
1. Virus: Mumps
2. Pus: acute suppurative parotitis
3. Stone: chronic calcular sialdenitis
4. Inclusions: cytomegalic inclusion disease
5. Mikuilcz cell: mikuilcz disease
.
16. Carcinoma of Large Intestine
"‫ ﻓﺒﻴﺘﺤﺴﺪوا ﻣﻦ "ﻗﺮاﻳﺒﻬﻢ" و"ﺟ�اﻧﻬﻢ‬،‫ﺑﺘﺎع اﻷﻏﻨﻴﺎء اﻟ� ﺑﻴﺎﻛﻠﻮا ﻟﺤﻤﺔ ﻛﺘ�ة وﺳﻠﻄﺔ ﻗﻠﻴﻞ‬
Inc. Dietary fat
Dec. Fibers
Carcinoma ‫ ﺑﻴﺒﻘﻰ‬Dysplasia ‫ ﻻﻧﻪ ﳌﺎ ﺑﻴﺤﺼﻞ ﻟﻪ‬Ulcerative colitis‫ﻗﺮ�ﺒﻪ اﻟـ‬
‫ واﺧﻮاﺗﻬﺎ‬Adenoma‫ﺟ�اﻧﻪ اﻟ� ﻋ� ﻃﻮل ﺟﻤﺒﻪ ﻓﺒﻴﺒﻘﻰ اﻟـ‬
88 ‫ص‬
.
17. Carcinoma of stomach
Predisposing factors: 5 A
• A → Autoimmune chronic gastritis
- 73 -
• A → Adenomatous polyp
• A → peptic Ulcer (pronunciation U=A)
• A → Blood group A
• A →‫( أﻛﻞ‬smoked food ,food with nitrites)
18. Complication of dysentery (amoebic and bacillary)
7 =(5 common + 2different)
1:5 Common in both
haemorrhage, fibrous stricture& perforation ‫(ﻓﻴﻜﻮﻧﻮا‬3 ulcer) ‫ﻋﻠﺸﺎن ﻫﻤﺎ‬
intussusception&rectal prolapse ‫ ( ﻓﻴﻜﻮﻧﻮا‬2 dysentery) ‫ﻋﻠﺸﺎن ﻫﻤﺎ‬
2- 2 different
1. bacillary dysentery
‫دي ﺑﻜﺮﺘ�ﺎ ﻓﻬﺘﻌﻤﻞ‬
secondary infection
toxin ‫وﺑﺘﻄﻠﻊ‬
toxaemia ‫ﻓﻬﺘﻌﻤﻞ‬
2. amoebic dysentery
‫ﺑﺘﻌﻤﻞ ﺣﺎﺟﺘ� ﻋ� اﺳﻤﻬﺎ‬
amoeboma & amoebic abscesses (spread)
19. Complications of Acute Appendicitis:

‫ ﺑﺘﻘﻮﻟﻜﻢ ﺑﺎي ﺑﺎي ﺑﻌﺪ ﻗﺮوووون ﻣﻦ ﺳﻴﻞ اﻟﺪم‬،‫ﻋﺼﺎﺑﻪ اﺳﻤﻬﺎ ﻣﺎس ﻣﺘﺨﺼﺼﻪ ﻲﻓ اﻻﻏﺘﺼﺎب‬
GANG, gangrene
MASS, Appendicular mass
RAPE, Rupture
PYE, pyemia
CHROON, chronicity
CELE, mucocele
- 74 -
Chapter Six |
Diseases of the liver
1. Types and pathological features of biliary cirrhosis
I. Primary biliary cirrhosis (Intrahepatic biliary obstruction)
Sex
female to male ratio 9:1
Aetiology
autoimmune disease
Gross
liver is enlarged, green with micronodular cut surface
Microscopy
4 stages
1. The stage of florid duct lesions

Lymphocytes and plasma cells surround the medium sized ducts associated with
focal disruption of the duct basement membrane. Duct epithelial necrosis may
occur. Some inflammatory cells may infiltrate the duct endothelium through the
disrupted basement membrane. Granuloma may develop around the ducts
.Finally most of these ducts disappear
2. Stage of ductular proliferation

The number of large bile duct is diminished, this is followed by proliferation of
small ductules.
piecemeal necrosis may occur, ductopenia differentiates this condition from
chronic hepatitis.
- 75 -
3. Stage of scarring
4. Stage of established cirrhosis

Due to progressive liver injury caused by bile retention due to ductopenia
.Regeneration nodules are usually micronodular.
II. Secondary biliary cirrhosis (extrahepatic biliary obstruction)
Aetiology
obstruction of extrahepatic bile ducts
1. Congenital biliary atresia
2. Gall stone
3. Compression by large lymph nodes
4. Equal male to female ratio.
Gross
liver is enlarged, green with micronodular cirrhosis.
Microscope
- Extra and intrahepatic ducts show bile stasis, it may show neutrophils.
- Prolonged bile stasis lead to progressive liver necrosis then cirrhosis.
2. Enumerate types of liver abscesses and discus the pathological features of them
I. Solitary abscesses
1. Amoebic abscess
2. Infected hydatid cyst
3. Following penetrating injury
4. Complicating cholecystitis
II. Multiple abscesses

1. Amoebic abscess may be multiple
2. Pyemic abscesses
3. Actinomycotic Abscesses
4. Complicating cholangitis
3. Give account on chronic active viral hepatitis
Definition
- 76 -
Chronic necro-inflamatory disease caused by HCV or HBV, the pathological changes

start at the interface, between hepatic lobules and portal tracts, that is why it
Gross
mild hepatomegaly
Microscope
I. inflammation
- Portal inflammation: expansion of the portal tract by chronic inflammatory cells
(mainly lymphocytes), bile duct walls may be inflamed
- lobar inflammation: usually mild
II. necrosis
Piecemeal necrosis: Destruction of liver cells at the limiting plates of liver lobules,
liver cells become detached, apoptosis may occur resulting in formation apoptotic
bodies “acidophilic bodies “ which become phagocytized by Kupffer cells.
Spotty bridging or multi-acinar necrosis occur in severe cases
a. Fibrosis
(Range from absent to very marked, the later is observed when cirrhosis
develop)It may be portal or bridging fibrosis or bridging accompanied by
cirrhosis
b. Other features
1. Ballooning of hepatocytes.
2. Steatosis of hepatocytes.
3. Ground glass hepatocytes.
4. hepatocellular dysplasia.
5. Cholestasis.
Complications
1. Post hepatitic cirrhosis
2. Liver failure
3. Hepatocellular carcinoma
4. Acute viral hepatitis
Aetiology
- 77 -
HAV(commonest), HEV, HBV, HCV
Gross
Liver is enlarged and yellowish green (bile stained)
Microscope
- Hydropic degeneration of hepatocytes
- Necrosis of hepatocytes, commonly central
- It may also be necrobiosis or focal necrosis
- Some of necrotic cells appear acidophilic, shrunken ( Councilman bodies)
- Inflammatory cells: appear around necrotic cells, in the adjacent portal
tract(lymphocytes, macrophages and plasma cells)
- Cholestasis: retention of bile inside cytoplasm of hepatocyte and inside the bile
canaliculi (which are obstructed by congested hepatocytes)
- Kupffer cells: engulf bile and undergo hyperplasia.
- Framework is not affected.
Termination (fate)
1. Complete recovery in 95% or more in hepatitis A
2. Acute fulminating, more common with B, C, E (during pregnancy) than A
3. Chronic hepatitis, carrier not due to A, E
5. Discus pathology of cirrhosis.
Gross
Size:
shrunken, may be enlarged (in biliary cirrhosis)
Consistency:
firm due to fibrosis
Cut surface:
nodular
1. Micronodular: 2-3 ml in diameter
2. Macronodular: more than 3 ml
3. Mixed micro, macro
Color:
- 78 -
- Yellow in nutritional, alcoholic cirrhosis.

- Green in biliary cirrhosis
- Dark brown in haemochromatosis
Microscope:
Loss of normal architecture and replacement by:
Regeneration nodules: proliferating liver cell plate with irregular sinusoids, central vein
may be absent or eccentric.
Fibrous septa: around regeneration nodule showing chronic inflammatory cells and
proliferating bile duct.
6. Causes of liver enlargement
1. Inflammatory diseases (viral hepatitis, liver abscess, malaria, granuloma)

2. Degeneration diseases: mainly steatosis in alcoholic, diabetes, obese.
3. Metabolic disorders: as collagen storage disease m hemochromatosis.
4. Blood diseases: leukaemia.
5. Neoplastic disease: benign & malignant (1ry or metastasis).
6. Some types of cirrhosis: biliary cirrhosis.
7. Amyloidosis.
8. Vascular disorders: nutmeg liver, Budd Chiari, veno-occlusive disease.
7. What is effects and manifestations of hepatocellular failure
- Jaundice
- Hypoproteinaemia due to decreased formation of plasma ptns.
- Vitamin deficiency (vit. K, A, B12, folic acid,…)
- Coagulation defects due to deficiency of fibrinogen, prothrombin and factors V, VII, IX,
X
- Anemia due to repeated hemorrhage, hypersplenism & B12 and folic acid deficiency
- Hypoglycemia due to defect in CHO metabolism
- Hormone disturbance due to decreased inactivation in the liver:
1. elevation of serum aldosterone.
2. elevation of serum estrogen which leads to palmar erythema, arterial spider in
- 79 -
both sexes. Gynecomastia, testicular atrophy and loss of libido, axillary and pubic
hair in males. Menstrual disturbances in females.
- Ascites due to portal hypertension, hypoproteinaemia and salt and water retention.
- Hepatic encephalopathy, hepatic coma: Neurological disturbances due to toxic
amines not detoxified in the liver.
- Foetor hepatitis: This is peculiar sweetish smell at the mouth due to presence of
methyl mercaptan.
- Renal failure.
8. Discuss Portal hypertension: causes and effects
Causes:
1. Compression of the portal vessels by regeneration nodules and fibrosis.
2. Development of anastomosis between portal veins and hepatic arteries.
Effects:
1. Splenomegaly followed by hypersplenism which lead to pancytopenia.
2. Varicosities: esophageal varices, piles, Caput medusa,…
3. Ascites
4. Congestion of stomach and intestine.
- 80 -
Chapter Seven |
Diseases of Gall Bladder, Pancreases, Peritoneum
GIVE AN ACCOUNT
1. Give an account on acute cholecystitis (aetiology, pathology and

complications)
Aetiology
1. chemical irritation: by concentrated bile if cystic duct is impacted by a stone
2. pancreatic enzymes irritation in case of pancreatic reflux
3. bacterial infection (strept., E. coli, typhoid bacillus)
Pathology
Gross
1. Serosal covering is opaque
2. Wall is hyperaemic swollen
3. Mucosa is ulcerated
4. Turbid bile may be mixed with pus or blood
5. Empyema of gallbladder (distension with pus) in severe cases if cystic duct is
obstructed
Microscopy:
Mucosal shedding PMNs pus cells dilated capillaries
Complications
1. empyema
2. gangrene as distension of gall bladder will compress vessels appearing black and
friable
- 81 -
3. perforation leading to pericholecystic liver abscess

4. chronic cholecystitis
2. Etiology and types of gall stones, their effect? (2003, 2008)
Etiology
I. Abnormal composition of bile

⬆ excess cholesterol due to hypercholesterolemia (e.g obesity) ➡ cholesterol
stone
Excess bilirubin in case of haemolytic jaundice ➡ pigment stone
Decreased water in hot climate
Decreased concentration of bile salts (loss of emulsification) ➡ mixed stones
Primary parathyroidism
II. Stasis of bile: due to pregnancy or obstruction of cystic duct lead to ➡ concentration
of bile due to absorption of water ➡ infection
III. Infected (cholecystitis): due to

Decrease of bile salts (emulsifying factor)
Formation of anucleus (bacteria, fibrin, cells….) around which constituents
become precipitated.
Types
I. Pure stones
• 10%
•Cholesterol ➡ actually solitary, yellow, 1_5 in diameter, with mamillated
surface, cut section show radiation
•Pigment ➡ multiple dark, small with smooth surface, consist of calcium
bilirubinate
•Calcium carbonate ➡ single or multiple, chalky white with smooth surface,
very rare
II. mixed stones

•80%
- 82 -
•Common with association with chronic cholecystitis (infected stones) due to

formation of anucleus (bacteria, fibrin, shed epithelial cells, inflammatory cells)
and due to decreased bile salt concentration
•Multiple
•1:1.5 cm
•With faceted surface

•Cut section showes a central nucleus surrounded by concentric laminae of
yellow cholesterol, Bile pigment (dark), calcium carbonate (whitish)
III. Combined stones

•10%
•If a cholesterol stone exists in infected gall bladder, it may act as nucleus
around which other bile constituents may precipitate
Effect & complication
I. Migration of stones: lead to biliary colic, biliary obstruction
II. Obstruction
1. Cystic duct obstruction ➡lead to acute cholecystitis, empyema, pancreatitis
2. Common bile duct obstruction ➡ obstructive jaundice ascending cholangitis,
secondary biliary cirrhosis
3. Obstructive ampulla of vater ➡ acute hemorrhagic pancreatitis
4. Intestinal obstruction (gall stone ileum) ➡ occurs when inflamed gall bladder get
adherent to loop of intestine accompanied by fistula formation through which a big
gall stone may pass causing intestinal obstruction
III. Infection ➡ cholangitis, andcholecystitis
IV. Squamous metaplasia, malignancy

3. Give an account on pathological features complications of acute hemorrhagic
pancreatitis
Pathological features
1. Swollen with areas of hemorrhage and necrosis
2. Secondary infection leading to suppuration (pus formation)
3. Fat necrosis due to the action of pancreatic lipase on peritoneal fat cells, (glycerol
and F.A later combined with ca causing patches of calcium soap
- 83 -
4. Rise of serum amylase and lipase

5. Chemical peritonitis: the peritoneal cavity contains brownish serous fluid
(pancreatic ascites) the fluid contains altered blood, fat globules and high level of
amylase
Complications:
1. Shock and death
2. Gangrene (rare) leading to severe toxaemia and death
3. Pancreatic pseudocyst:a cyst with fibrous wall no epithelial lining and bloody
contents
4. Chronic pancreatitis following acute attacks. pancreas appears rigid and nodular
due to fibrosis
5. Steatorrhea and D.M
4. Give an account on carcinoma of pancreas
Risk factors
1. Diabetes mellitus particularly in females
2. Dietry factors as high fat diets
3. Chronic pancreatitis
4. Cigarette smoking
Site
1. Head of pancreas
2. Body and tail (less common)
Grossly ➡
infiltrative irregular hard, grayish mass affecting head, body or tail of pancreas
Microscopic ➡
90% arising from duct, 1% from acini. It's commonly well differentiated
adenocarcinoma with marked fibrosis and perineural invasion. Other types include
➡ adenosquamous carcinoma and anaplastic carcinoma
Spread
I. Direct
1. From carcinoma of head to common bile duct causing obstructive jaundice, to
duodenum leads to duodenal obstruction
- 84 -
2. From carcinoma of body, tail ➡ to spleen, kidney and vertebrae no jaundice
II. Lymphatic➡ to regional lymph nodes
III. Blood ➡ to liver, lungs, etc…
IV. Trancelomic spread ➡ associated with hemorrhagic ascites.
E N U M E R AT E
1. Four different complications of gall stones ➡ see question 2
2. Causes of suppurative pancreatitis
1- Obstruction of ampulla of vater by gall stones, thus bile passes into pancreatic duct
and activates trypsinogen into trypsin which digest the pancreatic tissue
2- Excess alcohol abuse ➡ ⬆ secretion of pancreatic juice➡ rupture of pancreatic duct
3- Accident surgical injury of pancreas
4- Hyperparathyroidism
5- Polyarteritisnodosa
6- Viral and bacterial infections
- 85 -
Chapter Eight |
Disease of the urinary system
GIVE AN ACCOUNT ON
1. Congenital anomalies of the kidney
Pathological features and complications of polycystic kidney

1. Agenesis.
2. Hypoplasia.
3. Ectopic kidney.
4. Horse-shoe kidney.
5. Supernumerary kidney.
6. Double ureters or pelvis.
7. Congenital cystic kidney:
I. Adult type of polycystic kidney disease

It may be associated with cystic liver and aneurysm
Pathogenesis:
- autosomal dominant inheritance

The cysts are believed to be due to failure of communication between
convoluted and collecting tubules
Gross:
- Both kidneys are enlarged and show small or large cysts.
- The cysts contain either clear or hemorrhagic fluid (bluish or brown).
- Their lining is smooth.
- They don’t communicate with renal pelvis.
- They grow as the patient grow causing pressure atrophy on kidney
parenchyma.
Microscopy:
- 86 -
Cysts are lined by cuboidal or flattened epithelium
Complications
a. Hematuria.
b. Secondary infection.
c. Hypertension.
d. Chronic renal failure.
II. Infantile polycystic disease of kidney

- A rare condition.
- Associated with congenital hepatic fibrosis.
- Autosomal recessive inheritance.
- Renal cystic affection is much more than the adult type.
- Death occurs during infancy or childhood due to renal failure.
2. Pathogenesis, pathological features & fate of post streptococcal G.N
Acute diffuse proliferative L.N
Aetiology and pathogenesis:

- It is an immune complex disease affecting children and young adults.
- It states as an upper respiratory infection with nephrogenic strains of group A beta
hemolytic streptococci.
- Within 1-4 weeks Ab are grouped & combine with streptococci Ag
Immune complexes which are deposited on the basement membrane of glomerular
capillaries → complement activation → destruction of glomerular capillaries by:
a. Lytic effect of complement.
b. Attraction of neutrophils and release their proteolytic enzyme.
Gross:
- Mild bilateral kidney enlargement.
- Cortical edema and petechial haemorrhage.
Microscopy:
1. Glomeruli: enlarged and show
a. Proliferation of epithelial, endothelial, mesangial cells
b. Several neutrophils in the glomerular capillaries
c. Bowman’s capsule space shows neutrophils, erythrocytes and some albumin
- 87 -
2. Tubules show cloudy swelling and casts (mainly blood cells)

3. Interstitium: edema and neutrophils
4. Electron-Microscopy “Humpy Lumpy” immune complex deposit
These are subepithelial between podocytes and basement membrane
5. Immunofluorescence
the deposit consists of IgG, IgM and complement
Clinical and general manifestations
I. Fever and rigors.
II. Nephritic syndrome is the classic presentation it consists of:

1. Hematuria.
2. Hypertension.
3. Proteinuria.
4. Oliguria.
Nephritic edema (stains in lids, particularly in the morning, then they become
generalized).
III. Urine analysis:

- Oliguria
- Hematuria (Coca-Cola like)due to altered blood
- Mild proteinuria
- High specific gravity (1035)
- Contains casts ( mainly hyaline and blood cells)
IV. blood analysis

- mild rise of urea and creatinine
- mild anemia
V. hypertension.
Fate
1. recovery in more than 95% of children and 2/3 of adults.
2. development of rapidly progressive G.N or chronic G.N
3. rarely, death from acute renal failure.
3. Aetiology and pathological features of pyelonephritis.
Aetiology → predisposing factors
- 88 -
I. Low immunity as in cases of:

a. D.M
b. AIDs
c. Immunosuppressive therapy
II. Urinary obstruction:

- stasis of urine favours bacterial growth.
III. Urinary tract instrumentation.
IV. females are commonly affected than male because of:

- shorter and wider urethra.
- pregnancy: lead to urine stasis.
•Bacteria: E.coli (the commonest)
Staphylococci, streptococci, pseudomonas, typhoid bacilli
• Routes:
1. Blood spread from distant infection
2. Ascending through submucosa of ureter or periureteric lymphatics or
submucosa of ureter
3. From colon through intercommunicating lymphoid
Pathology:
Tow types, commonly bilateral
Acute pyelonephritis Chronic pyelonephritis

Enlarged Convoluted asymmetrically
Gross picture size
Smooth Irregular surface depressions
surface
Strips easily adherent
capsule
Small cortical abscess + streaks of scarred cortex and medulla
Cut section pus along medullary rays Not demarcated form each other
Contain pus scarred distorted
Pelvis and
calyx
- 89 -
1. Interstitium of the kidney and 1. Interstitium of the kidney and pelvis:

Microscopic picture pelvis: a. endarteritis obliterans.
a. Dilated capillaries b. lymphocytes, plasma cells and
b. Neutrophils, pus cells, macrophages.
macrophages. c. fibrosis, it may surround
c. oedema. glomeruli leading to glomerular
ischemia ending with glomerular
fibrosis.
2. Tubules: Fibrotic, cystic or contain

2. tubules: degeneration, thyroid-like casts
inflammation and leucocytic cysts.
1. mild case: recovery. 1. Hypertension.
Fate and complications
2. severe case: acute renal failure. 2. Chronic renal failure.
3. some cysts develop pyonephrosis
or progress to chronic phase.
4. Aetiology & pathological features of hydronephrosis.
Aetiology
incomplete or intermittent urinary tract obstruction this may lead to
‫ﻣﻦ ﺗﺤﺖ ﻟﻔﻮق‬
I. Urethral lesions :
a. congenital lesions:
1. phimosis
2. stenosis of external urethral meatus
3. prostatic urethral valves
b. acquired causes:
1. post traumatic or post inflammatory urethral stricture
2. urethral tumors
II. prostatic enlargement :
a. senile enlargement.
b. carcinoma.
- 90 -
III. Bladder neck obstruction

a. functional neuromuscular incoordination as in tabes dorsalis
b. inflammatory stricture as in bilharzial fibrosis
c. tumor
d. stones
IV. ureteric lesions
1. inflammatory stricture as in bilharzial fibrosis
2. tumors
3. stones
4. pregnancy
5. retroperitoneal fibrosis
V. renal pelvis
1. stone
2. tumors
3. pressure by an aberrant renal artery
4. kinked pelvis & ureter
Pathology
- hydronephrosis may be unilateral due to unilateral ureteric or pelvic lesions
- may be bilateral due to urethral, prostatic or bladder neck lesions
I. bilateral hydronephrosis is associated with:

- hypertrophy, dilatation & trabeculation of the bladder
-bladder diverticula may develop due to pouching of the mucosa through muscle
layers after marked bladder dilatation
-bilateral hydro ureter . they appear hypertrophied, dilated, elongated, tortuous.
-distention of pelvis and ulcers with urine lead to pressure atrophy and flattening,
then cupping of pyramids followed by disappearance of the whole pyramid &
progressive atrophy of renal parenchyma
II. Gross:
the affected kidney is enlarged with bossy surface
cut section reveals a multi localized sac distended with
urine
Complication
1. Secondary infection → pyonephrosis.
2. Hypertension.
3. Stasis → stone formation.
- 91 -
4. Chronic renal failure in bilateral cases.

5. Bladder diverticula may be complicated by secondary infection, stone formation &
carcinoma.
5. Pathological features & complications of bladder carcinoma
Schistosoma hematobium, most imp predisposing factor in Egypt.
cancer develops due to
1. Development of bilharzial urethral precancerous lesions as cystitis glandularis,
squamous metaplasia, leukoplakia & dysplasia
2. Tryptophan metabolites released from the worm into the bl. & excreted in urine
are carcinogenic
3. 2ry infection of bilharzial ulcer is common . gram –ve bacteria as E.coli change
urinary & ureteric into nitrosamine → carcinogenic particularly to metaplastic
urothelium.
chemical carcinogen
1. Bladder cancer is more common in industrial areas, particularly those associated
with petrochemicals
2. Cigarette smoking
3. Aniline dye
Other risk factors

1.Villous papilloma
2. HPV is controversial
3. Chronic cystitis
4. Stones
5. Ectopic vesica
Gross picture
Bladder cancer whether bilharzial or not assume one of the following patterns:
1. Exophytic pattern
a. papillary pattern / villous pattern . it's a common pattern mostly in non-bilharzial
cancer but can be present in both
b. solid nodular pattern polypoid or cauliflower fungating pattern
- 92 -
2. Endophytic patterns
a. ulcerative pattern
b. infiltrative pattern
3. Combined patterns
Microscopic pic
1. Urothelial (transitional cell ) carcinoma
a. papillary type: exophytic villous structure covered by several layers of malignant
urothelial cells showing low or high grade nuclear anaplasia. The underlying
laminae may or may not be invaded
b. solid (non papillary): malignant urothelial cells form solid groups that invade
lamina or deeper . solid pattern is more commonly a high grade tumour
2. Squamous cell carcinoma:

classical or verrucous types . the classical type of squamous cell carcinoma mostly
develops on top of bilharzial cystitis
3. Adenocarcinoma
4. Mixed pattern
5. Rare types as neuroendocrine tumors
Effect & complication
1. Spread:
Direct → prostate, seminal vesicle, ureters, rectum & vagina
lymphatic → iliac & para-aortic lymph nodes
Blood → late to lungs, liver, bone,….
2. Urinary obstruction
hydro-ureter, hydro-nephrosis, renal failure
3. Infection
cystitis, pyelonephritis, pyoureter & pyonephrosis
4. hematuria
5. Fistula formation with rectum or vagina due to direct spread
6. Microscopic patterns of lupus nephritis
- 93 -
class I:
normal microscopic pattern
class II:
mesangial lupus nephritis
mild ++ of mesangial matrix & mesangial cells of the glomeruli: mesangial deposits of
IgG &C3 are detected. Clinical symptoms are mild.
class III
focal proliferation glomerulonephritis:
focal means affection of < 50% of glomeruli or total glomerular capillaries.
clinically nephrotic syndrome in 30% of cases
class IV
diffuse proliferative G.N.
diffuse means more than 50%
this is most common severe form
all glomeruli show diffuse mesangial hypercellularity commonly with thickening of
capillary loops due to fibrinoid necrosis( wire loop lesions).
- Crescentic lesions may also develop.
- clinical effect include 50% nephrotic syndrome & renal failure ultimately develops
Class V
- membranous G.N.
characterized by thickening of glomerular capillaries basement membrane without
cellular proliferation.
- clinically nephrotic syndrome
Class VI
- advanced sclerosing G.N.
- Global glomerulosclerosis, affecting > 90% of the glomeruli .
7. Renal failure
Definition
this is failure of the kidney to eliminate the toxic compounds into urine that normally
exist in blood.
Types and causes
- 94 -
1) acute renal failure

a. pre-renal causes as shock e.g. due to burns or hemorrhage
b. Renal causes as acute tubular necrosis, acute pyelonephritis and acute G.N
c. post renal causes as calculus anuria due to sudden ureteric obstruction by stones
2) chronic renal failure

Due to chronic bilateral kidney disease as
1. amyloidosis
2. chronic pyelonephritis
3. chronic G.N
4. hydro nephrosis
5. pyonephrosis
6. renal tumors
Pathogenic features
a. Blood changes 3R & 2A

1. rise of urea, creatinine & other non protein nitrogenous compounds
2. retention of phosphates & lowering of calcium
3. retention of sodium and potassium
4. acidosis
5. anemia due to toxic depression of bone marrow & reduced erythropoietin
formation by the kidney
b. urine volume
1. in case of acute uraemia, oligo-anuria is usual
2. in case of chronic uraemia, polyuria
c. organ lesions
1. serous membranes, fibrinous pleurisy & fibrinous pericarditis
2. skin is pale & shows petechial hemorrhage as well as greyish and brownish
discoloration related to urea or urochrome pigment deposition
3. GIT: colitis, gastritis, enteritis & colitis
4. lungs: pulmonary oedema & infection in addition uremic fibrinous pleurisy
5. cerebral oedema leading to tremors, convulsions & coma.
8. pyonephrosis
Definition
a condition in which pelvis & calyces are markedly distended with pus → atrophy of renal
tissue.
- 95 -
Aetiology
“infection + ↑ urine volume”
1. pyelonephritis associated with urinary tract obstruction
2. Urinary tract obstruction “”hydronephrosis” followed by secondary infection
Pathology
1. Pelvis & calyces are distended with pus
2. Atrophic renal tissue
3. Spread of infection to surrounding “perinephritis” → fibrosis & fixation of kidney
4. chronic renal failure in bilateral cases.
9. urinary bladder stone “Enumerate complication of renal calculi”
Definition
They are precipitation of urinary crystalloids in renal pelvis or in the bladder.
Aetiology
I. Disturbance of composition urine
a. decreased water content (concentrated urine)

e.g. due to excessive sweating.
b. increased crystalloids:
- Excess Calcium as in hyperparathyroidism.
- excess uric acid and urates in cases of gout.
- Excess oxalates due to:
1. ++ intake in diet (mango, tomato).
2. hereditary metabolic error.
- Familial cystinuria.
II. Stasis of urine
due to urinary obstruction:
a. stasis allows easier precipitation of crystalloids of urine.

b. Stasis predisposes to infection
III. Urinary infection

It predispose to precipitation of urinary crystalloids through:
a. formation of a nucleus (pus cell, detached necrotic cells)

b. change of pH in urine
- 96 -
-alkalinity in pyogenic infections → precipitate calcium, Mg, NH4.

- Phosphate (triple phosphate stone), occurs in alkaline urine.
- +++ acidity (in case of E. coli). This favours precipitation of oxalates & urates.
Types of stones
a. primary (metabolic) stones

UTI is not important for their formation.
1. calcium oxalate stone 60%

it forms in acidic urine, usually occur in renal pelvis and are multiple hard with
spiny surface.
This leads to injury & hemorrhage of urinary mucosa → dark staining of stones.
2. uric acid & urate stones 8%

- in acidic medium
- in renal pelvis
- single, hard & smooth surface
- yellowish brown in color
3. cysteine stones 2%
- soft
- yellowish green
b. secondary (infected) stones:

Triple phosphate stone (30%)
- it develops in alkaline urine.
- usually single, large white and friable with a smooth surface.
- commonly forms in urinary bladder but May form in renal pelvis and calyces
casting their shape ( Stag Horn stone).
Complication
1. Migration from renal pelvis to ureter or bladder causing pain or urinary obstruction
2. Urinary obstruction leading to hydroureter, hydronephrosis & sometimes calculus anuria
3. Urinary infection leading to cystitis, pyelonephritis, pyoureters & pyonephrosis
4. Injury of urinary mucosa (particularly by oxalate stones) this leads to hematuria
5. Squamous metaplasia
6. squamous cell carcinoma may occur on top of metaplasia
10. Minimal change G.N (lipoid nephrosis)
Aetiology & pathology
- 97 -
- Children are affected

- Aetiology is unknown, although antibodies or component are not detected in the
glomeruli, still an immune mechanism is suspected because:
a. many cases follow respiratory infections
b. Excellent response to corticosteroids
Gross
unremarkable changes.
Microscopy
a. Unremarkable light microscopic glomerular changes.
b. the living cells of the proximal convoluted tubules may show slow lipids (due to
reabsorption of lipoprotein leaked from the glomeruli).
c. E.M & immunofluorescence.
Diffuse effacement of the foot process of the visceral epithelial cells.
No immunoglobulin deposits
Clinical pictures
Nephrotic syndrome
commonest cause of the syndrome in children.
Fate
the prognosis is usually excellent, most cases are cured by corticosteroid therapy.
11. Describe the Gross picture of chronic G.N
1.Both kidneys are symmetrically contracted.

2. Finely granular surface.
3. Adherent capsule that strips difficultly with decortication.
4. cut section shows:
a. atrophic cortex & medulla not demarcated from each other.
b. ++ peripelvic fat
c. prominent vessels and few cysts.
12. Nephrotic syndrome is characterized by:
- 98 -
a. Massive proteinuria (over 3.5 gm/day)

b. hypoalbuminemia (plasma albumin level is less than 3g %)
c. Severe generalized oedema due to lowered plasma osmotic pressure
d. hyperlipidemia and lipiduria.
Causes of nephrotic syndrome:
a. 1ry Glomerular Disease as:

Minimal change glomerulonephritis.
- Membranous glomerulonephritis.
- Mesangiocapillary glomerulonephritis.
- Focal proliferative glomerulonephritis.
- Focal segmental glomerulonephritis.
b. 2ry Glomerular Disease as:

- Renal amyloidosis.
- Lupus nephritis.
- Diabetic glomerulosclerosis.
13. What is meant by haematuria? and list its causes.
It means blood passing in urine.

a. Pre-Renal causes: (general causes)
1. Hypertension
2. blood diseases as leukaemia & purpura.
3. Vit. C & K deficiency
4. Drugs as salicylates & anticoagulants.
b. Renal causes:
1. Congenital as polycystic kidney.
2. Inflammatory as: Nephritic syndrome or Acute pyelonephritis.
3. Neoplastic as hypernephroma.
4. Vascular disorders as: chronic venous congestion & renal infarction.
5. Traumatic as: kidney injury due to accidents & bleeding following renal surgery.
c. Post-Renal causes:
1. Congenital: bladder diverticulum.
- 99 -
2. Inflammatory as: Bilharziasis: most common cause in Egypt

- Others types of cystitis as: acute & tuberculous.
3. Neoplastic as: tumors of renal pelvis, ureter or bladder.
4. Vascular disorders as: chronic venous congestion
5. Traumatic as:
traumatic injury by stones or due to instrumentation by metal catheters.
DEFINE
1. Acute tubular necrosis of k idney:
ischemic or toxic necrosis of the tubules of kidney. Proximal convoluted tubules in case
of toxic necrosis & several parts of all tubules in ischemic necrosis.
2. Nephrotic syndrome:
Syndrome of the kidney characterized by:

a. Massive proteinuria.
b. hypoalbuminemia .
c. Severe generalized oedema due to lowered plasma osmotic pressure.
d. hyperlipidemia and lipiduria.
3. Nephritic Syndrome:
Characterized by:
a. haematuria
b. oliguria
c. mild proteinuria
d. Hypertension
e. oedema of eye lids.
4. Pyelonephritis:
Infection of kidney ( interstitial tissue) & renal pelvis.

5. Pyonephrosis:
A chronic condition in which pelvis and calyces are markedly distended with pus 
atrophy of renal tissue.
6. Hydronephrosis:
- 100 -
A chronic condition in which pelvis and calyces are markedly distended with urine due
to urinary obstruction, followed by pressure atrophy of renal tissue.
8. Renal Failure:
This is a failure of kidneys to eliminate into urine the toxic compounds that normally
exist in blood.
- 101 -
Chapter Nine |
Male Genital system
GIVE AN ACCOUNT ON
1. The microscopic picture of testicular seminoma.
Many types:
1. Classical seminoma:
It consists of uniform large cells with abundant clear cytoplasm and large central
nuclei containing large nucleoli. The cells exist in groups separated by fibrous bands
invariably infiltrated by lymphocytes and plasma cells.
→ immunohistochemistry, cells are positive for placental alkaline phosphatase and
C-kit (CD117).
2. Spermatocytic seminoma:
It consists of cells showing marked size variation (a mixture of small cells, large cells
and bizarre giant cells)
Mitosis may be numerous and lymphocytic infiltration is absent.
3. Other types: such as:

a. Classic seminoma with trophoblastic giant cells.
b. Anaplastic seminoma (seminoma with high mitotic activity).
2. Seminoma:
Definition and origin:

malignant tumor arising from germ cells (seminiferous) of the testis, it is the commonest
testicular tumor (40%) and it has a better prognosis since it is radiosensitive.
Gross:
The testis is moderately enlarged, cut section shows a non-capsulated solid homogenous
pale yellow growth sometimes with small necrotic foci.
- 102 -
Microscope:
See above.
Age
- spermatocytic seminoma occurs in old age groups (around 65 years)
- Other types of seminoma occur around the age of 30-40 years.
Spread of seminoma and other malignant testicular tumors:

1. Direct: to testicular adnexa and scrotal wall.
2. Lymphatic: para-aortic lymph nodes.
3. Blood: lung, liver, bone and brain.
Prognosis
seminomas are radiosensitive tumors
1. Spermatocytic seminoma never metastasize and has excellent prognosis.
2. Classic seminoma stage1 (limited to testis) or stage 2 (spread to infradiaphragmatic
lymph nodes) have also excellent prognosis and over 95% of these patients are cured.
With stage 3 (metastasis) the prognosis is unfavourable.
3. nodular hyperplasia of the prostate.
At the age of 30 years the prostate normally weighs 20 gm. Benign prostatic hypertrophy
(BPH) affects 8% of men in their fourth decade but the incidence rises to 50% in men in
the 5th decade and 75% in men in the 8Th decade.
Pathogenesis
no predisposing factors or protecting factors (other than castration) have been
identified. However, recent studies relate BPH to an error in the metabolism of
dihydrotestosterone.
Gross
1. The weight of prostate in cases of BPH ranges between 35gm (mild cases) to 800 gm
or more. The average is around 100gm.
2. BPH affects the central and transitional zones of the prostate around the urethra. This
part becomes enlarged and exhibits a nodular cut section. The urethra is compressed,
the peripheral prostatic tissue is also compressed. The hyperplastic nodules may have a
solid or a spongy appearance.
Microscopy:
1. Hyperplastic glands: the glands are enlarged with numerous cystic forms, acini are
variable. Characteristically with double epithelial lining showing infoldings. The lumens
- 103 -
frequently contain inspissated glycoprotein material (corpora amylacea)

2. Hyperplastic fibromuscular stroma with lymphocytic infiltrates.
3. Prostatic infarcts are common in large prostates.
Effects and complications:
a. Compression of prostatic urethra leads to:

1. Difficult micturition.
2. Urine retention may occur.
3. Urinary continence may occur
b. Urinary tract obstruction 

1. Bladder hypertrophy, dilatation and diverticula.
2. Bilateral hydroureter and hydronephrosis renal failure.
c. others
1. Urinary stasis due to obstruction  infection
2. (Cystitis, pyelonephritis…etc)  stone formation.
4. enumerate effects and complications of senile(nodular) prostatic hyperplasia
See previous question

5. carcinoma of the prostate:
Definition
Primary malignant neoplasm arising from prostate.
Etiology
the exact etiology is unknown however the following are predisposing factors:
a. Age:
cancer prostate is extremely common. The incidence rises steadily with age. Most
cases occur after the age of 50 years
b. Most cases are hormone dependent (androgens), therefore carcinoma doesn’t
occur in persons castrated before puberty.
c. Premalignant lesions:
1. Prostatic intraepithelial neoplasia (PIN) was the accepted term of
premalignant prostatic lesions. PIN is characterized by hyperplastic glands
- 104 -
showing cellular atypia, I the form of cellular stratification, nuclear enlargement

and nucleolar prominence.
2. Atypical adenomatous hyperplasia (AAH).
Pathological features:
a. Serum markers of prostatic cancer:

1. Prostatic specific antigen: is very useful marker for diagnosis and follow up of
prostatic carcinoma. Normal serum value 0-4 it is elevated in prostatic cancer.
2. Acid phosphatase: is also secreted by tumor cells and is another useful
marker.
Gross picture:
Most carcinomas of the prostate arise from the peripheral zone, rarely carcinoma
arises from the transitional periurethral zone.
Cancer prostate varies in size and present as a hard poorly defined yellowish nodule
or multifocal nodules (80% multifocal).
Microscopic picture:
the commonest pattern is prostatic adenocarcinoma. It may be well differentiated,
moderately differentiated or poorly differentiated.
This grading was modified by Gleason and this is till now the most accepted
method of microscopic grading for adenocarcinoma.
He described 5 grades of prostatic adenocarcinoma:
Grade 1
closely packed uniform acini lined by a single cell layer.
Grade 2
small separated less uniform acini lined by a single cell layer.
Grade 3
Irregular separate acini, cribriform and papillary pattern.
Grade 4
infiltrative fused glands with solitary cells or clear cells.
Grade 5
solid sheets, strands or focal tumor necrosis. (Comedo pattern)
- 105 -
A final Gleason score, is made by adding numerical values of the two most
predominant grades (e.g, Gleason grade 3+4= score 7)
Gleason score system is interpreted as follows:

1. Low grade (well differentiated) Carcinoma corresponds to Gleason score 2-4
2. Medium grade (moderately differentiated) carcinoma corresponds to score 5-7
3. High grade (poorly differentiated) carcinoma corresponds to score 8-10
Immunohistochemistry: tumor cells are negative for both CK20 and CK7 but stain
for EMA and PSA.
Spread:
1. Direct spread: leads to invasion of prostatic capsule, prostatic urethra, bladder and
rectum. Perineural spread is also common
2. Lymphatic spread: to pelvic, retroperitoneal lymph nodes then to supradiaphragmatic
nodes.
3. Blood spread (LBLB) to bone (osteoblastic), lung, skin, brain, liver, penis and adrenal
glands.
Staging of prostatic carcinoma

T1: clinically inapparent tiny tumor.
T2: Tumor confined within the prostate.
T3: Capsular infiltration or invasion of seminal vesicles.
T4: infiltration to levator muscle or fixed to pelvic wall.
DEFINE
1. Cryptorchidism:
Failure of descent of one or both testis into the scrotum.

2. Seminoma
it is a malignant tumor arising from germ cells (seminiferous) of the testis. It is the
commonest testicular tumor (40%) and has a better prognosis since it is radiosensitive
3. Phimosis:
This is a congenital stenosis of the orifice of the prepuce.
- 106 -
Chapter Ten |
Diseases of the female genital system
E N U M E R AT E :
1. Four types of ovarian sex cord stromal tumors.
1. Granulosa cell tumor.

2. Theca cell tumor (Thecoma-Fibroma).
3. Androblastoma (Sertoli cell-Leydig tumor).
4. Gynandroblastoma (Mixture).
2. Complications of cervicitis.
1. Contact bleeding (during sexual intercourse).

2. Carcinoma on top of squamous metaplasia and dysplasia.
3. Habitual abortion due to ectropion.
4. Spread of infection → endometritis, salpingitis.
3. Predisposing factors of carcinoma of the cervix.
3 female, 1 male, 3 diseases.

1. Females with early age of 1st intercourse.
2. Females with multiple sexual partners (cancer cervix is common in prostitutes).
3. Multiparous females.
4. High risk male sexual partners (uncircumcised).
5. Chronic cervicitis.
6. Cervical dysplasia.
7. Human papilloma virus infection especially type (16- 18).
4. Causes of abnormal uterine bleeding (menorrhagia or metrorrhagia).
I. Dysfunctional uterine bleeding (DUB):

Caused by hormonal dysfunction without organic cause.
I.I. An ovulatory causes: (bleeding + infertility)
- 107 -
1. Exaggerated- disordered proliferative endometrium, due to unopposed action of

estrogen.
2. Endometrial hyperplasia.
3. Endometrial atrophy.
I.II. Ovulatory luteal phase defects:

1. Persistent corpus luteum → prolonged luteal phase → irregular shedding of
endometrium.
2. Inadequate luteal phase → bleeding and maybe infertility.
3. Irregular hormone response → bleeding and maybe infertility.
II. Local organic causes:

IAM BD
1. Inflammations as cervicitis.
2. Adenomyosis.
3. Malignant tumors as carcinoma of cervix.
4. Benign tumors as leiomyoma.
5. Disorders of pregnancy as abortion.
III. General causes of bleeding:

1. Hypertension.
2. Leukaemia, purpura, haemophilia.
3. Vitamin C or K deficiency.
5. Complications of puerperal sepsis.
4s +I
1. Severe toxaemia → toxic myocarditis + other toxic effects.
2. Septic thrombophlebitis → pyemia.
3. Septicaemia.
4. Direct Spread → peritonitis, salpingitis, or salpingo-oophoritis.
5. Infertility.
6. Neoplastic and non-neoplastic ovarian cysts.
I. Neoplastic cysts:
1. Cystic teratoma (dermoid cyst).
2. Cystadenomas (Serous & Mucinous).
3. Cystadenocarcinoma.
II. Non-neoplastic cysts:
- 108 -
1. Follicular cysts.
2. Stein- Leventhal syndrome.
3. Corpus luteum cyst.
4. Chocolate cysts.
5. Theca lutein cysts.
7. Complications of mucinous ovarian tumor.
1. Torsion of the pedicle → Ascites, haemorrhage & shock.

2. Rupture → pseudomyxoma peritonii.
3. Pressure effects on surrounding organs (bladder, rectum).
4. Malignant change (more common in papillary type).
5. Secondary infection.
DEFINE:
1. Puerperal sepsis.
It is acute inflammation of the uterus (endometrium mainly) following labour or

abortion.
2. Adenomyosis.
Presence of endometrial foci inside the myometrium.

3. Endometriosis.
Presence of endometrial tissue outside the uterine wall.

4. Dysgerminoma (germinoma).
It is a malignant tumor arising from germ cells of the ovaries. It's similar to testicular
seminoma.
5. Dysfunctional uterine bleeding.
It is uterine bleeding caused by hormonal dysfunction without organic causes.

6. CIN- III
Severe cervical dysplasia or carcinoma in situ.

Diffuse cellular atypia affecting the whole thickness of the cervical mucosa. In 30% of
cases→ invasive carcinoma.
- 109 -
CO MPAR E B E TW E E N :
1. Complete and partial mole.
Complete mole Partial mole

All chorionic villi → vesicles. Mixture of vesicles + normal villi.
No fetus. Fetus is anomalous, but present.

Present due to abnormal fertilization Present due to fetal anomalies and death.
(empty ovum with 2 sperms).
Normal diploid number of chromosomes Triploid no. of chromosomes (69 XXX or
(46 XX or 46 XY). 69 XXY).
Gross picture
Uterus → disproportionately large for the Uterus → proportionate for the age of
age of gestation. gestation.
Placenta → large mass composed of Placenta → slightly enlarged with fewer
vesicles, 1-30mm each. Appears like bunch vesicles.
of grapes.
Ovaries → Theca lutein cysts. Ovaries → No theca lutein cells.
Microscopy
All villi are vesicular with: Some villi are vesicular with:
1. Marked trophoblastic proliferation. 1. Mild trophoblastic proliferation.
2. Hydropic edematous cores → no 2. Hydropic edematous cores, with vessels
vessels. containing fetal erythrocytes.
Serum HCG is high (+ve pregnancy test). Serum HCG is lower than complete mole.
Complications
1. Massive uterine bleeding. 1. Less massive uterine bleeding.
2. Transformation into invasive mole or 2. Transformation into invasive mole or
choriocarcinoma (common) choriocarcinoma (uncommon).
- 110 -
2. Compare between mucinous and serous cystadenoma of the ovary, and

enumerate complications of mucinous cystadenoma.
Mucinous cystadenoma Serous cystadenoma

Gross features
Unilateral, pedunculated. Bilateral, may be pedunculated.
Assumes huge size. Small to moderate size (up to 30cm).
Multilocular. Unilocular.
Locules have smooth lining & contain Locules have smooth lining & contain clear
bluish mucinous material. serous fluid. May be papillary projections
are present (serous papillary
cystadenoma).
Microscopy
Cysts → lined by columnar mucin- Lined by cubical cells.
secreting cells.
Complications
See enumerate question.
WRITE A NOTE ON (GIVE AN ACCOUNT ON):
1. Pathological features and complications of cervicitis.
I. Cervical erosion:
1. It is red patch on external os that bleeds easily on touch.
2. Acute inflammation of external os:
a. Necrosis and shedding of stratified squamous epithelium.
b. Hyperaemia of sub epithelial tissue.
3. Columnar cells of endocervix creep and cover the bare external os, which are less
resistant than stratified squamous epithelium → bleeding on touch.
II. Nabothian follicles:

Inflammation involves endocervical glands → become distended with exudate,
leads to → multiple small cysts (retention cysts).
III. Squamous metaplasia:
- 111 -
In endocervical mucosa in chronic cases. May be associated with dysplasia → CIN

→ precancerous.
IV. Polypoid endocervicitis:

Develop in chronic cases (cervical polyps).
1. Gross:
Sessile, pedunculated, soft pink → easily bleed on touch.
2. Microscopy:
Covered by columnar or metaplastic stratified squamous epithelium.
Core shows:
a. Chronic inflammatory cells.
b. Fibrosis.
c. Proliferative endocervical glands.
V. Ectropion:
Eversion of cervical lips due to marked fibrosis.
VI. Persistent discharge (leucorrhoea).
Complications:
See enumerate question.
2. Pathological features, staging and spread of cervical carcinoma.
Pathology:
I. Cervical intraepithelial neoplasia (CIN):

Non-neoplastic precancerous lesions.
Gross:
Small - indurated patch.
Microscopy:
Cellular atypia, loss of polarity, no basement membrane invasion.
There are 3 grades:

1. CIN-I: atypia involves lower third of cervical mucosa (mild dysplasia).
2. CIN-II: atypia involves lower two thirds of cervical mucosa (moderate).
- 112 -
3. CIN-III: diffuse cellular atypia involves whole cervical mucosa (severe). 30% of
cases → invasive carcinoma (carcinoma in situ).
II. Invasive carcinoma:
Gross:
Starts as small-indurated nodule. While growing maybe:
1. Exophytic: (protrude in vagina): Verrucous mass or polypoid fungating
mass.
2. Endophytic: (deeply invading): Nodular infiltrative or ulcerative.
Microscopy:
1. Squamous cell carcinoma (keratinized and non-keratinized) 90%.
2. Adenocarcinoma from endocervical mucosa 5%.
3. Adenosquamous carcinoma - rare.
4. Undifferentiated carcinoma.
Spread:
1. Direct:
- Downwards to upper vagina.
- Upwards → obstruction of cervical canal → pyometria (due to 2ry
infection) → pus in the uterus.
- Anterior →to the bladder → fistulae.
- Posterior → to the rectum → fistulae.
-Lateral → ureters → ureteric obstruction → renal failure.
2. Lymphatic:
To regional lymph node (pelvic).
3. Blood:
Late to the lung, liver, bone, and brain.
Staging:
Stage 0: CIN – III = carcinoma in situ.
Stage I: carcinoma confined to cervix.
Stage II: carcinoma extending to upper vagina.
Stage III: carcinoma extending to pelvic wall.
Stage IV: carcinoma extending to nearby organs or distant spread.
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3. Puerperal sepsis (pathological features, etiology, complications)
�‫ اﺗﻜﺮر ﻛﺘ‬،‫ﻣﻬﻢ ﺟ ًﺪا‬
Aetiology:
Causative organism:
Pyogenic bacteria: streptococcus hemolyticus. Less common E.coli.
1. Retained clots or placental fragments.
2. Low immunity.
Route of infection:
1. Endogenous: direct from vagina, or through blood from distant infection.
2. Exogenous: contaminated gloves, instruments, … etc.
Gross:
1. Uterus → subinvoluted and soft.
2. Endometrium → yellow purulent exudate.
3. Myometrium veins → septic thrombi.
Microscopy:
1. Endometrium → septic endometritis → necrosis, neutrophils + pus cells &
dilated capillaries (acute inflammation).
2. Myometrium (severe cases) → septic myometritis (myometrial abscesses).
Complications:
See enumerate.
4. Endometriosis.
Definition:
Presence of endometrial tissues outside the uterine wall.
Sites:
I. Genital:
1. Ovaries.
2. Fallopian tubes.
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II. Extra genital:

1. Wall of urinary bladder.
2. Recto-vaginal septum.
3. Pelvic peritoneum.
4. Umbilicus.
5. Lungs.
6. Lymph nodes.
Pathogenesis:
Still unknown.
1. Ovarian- tubal – pelvic types may be due to regurgitation & implantation of shed
menstrual endometrial glands.
2. May be due to metaplasia of serosal cells covering ovary.
3. May be due to lymphatic or vascular emboli of endometrial tissue.
Complications:
1. Pain.
2. Hemorrhage in affected area.
3. Ovaries → chocolate cysts.
4. Peritoneal hemorrhage → maybe followed by fibrosis + adhesions.
5. Adenomyosis.
Definition:
Presence of endometrial foci inside the myometrium.
Pathogenesis:
Foci → derived from basal layer of endometrium.
Gross:
1. Uterus is enlarged.
2. Thick myometrium with small greyish or bleeding foci.
Microscopy:
Myometrium has foci formed of endometrial glands and stroma (adenomyosis), or
stroma only (stromal endometriosis).
Complications:
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1. Menorrhagia.
2. Dysmenorrhea.
6. Cervical intra-epithelial neoplasia.
See cervical carcinoma.

7. Endometrial hyperplasia.
Definition:
- It's a common condition.
- Occur around menopause
- Has precancerous potential, which increases if there is atypia and gland complexity.
Etiology:
Prolonged estrogen stimulation:

1. Repeated anovulatory cycles (premenopause).
2. Estrogen secreting tumors (granulosa cell tumor).
3. Prolonged estrogen therapy.
4. Others, as: polycystic disease of the ovary & adrenal hyperfunction.
Gross:
1. Uterus → mildly enlarged.
2. Endometrium → thick polypoid.
Microscopy:
Stroma and glands are hyperplastic (glandular hyperplasia)
I. Simple hyperplasia (cystic):

1. Crowded glands with many cysts (a Swiss-cheese appearance).
2. Glands lined by columnar cells.
It may be in the form of:

a. Simple hyperplasia with no atypia (mostly).
b. Simple hyperplasia with atypia (rare).
II. Complex hyperplasia (adenomatous):

1. Crowded back to back glands.
2. Lined by columnar cells.
It may be in the form of:
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a. Complex hyperplasia with no atypia (less common).

b. Complex hyperplasia with atypia (common) → the most precancerous of all.
Complications:
1. Abnormal uterine bleeding (dysfunctional uterine bleeding). It may be:

a. Menorrhagia: excessive prolonged menstruation.
b. Metrorrhagia: irregular bleeding.
2. Malignancy:
Commonly on top of atypical hyperplasia.
8. Leiomyoma (Pathological features, secondary changes).
Pathological features :
Gross:
1. Single or multiple.
2. Occurs in:
a. Myometrium (intramural – interstitial).
b. Beneath serosa (subserous).
c. Beneath endometrium (submucous).
3. Sharply circumscribed, round and firm.
4. Uncapsulated, may acquire false capsule of surrounding muscles.
5. Cut section is greyish brown with whorly appearance.
Microscopy:
1. Interlacing bundles of smooth muscle cells which are spindle in shape.
They differ from fibroblasts in:

a. Having abundant eosinophilic cytoplasm.
b. Rod shaped nuclei with non-tapering (blunt) ends.
2. Fibrous stroma with blood vessels. It increases after menopause → called Fibroid
or fibromyoma.
Secondary changes:
1. Dystrophic calcification.
2. Hyaline degeneration.
3. Myxomatous degeneration.
4. Cystic changes.
5. Ulceration of endometrium & 2ry infection.
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6. Malignancy (rare).
7. Ischemic necrosis (red degeneration) during pregnancy due to vascular thrombosis.
Tumor is red and necrotic.
9. Mucinous and serous cystadenoma of the ovary. Or write a note on benign
cystic surface epithelium tumors of the ovary.
See comparison (common question).

10. Non-neoplastic ovarian cysts.
.‫ﺳﺆال ﻣﻬﻢ‬
I. Follicular cysts.
1. Multiple small cysts arising from non-rupturing Graafian follicles.
2. Lined by granulosa cells.
3. Contain clear fluid.
II. Stein-Leventhal syndrome.

1. Polycystic ovaries showing many follicular cysts.
2. There is hirsutism, oligo menorrhea, and infertility.
III. Corpus luteum cysts.

1. Single, large cyst arises from corpus luteum.
2. Intracystic hemorrhage is common.
IV. Chocolate cysts.

Hemorrhagic cysts in ovarian endometriosis.
V. Theca-Lutein cysts.
Multiple cysts lined by luteinizing theca cells in placental tumors.
11. Give the gross picture of benign mature ovarian teratoma.
Gross:
Size:
The tumor is large.
Components:
1. Dermoid ridge which is solid and covered by skin.
2. The rest of the tumor is cystic and contains mature structures: tufts of hair, teeth
& other structures.
12. Germ cells tumors of the ovary.
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They constitute about 10% - 15% of ovarian neoplasms (similar to GCT of testis).
I. Dysgerminoma.
A malignant tumor arising from germ cells, similar to testicular seminoma.
Gross:
a. Solid greyish, unilateral or bilateral.
b. Affecting young females.
Microscopy:
a. Large pale tumor cells.
b. Large nuclei with prominent nucleoli.
c. Separated by stroma rich in lymphocytes.
II. Teratoma.
1. Mature teratoma:
a. Benign.
b. Most common, usually cystic (Dermoid cyst - See before).
2. Immature teratoma:
a. Malignant.
b. Grossly: hemorrhage and necrosis.
c. Microscopy: mixture of tissues from different origins (ecto – endo – mesoderm)
some are immature (malignant).
III. Others (which may be classified among teratoma):
1. Embryonal carcinoma:
a. Undifferentiated teratoma.
b. Consists of primitive cells, high anaplasia with multiple mitosis.
2. Terato-carcinoma:
Mixture of embryonal carcinoma and classic teratoma.
3. Mono-dermal teratomas:
a. Struma ovarii → benign → only thyroid tissue is present.
b. Carcinoid tumor → similar to that of GIT.
c. Choriocarcinoma → malignant trophoblasts secrete HCG hormone
IV. Yolk sac tumor (Endodermal sinus tumor):
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a. Gross: Solid and cystic areas.

b. Microscopy: very primitive cells exhibiting → (microcytic, hepatoid, clear cells and
papillary structures) → resembling normal yolk sac.
c. It is positive for α-feto protein (AFP).
13. Choriocarcinoma.
Arises de novo or on top of invasive mole, complete mole or rarely partial mole.
Gross:
1. Uterus → enlarged, no fetus.
2. Uterine cavity → filled with large hemorrhagic necrotic mass that invades
myometrium.
3. Ovaries → show theca lutein cysts.
Microscopy:
1. Large sheets of malignant cytotrophoblast and syncitiotrophoblast.
2. Extensive necrosis and hemorrhage.
3. No chorionic villi.
Pregnancy test:
Positive → elevated HCG.
Spread:
1. Direct: uterine perforation and massive peritoneal hemorrhage.
2. Blood: lungs, bones, liver (early).
3. Lymphatic (late).
14. Hydatidiform (vesicular) mole.
See comparison (complete & partial mole).

15. Endometrial carcinoma.
Definition:
1ry malignant neoplasm arising from endometrium.
Etiology:
Uncommon, occurs mainly after menopause.
Nulliparity & endometrial hyperplasia (+ its predisposing factors, see before).
Pathology:
- 120 -
Site:
Common in fundus.
Gross:
1. Enlarged uterus.
2. The tumor maybe:
a. Fungating polypoid mass (exophytic).
b. Diffuse infiltrating carcinoma (endophytic).
Microscopy:
1. Adenocarcinoma or papillary adenocarcinoma (commonest).
2. Adenoacanthoma: adenocarcinoma in which some malignant glands show
squamous metaplasia.
3. Adenosquamous carcinoma: Mixture of adenocarcinoma & squamous
carcinoma.
Spread:
1. Direct: Fallopian tubes, cervix, bladder, .. (nearby organs).
2. Lymphatic: early to regional (pelvic) LNs.
3. Blood: late to lungs, liver, bone, brain, ...
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Chapter Eleven |
Diseases of the Breast
GIVE AN ACCOUNT ON:
1. The GP of carcinoma of female breast
I. Intra-duct carcinoma:
Non capsulated mass composed of enlarged ducts, many of which contain yellowish
necrosis material.
II. Infiltrating duct carcinoma:
1- Scirrhous carcinoma:
Ill-defined hard greyish mass that give a gritty sensation on cutting
• Retraction the nipple or skin dimpling due to adherence of tumor to skin &
retraction of fibrotic stroma.
• Peau d’orange: mammary skin appears mamillated (like the peal of an orange)
due to lymphedema which leads to forward pushing of the skin except at points
of skin anchorage.
• Inflammatory carcinoma: sometimes, breast become swelling, redness &
tenderness.
• Micro-calcification.
2- Paget’s disease:
The nipple is red, ulcerated & scaly.
3- Medullary carcinoma:
Fairly defined soft mass with area of necrosis & hemorrhage
the cut surface bulges.
2. Mammary cystic hyperplasia (fibrocystic disease)
Aetiology:
Exaggerated response to estrogen (at the age of 35-50years)
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Gross:
• May be unilateral or bilateral.
• Irregular greyish firm non-capsulated mass or masses with scattered variable-sized
cysts, the cysts contain clear or hemorrhagic fluid and may appear yellowish brownish or
blue.
MP:
1- Epithelial hyperplasia:
• Adenosis:
Increased number of acini/ductules  increased sized of lobules.
•Lobular hyperplasia:
Cell lining the acini are hyperplastic forming many layers may associate with
cellular atypia.
• Ductal hyperplasia:
The ducts are lined by many layers of cell (epitheliosis), sometimes with
papillary formation (papillomatosis), may associated with atypia.
2-Cysts:
Dilated ducts containing secretions
3-Apocrinemetaplasia:
Large with abundant eosinophilic cytoplasm resembling cells of apocrine sweat
glands
4- Fibrosis.
5- Sclerosing adenosis:
Adenosis with extensive fibrosis that distorts & compresses the hyperplastic
ductules giving a false impression of invasive cancer
3. Types of breast mass
1- Neoplastic diseases:
Benign & malignant tumors
2- Hyperplastic diseases:
Fibrocystic disease
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3- Inflammatory diseases:
Chronic abscess, mammary duct ectasia & TB Mastitis
4- Traumatic lesions:
Fat necrosis & hematoma
4. Spread & staging of breast carcinoma
I. Spread:
1- Local spread:
To skin and chest wall
2- Lymphatic spread:
• Lymphatic emboli:
Lead to metastases in axillary lymph nodes. Further spread leads to metastases in
infraclavicular & sometimes supraclavicular nodes, internal mammary nodes.
• Lymphatic permeation:
Leads to lymphedema causing:
- Peau d’orange: mammary skin appear mamillated (peal of orange)
- Cancer-en-cuirasse: hardening and fixation of breast due to lymphedema and
invasion of pectoral muscle
3- Blood Spread:
To lung, liver, bone.
II. Staging:
TNM staging
Tis: in situ lobular or duct carcinoma
T1: tumor 2 cm or less in longest dimension
T2: tumor 2-5 cm
T3: more than 5 cm
T4: any size with invasion of the skin or chest wall
N0: no LN metastases
N1: metastases to 1-3 ipsilateral axillary LN
N2: 4-9 ipsilateral axillary LN
N3: 10 or more ipsilateral axillary LN
M0: no evidence of distant metastases
M1: Distant metastases
- 124 -
LIST
Six precancerous factors, lesions for mammary carcinoma
1- Heredity: mutation of BRCA genes

2- Early menarche or late menopause.
3- Nulliparity.
4- Endogenous hyperoestrinism.
5- Obesity: local synthesis of estrogen with in fat depot.
6- Fibrocystic disease with atypical hyperplasia.
7- Duct papilloma.
8-breast carcinoma in one side increase risk of cancer development in the other.
9-milk factor (virus): only in experimental animals
5. Pathology of intra-ductal breast carcinoma
GP:
Non-capsulated mass composed of enlarged ducts, many of which contain yellowish
necrotic material when the mass is squeezed; the necrotic material comes out of the cut
surface like a tooth paste.
MP:
The ducts are enlarged & lined by several layers of malignant cells without invasion of
basement membrane. Intra-ductal cell proliferation may assume several patterns:
cribriform, papillary & comedo pattern.
-Comedo pattern appears as central eosinophilic necrosis filling the lumen of the ducts
& surrounded peripherally by few layers of malignant cells, this pattern is more rapidly
followed by infiltration.
6. Benign tumors of the breast
1- Duct papilloma:
Usually in middle aged females.
Gross:
Small pedunculated branching mass
Microscopy:
Vascular cores covered by columnar cells
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Effects:
• Bleeding per nipple.
• Malignant change.
2- Fibro-adenoma:
Most common benign tumor in the breast
Young age: 15-25 years
Gross:
• Capsulated rounded or oval mass ranging from less than 1 cm to more than 10 cm
in diameter.
• Usually single but more than one can occur
• Cut section is uniform greyish white and shows slits
• the commonest site is upper outer quadrant
Microscopy:
• Consist of proliferated ductules lined by regular epithelium and myoepithelium
and surrounded by abundant fibroblastic stroma.
• Ductules may be patent with recognizable lumens (pericanalicular)
• Ductules may appear compressed due to excess stroma (intracanlicular)
• Mixed type is not uncommon
• No difference between the two types clinically
Malignant change is rare and if present it is malignant in situ
3- Phyllodes tumor:
Uncommon, Occurs in middle aged females
Gross:
• Capsulated large mass. 10-15 cm
•Cut section: myxomatous,cystic areas and leaf like clefts and slits (phyllodes)
Microscopy:
Resembles intracanalicular fibro-adenoma but stroma is very cellular
Effects:
• Breast enlargement
• Malignant phyllodes (uncommon)
4- Others:
Lipoma, hemangioma, neurofibroma and others
- 126 -
7. Mammary carcinoma of lobular origin
Less than 10% of cases

1- Lobular carcinoma in situ: acini are distended with small malignant cells with no
invasion of basement membrane. It may change to invasive type
2- Infiltrative lobular carcinoma: They are small malignant cells typically invading the
stroma in the form of linear cords (Indian file pattern).
Both types invasive and in situ lobular carcinoma have a high incidence of multicentricity
and bilaterally.
8. Paget’s disease of the breast
The disease is characterized by:

• Mammary carcinoma: Intra-duct or invasive.
• Eczema of the nipple due to transductal intraepidermal spread
Gross:
Nipple is red, ulcerated and scaly
Microscopy:
The epidermis is infiltrated by large-sized neoplastic cells with clear cytoplasm and large
hyperchromatic nuclei (Paget’s cells)
- 127 -
Chapter Twelve |
Diseases of Bones and Joints
GIVE AN ACCOUNT ON:
1. Paget's disease of bone.
Definition:
One of the types of osteodystrophies (abnormalities of bone growth & structure),
characterized by bone decalcification followed by excess deposition of weak bone
leading to bone thickening.
Aetiology:
• Unknown.
• Affects old males.
• Very rare in Egypt.
Pathology:
Characterized by "collage of matrix madness" where affected bones show:
• Osteolytic phase: areas of furious bone resorption by osteoclasts.
• Osteoblastic phase: Hectic bone formation.
• Osteosclerotic phase: Net result is increased bone density leading to bone
deformities, as:
- Skull enlargement with narrowing of its foramina.
- Bending of long bones.
Complications:
• Pathological fracture.
• Precancerous (sarcomatous transformation) → Osteosarcoma, Chondrosarcoma or
fibrosarcoma.
• High output heart failure.
2. Acute hematogenous osteomyelitis.
Definition:
- 128 -
Blood-borne acute suppurative inflammation of bone & bone marrow
Aetiology:
(More common in children)
1- Causative organism:
• Staph. Aureus in 80-90% of cases
• Less commonly E. coli, pneumococci, streptococci,
2- Mode of transmission:
Blood spread (bacteremia) from distant infections following trivial injuries (as
intestinal mucosal abrasions &vigorous chewing of hard foods)
3- Predisposing factor:
Bone trauma, especially in children
Site:
• Long bones are more commonly affected then vertebrae.
• Lesions are localized at sites of most vascularity >>metaphysis in children, because it's
the most vascularized part of bone and normally the flow is slow ,moreover the
metaphysic is the most common part subjected to trauma .
>>epiphysis in infants and adults
• in infants and adults: epiphysis may be also affected.
1. The initial lesion is a suppurative focus (1) in the metaphysis (most vascular part of
long bones).
2. The organism spreads through penetrating the endosteum & reaches the periosteum
causing sub-periosteal abscess (2).
3. Rupture of sub-periosteal abscess → sinuses (3).
4. Bone necrosis (4) occurs; due to:
• Bacterial toxins.
•Ischemia; due to stretching, compression or thrombosis of periosteal vessels.
5. Separation of necrotic bone by action of osteoclasts. The separated part is called
sequestrum(5)& its margins are serrated.
6. Gradual thickening of periosteum due to new bone formation (involucrum)(6).
7. The sinuses now appear as thick-walled holes called cloacae(7) (this occurs in chronic
phase).
- 129 -
Complications:
1- Pathological fracture.
2- Spread of infection:
• Direct → Arthritis, myositis, neuritis …
• Blood → Toxemia, septicemia & pyemia.
3- Chronicity → chronic suppurative osteomyelitis, leading to:
• 2ry amyloidosis
• Squamous cell carcinoma as a result of epithelialization of sinuses
3. Giant cell tumor of bone (Osteoclastoma).
Definition:
Locally-malignant neoplasm arising from bone usually occurs after the age of 20 years
but may occur in younger ages. Maybe malignant in 10-20% of cases
Site:
• The most common sites are around knee joint (distal femur & proximal tibia).
• The tumor involves both epiphysis & metaphysis.
1- Grossly:
• The tumor forms an eccentric mass that erodes the subchondral bone → the
covering cortical bone becomes markedly thinned (egg shell-like).
• The tumor tissue is greyish brown & shows areas of cystic degeneration &
hemorrhage.
2- Microscopy:
• Mononuclear neoplastic cells of unsettled origin (maybe osteoblastic or
fibroblastic): oval stromal cells with dark nuclei & different grades of atypia ranging
between mild & marked.
• Multinucleated (up to 100 nuclei) non neoplastic giant cells: formed as a result of
fusion of monocytes-macrophages (osteoclasts).
• Collagenous stroma, vessels & areas of hemorrhage.
3- Radiological features:
Appears as an eccentric lytic lesion with an adjacent thinned cortex and with
minimal or no periosteal reaction (Soap-bubble appearance in epiphysis)
- 130 -
Spread:
• Local spread only (in 80-90% of cases).
• Distant (blood) spread occurs only in 10-20% of cases with a malignant behaviour.
4. Sites, pathological & radiological features of multiple myeloma.
Site:
Bone marrow of axial skeleton (skull, vertebrae, sternum, pelvis & ribs)
1- Grossly:
• Often arise as multiple tumors (myelomatosis).
• Rarely start as a solitary tumor then becomes multiple.
• The tumors appear as soft red nodules.
2- Microscopy:
Malignant plasma cells at different stages of maturation
3- Radiology:
Multiple osteolytic defects
5. Causes of death in multiple myeloma.
1- One & bone marrow destruction, leading to:

• Pathological fractures.
• Pancytopenia.
• Hypercalcemia & metastatic calcifications.
2- Production of abnormal immunoglobulins (Bence-Jones proteins), leading to:
• Bence-Jones proteinuria: These proteins form casts that block renal tubules. They
can be detected in urine by heating (they coagulate at 55oC & are dissolved at
85oC).
• Low immunity → recurrent infections.
• Amyloidosis in 25% of cases.
3- Blood spread → plasma cell leukaemia.
4- Renal changes (myeloma nephrosis):
• Common, leading to renal failure.
• Include: blockage of renal tubules by protein casts, nephrocalcinosis &
pyelonephritis.
6. Articular & extra-articular lesions of rheumatoid arthritis.
- 131 -
I. Articular (joint) lesions:
Site:
• Polyarthritis, symmetrical bilateral affection, involved joint is swollen painful &
stiff.
• Mainly involves small joints of hands & feet (esp. inter phalangeal joints).
• May also affect large joints as knee, hip & elbow.
Lesions include:
1- Chronic inflammation of synovial membrane:
Grossly:
Swollen redundant synovium, showing exaggerated villous projections.
Microscopy:
• Fibrinoid necrosis.
• Increased vascularity.
• Numerous lymphocytes, plasma cells & histiocytes.
• Synovial cell hyperplasia.
• Osteoclastic activity on underlying bone → bone erosion.
2- Excessive granulation tissue formation:

• It creeps under the articular cartilage within the eroded bone and also over the
articular cartilage & may communicate on both surfaces forming pannus.
• This leads to fibrous ankylosis.
3- Articular cartilage destruction:

• This is due to action of collagenase & other proteases released in pannus.
• This is followed by fibrous or bony ankylosis → the joints appear swollen,
spindle-shaped & deformed.
II. Extra-articular lesions:

1- Rheumatoid nodules:
• Subcutaneous nodules that develop over bony prominences, commonly around
the elbow.
• 1-2 cm in diameter.
• Microscopy: area of fibrinoid necrosis of collagen surrounded by palisading
histiocytes.
2- Heart lesions:
- 132 -
Rheumatoid nodules affecting valves & pericardium

3- Vascular lesions:
Arteritis & phlebitis may occur.
4- Lymphoid hyperplasia &enlargement of lymph nodes & spleen.
5- Amyloidosis.
NB:
• Felty's syndrome: rheumatoid arthritis in old age accompanied by splenomegaly
& pancytopenia.
• Still's disease (Juvenile rheumatoid arthritis): occurs in patients fewer than 16 with
acute onset, high fever, leucocytosis, and splenomegaly and skin rash.
7. Osteoarthritis.
Definition:
• A common degenerative disease characterized by primary abnormalities in the
articular cartilage of large weight bearing joints (esp. knee & hip joints) and spine.
• It is a disease of elderly (females more common than males).
• When younger patients develop osteoarthritis, it's 2ry to a predisposing abnormality in
the joint.
Types:
1. Primary osteoarthritis (95%):

Affects old age; as a result of "wear & tear" of the joint
2. Secondary osteoarthritis (5%):

Affects any age; as a result of:
a. Chronic joint stress:

As in obesity & occupational strains
b. Abnormal joint mechanics, e.g.:

• Defective nerve supply to the joint (Charcot's joint) as in spinal cord lesions
(tabes dorsalis of syphilis …)
• Congenital joint deformities as angulations & malalignment.
• Acquired joint deformities as post-traumatic or post-inflammatory injury.
c. Systemic disease: as DM & hemochromatosis.
- 133 -
Site:
Large weight-bearing joints (esp. knee & hip joints) and spine are the most common
sites.
Main lesions include:
1. Articular cartilage & bone lesions:

• Degeneration & softening of articular cartilage → central part of articular cartilage
disappears & underlying bone is exposed.
• Proliferation of peripheral parts of cartilage → cartilaginous lippings.
• Ossification of cartilaginous lippings → bony projections (osteophytes).
•Separated portions of degenerated cartilage may float freely in joint "joint mice".
• Underlying bone undergoes progressive eburnation.
2. The synovium:
May show mild chronic inflammation &osteo-cartilaginous metaplasia
8. Osteosarcoma
9. Chondrosarcoma
Osteosarcoma Chondrosarcoma
Primary malignant neoplasm • Primary malignant neoplasm
Definition arising from Osteogenic (secrete arising from chondrogenic cells
bone matrix) cells of bone (secreting cartilaginous matrix)
(osteoblasts). (chondroblasts).
• Less common than
osteosarcoma
(‫)ﺗﺪوﺑﻲ‬ (‫)دوب‬
Predisposing
factors: • Trauma. • Paget's disease of bone.
• Irradiation. • Fibrous dysplasia.
• Paget's disease of bone. • Chondroma & osteochondroma.
• Fibrous dysplasia.
• Osteochondroma
• Children& young adults (usually Affects any age, most commonly

Age: below 20). in the 4th decade.
• In old age on top of Paget's
disease of bone.
- 134 -
Any bone may be affected, but Arises in any bone, but most
Site: the most common sites include: commonly in central portions of
skeleton: pelvis, shoulder & ribs.
• Distal femur & proximal
tibia (ends of bones around
knee joint) "60%".
• Proximal femur "15%".
• Proximal humerus "10%".
The tumor starts in metaphysic
Pathological Grossly: Grossly:

features • The tumor forms a large The tumor grows within
mass which extends the medullary canal, low
within the medullary canal grade tumors show
& destroys bone cortex. reactive thickening of
• The periosteum is cortex but high grade
elevated, and then penetrate the cortex and
becomes penetrated. periosteum extending to
• Extension of periosteum the adjacent soft tissue
within the adjacent soft forming a large mass wit
tissue occurs→ severe areas of He and necrosis
hemorrhage & necrosis. calcific and myxomatous
• Well differentiated changes are common
tumors are usually hard
(osteosclerotic), while
undifferentiated tumors
Microscopy:
are usually soft
(osteolytic). •Tumor cells:
Microscopy: In low grade tumors the

chondrocytes show low
The tumor consists of:
grade atypia and
• Tumor cells: minimal mitoses but in
hugh grade they show
Pleomorphic and
pleomorphism, dark
include spindle & giant
nuclei and prominent
cell forms with large
mitoses
dark nuclei showing
abnormal mitotic •Matrix:
activity (criteria of
Hyaline matrix is more
anaplasia).
abundant in low grade
- 135 -
tumors myxoid changes

• Matrix:
and spotty
Consists of osteoid calcifications are
tissue (more common, but
prominent in well
differentiated tumors). • Hemorrhage & necrosis
There may be also are more common in high
collagenous & grade tumors.
cartilaginous matrices.
• Thin-walled vessels,
which may be very
numerous
(telangiectatic
osteosarcoma).
• Areas of hemorrhage &
necrosis.
• Tumors rich in bone matrix may Mottled densities; due to spotty

Radiological show sun-ray appearance in X- calcifications.
features: ray films.
• Periosteal elevation maybe
associated with reactive bone
formation in the triangle between
the cortex & elevated
periosteum →Codman's
triangle in X-ray films.
• Direct to surrounding soft • Low grade tumors spread only
Spread: tissue. locally.
• Blood spread to lung & others • High grade tumors spread both
locally (to surrounding soft tissue)
and by blood (lung …).
A highly malignant tumor with Better than osteosarcoma

Prognosis: rapid spread & poor prognosis
- 136 -
10. Ewing's sarcoma (1991).
Definition:
Primary malignant neoplasm of unsettled origin, most likely from primitive
neuroectodermal cells
Site:
• Arises in the medullary canal of diaphysis of long bones, esp. femur, or in flat bones of
pelvis.
• May also arise in soft tissue (called primitive neuroectodermal tumor PNET).
Age:
5-20 years, but PNET may occur in older age groups.
Gross picture:
Soft mass with extensive hemorrhage & necrosis that destroy bone cortex
Microscopy:
• Round cells with dark nuclei.
• Cytoplasm contains glycogen (to differentiate them from cells of other malignant
round cell tumors as lymphoma & neuroblastoma).
Radiological features:
A lytic destructive bone lesion with a characteristic bone reaction in the form of layers
(onionskin-like fashion).
Spread:
Direct & by blood
- 137 -
DEFINE.
1. Rheumatoid arthritis.
• Systemic autoimmune collagen disease, more common in females between 30-50

years.
• Stimulus is unknown, maybe viral or bacterial.
• Autoantibodies are formed & initiate an inflammatory reaction → inflammatory cells
release cytokines (as TNF & interleukins) and proteolytic enzymes (as proteases) →
destruction of joint structures.
2. Osteomyelitis.
Inflammation of bone & bone marrow
Classification:
I. Bacterial:
1. Acute suppurative osteomyelitis:
Hematogenous or non hematogenous
2. Chronic osteomyelitis:
Non- specific (suppurative) or specific (tuberculous or syphilitic)
II. Non-bacterial:
1. Viral osteomyelitis.
2. Sarcoidosis.
3. Radiation osteomyelitis.
3. Osteoarthritis (OA).
• A common degenerative disease characterized by primary abnormalities in the

articular cartilage of large weight bearing joints (esp. knee & hip joints) and spine.
• It is a disease of elderly (females more common than males).
• When younger patients develop osteoarthritis, it's 2ry to a predisposing abnormality
in the joint.
4. Paget's disease of bone.
One of the types of osteo-dystrophies (abnormalities of bone growth & structure),

characterized by bone decalcification followed by excess deposition of weak bone
leading to bone thickening.
- 138 -
E N U M E R AT E (C L A S S I F Y ) :
Primary bone tumors
Origin Benign Locally-malignant Malignant

Osteoma. Osteosarcoma.
Osteogenic (from Osteoblastoma
osteoblasts)
Chondroma. Chondrosarcoma.
Chondrogenic Chondroblastoma.
(from Chondromyxoid
chondroblasts) fibroma.
Osteo-Chondroma
Developmental
Fibroma. Fibro-sarcoma.
Fibroblastic
Chordoma. Chordoma.
Notochord
remnants
Adamantinoma. Adamantinoma.
Epithelial
Hemangioma. Angio-sarcoma.
Vascular
Schwannoma. Malignant
Neurogenic Schwannoma.
Lipoma. Liposarcoma.
Adipose tissue
Myeloma.
Bone marrow Lymphoma.
Leukemia.
Ewing sarcoma
Primitive (PNET)
neuroectodermal
cell
Giant cell tumor. Giant cell tumor.
Unsettled origin
- 139 -
Benign fibrous Malignant fibrous

Fibrohistiocytic histiocytoma. histiocytoma.
MENTION:
A disease characterized by degeneration of articular cartilage & development of

osteophytes.
Osteoarthritis.
- 140 -
Chapter Thirteen |
Diseases of lymphoid tissue
GIVE AN ACCOUNT:
1. Hodgkin’s lymphoma
Definition
It’s the common lymphoma. It occurs at any age and usually starts in cervical lymph
nodes.
I.Gross:
Different types of lymphomas have worse or less similar gross features.
1- The affected nodes are enlarged, firm with homogenous greyish pink cut section. The
enlarged nodes are first discrete, but they become fused due to capsular invasion leading
to formation of irregular large fixed mass.
2- Affection of Spleen → Multiple (usually) greyish nodules → splenomegaly
3- Affection of extra-nodal sites similarly appears as greyish pink nodules.
II. Microscopy:
II.I Loss of nodal architecture and replacement of nodal tissue by:

• Neoplastic cells: their histogenesis (origin) is not settled
1- Reed-Sternberg Cells (RS cells):
these are large cells 30-60μ in diameter with amphophilic cytoplasm and
multiple (commonly two) mirror image nuclei containing large eosinophilic
nucleoli
2- Mononuclear Hodgkin’s cell:
it’s smaller than RS cell, with a single nucleus having an eosinophilic nucleolus.
The cytoplasm is amphophilic.
3- Lacunar cell:
it resembles RS cells but with shrunken cytoplasm that creates a clear space
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between the shrunken cytoplasm and the cell wall. It’s the most common cell in
nodular sclerosing type
4- L and H cells (atypical lymphocyte and histiocytes cells)
these are large mononuclear cells with twisted or lobulated nuclei and multiple
small nucleoli
•Non-Neoplastic (reactive) cells:
A variable mixture of lymphocytes, plasma cells, neutrophils, eosinophils, and
macrophages
• Necrosis and fibrosis: may occur.
II.II Histological classification HL: Rye’s classification.

1- Nodular Lymphocyte predominant type (5%):
It’s characterized by nodules of reactive lymphocytes with their central portions
showing predominance of L and H cells with no or few RS cells. Prognosis is good
2- Lymphocyte rich type (5%):
Characterized by diffuse background composed of reactive lymphocyte with many
mononuclear Hodgkin’s cells and vary rare RS cells. Good Prognosis.
3-Nodular Sclerosing Type (60%):
It’s characterized by numerous lacunar cells in addition to RS cells. There are
variable reactive cells. Thick bands of Collagen occur and may divide the node into
nodules. It has a relatively good prognosis.
4- Mixed cellularity Type (25%):
There are numerous RS cells and Hodgkin’s mononuclear cells associated with a
mixture of reactive cells (lymphocytes, plasma cells, eosinophils, histiocytes…).
This type is more aggressive than the previously mentioned 2 types.
5- Lymphocyte Depletion Type (1-5%):
It’s characterized by very numerous RS cells and Mononuclear Hodgkin’s cells.
Lymphocytes are very few. Necrosis and diffuse fibrosis may occur. Prognosis is
poor. Recently there is a trend to classify this type independent of Hodgkin’s
lymphoma.
Remark
Lymphocyte predominant types can (if untreated) change into mixed cellularity or
lymphocyte depletion type. Nodular sclerosing type doesn’t change to other types.
• The original Rye’s classification did not include nodular lymphocyte predominant
type (only recently identified as a separate entity)
- 142 -
III. Clinical Features:

1- Enlarged L.N.s and may be Splenomegaly
2- Systemic manifestations: Hodgkin’s lymphoma may be associated with:
a) Intermittent Fever
b) Anemia
c) Night Sweats
d) Loss of Weight
* The presence of these manifestations indicates a more aggressive disease course.
IV. Clinical staging of HL:

It’s decided into 4 stages (I, II, III,IV) each stage is further subdivided according to the
presence or absence of systemic manifestations into (A) absent, (B) present.
Example: stage IIIB or stage IIIA
Stage I: The disease is limited to only one group of L.N.s e.g. cervical.
Stage II: Two or more groups of nodes but to one side of the diaphragm (above or
below)
Stage III: Many groups of L.N.s above and below the diaphragm (including spleen)
Stage IV: Affection of non-lymphoid organs due to blood spread.
2. Lymphadenitis:
It’s a common disorder
I. Acute Bacterial Lymphadenitis
Aetiology:
It affects L.Ns draining acute infective lesions e.g. cervical L.Ns in case of acute
tonsillitis or tooth infection and mesenteric nodes in case of Typhoid Fever or Acute
Appendicitis.
Pathology:
Enlarged discrete nodes showing congested capillaries, neutrophils and
macrophages
II. Acute Viral Lymphadenitis:
a) Measles
b) Infectious Mononucleosis
- 143 -
Define and Aetiology:

An infective disease caused by Epstein Barr Virus characterized by fever, sore
throat, generalized L.N enlargement and sometimes splenomegaly.
Pathology:
• Generalized L.N enlargement:
the affected node show striking Para cortical blast transformation
• Splenomegaly
the peripheral blood shows lymphocytosis with many abnormal T-Lymphocytes.
• Lymphocytic infiltration of liver, brain, meninges may sometimes occur
• The disease is usually self-limited
III. Acute Chlamydial Infection:

In case of Lymph granuloma Venereum
IV. Chronic Non-specific Lymphadenitis:
Aetiology:
Occurs in L.Ns draining areas of chronic bacterial infections
Pathology:
The affected nodes are enlarged, firm and discrete. Microscopically they show
chronic inflammatory cells associated with reactive follicular hyperplasia.(enlarged
follicles with reactive prominent germinal centres) and/ or sinus histiocytes.
V. Chronic Specific/Granulomatous Lymphadenitis: e.g.

T.B
• Atypical Mycobacteriosis
• Sarcoidosis
• Leprosy
• Syphilis
• Toxoplasmosis
- 144 -
LIST
1. Causes of L.N enlargement. Describe microscopic picture of one of them.
1- Acute Chronic Lymphadenitis

2- Reactive L.N hyperplasia
3- L.N tumours
Primary = lymphoma
Secondary = metastasis
4- Blood disease: mainly leukaemia
5- Some metabolic storage diseases.
2. Causes of splenomegaly:
I. Infectious:
1- Bacterial: as T.B, typhoid and septicaemia
2- Viral: infectious mononucleosis
3- Parasitic: as bilharzia, malaria, kala-azar, hydatid cyst ….
II. Vascular disorders:

1- Portal hypertension due to cirrhosis or hepatic bilharziasis
2- Chronic venous congestion: due to right sided heart failure
3- Recent infarcts
III. Blood diseases:

1-leukaemia
2- haemolytic anemia
3- Polycythemia Vera
4- thrombocytopenia
IV. Tumors:
1- Malignant: Primary or secondary
2- Benign
V. Metabolic disturbances:
As amyloidosis, hemochromatosis and lipid storage disease
VI. Hypersplenism:
- 145 -
- Splenic enlargement with increased destructive activity to blood cells leading to

pancytopenia.
- It may be primary or secondary.
- 146 -
Chapter Fourteen |
Haematopoietic disorders
GIVE AN ACCOUNT ON:
Major types and pathological features of chronic leukaemia
Chronic myeloid Chronic lymphocytic

leukaemia leukaemia
25-60 Commonest
Age leukaemia in old
person >50
Hyper-cellularity with Show scattered foci of
Bone marrow increased myeloid small mature
cells “granulocytes” lymphocytes in a
including eosinophils background
The total leucocyte Lymphocyte count is
Peripheral blood count rises to 75,000- up to 100,000
250,000. Most cells are mature
Most of the cells are lymphocytes
mature granulocytes
and late myelocytes
Hepatomegaly, Hepatomegaly,
splenomegaly, splenomegaly,
generalized lymph generalized lymph
node enlargement. node enlargement
Other organ may (L.N Show picture
of small diffuse
show leukaemia
lymphocytic
infiltrate
lymphoma).
Other organ may
- 147 -
show leukaemia
infiltrate
1- Gout is a common 1- Autoimmune

Complications complication due to haemolytic anemia.
excess production of 2- Lowered immunity,
uric acid. thus infections is
2- Lowered immunity, common.
thus infections is
common.
DISCUSS
The pathology of chronic lymphocytic leukaemia
See before
MENTION AND GIVE A VERY SHORT ACCOUNT ON
Four complications of pernicious anemia
1. Atrophic gastritis with deficient production of intrinsic factor (Gastric carcinoma is a

complication)
2. Sub-acute combined degeneration of the spinal cord in up to 10% of cases
3.Hemosiderosis due to impaired utilization of iron by the bone marrow
GIVE AN ACCOUNT ON
Polycythemia
Def.:
Increased blood erythrocytes
It may be:
- 148 -
1. Secondary “reactive” type due to bone marrow stimulation in case of hypoxia (high
altitudes, chronic lung disease, congenital cyanotic lung disease).
2. Primary “Polycythemia Vera”
A serious neoplastic disease of bone marrow. There is a marked increase of peripheral
RBCs leading to marked increase in blood viscosity. Thrombosis is common leading to
infections. Splenomegaly occurs
- 149 -
Chapter Fifteen |
Diseases of the endocrine glands
E N U M E R AT E
Types of thyroiditis
• Hashimoto’s thyroiditis
• Reid’s thyroiditis
• Granulomatous (sub-acute or de Quervainis) thyroiditis
• Acute thyroiditis
• Other types→ tuberculous, syphilitic& fungal thyroiditis
GIVE AN ACCOUNT ON
1. Hashimoto’s thyroiditis
I. Aetiology:
Autoimmune, type II hypersensitivity (cytotoxic T-cell mediated reactions)
II. Gross:
• Symmetrically enlarged thyroid lobes
• Consistency → firm, rubbery gland
• Colour → the normal red brown colour of the gland is replaced by pale greyish white
appearance
III. Microscopy:
• Extensive replacement of the thyroid by lymphocytes which may sometimes form
follicles
• Marked atrophy of the follicular epithelium
• the residual follicular cells commonly transform into large pink cells (Ashkenazy or
Hurthle cells)
- 150 -
2. Nodular goiter
I. Aetiology & pathogenesis:

• Nodular goitre may develop on top of diffuse goitre
•It’s believed that nodular goitre is due to:
Repeated cycles of iodine deficiency (thyroid hyperplasia) & iodine correction
(thyroid involution) which creates an abnormal gland rhythm accompanied by
irregular vascularity, irregular hyperplasia & irregular fibrosis leading to formation
of one or multiple nodules (multi-nodular goitre)
II. Gross:
• Asymmetrically enlarged thyroid lobes with nodular surface & cut section
• Nodules are variable in size & shape and separated by fibrous tissue
• some nodules are firm and others show a gelatinous colloid pattern
• Secondary changes are common as cystic changes, haemorrhage & dystrophic
calcification
III. Microscopy:
• The thyroid follicles are very variable reflecting the abnormal gland rhythm
• some follicles are normal, others are hyperplastic or colloid distended, separated by
fibrous tissue infiltrated by lymphocytes
• Cystic follicles may show hyperplastic papillary epithelial projections
• Haemorrhage & calcification are common
IV. Complication:
1-Pressure effect
2-Retrosternal extension
3-Toxic transformation (secondary or toxic nodular goitre)
4-Malignant transformation
3. Grave’s disease (diffuse toxic goitre or exophthalmic goitre)
I. Pathogenesis:
• Autoimmune disease characterized by hyperthyroidism with exophthalmic
• it’s believed to be due to: antibody termed LATS (long acting thyroid stimulator)
• Nowadays it’s believed to be due to complex of autoantibodies:
1-Thyroid stimulating immunoglobulins (TSI):
They act on TSH receptors mimicking the action of TSH
2-Thyroid growth stimulating immunoglobulins (TGI):
- 151 -
They initiate the growth of thyrocytes

• Mechanism of exophthalmos is unclear but it was found that TSI has fibroblast
stimulating action, so may stimulate fibroblastic proliferation of the retro-orbital tissue
leading to exophthalmos
II. Gross:
• Moderate diffuse symmetrical thyroid enlargement
• Cut section is pink due to high vascularity
III. Microscopy:
1-Thyroid follicles:
• Follicles are hyperplastic
• lined by tall columnar cells which may form papillae
• Colloid: pale, scanty, and vacuolated at the periphery (due to rapid absorption of
thyroid hormones)
2-Thyroid stroma:
• Blood vessels: highly vascular stroma
• Stroma: lymphocytic infiltration
IV. Other pathological features:

1-Exophthalmos: protrusion of the eyeballs with risk of infections and blindness
2-Pretibial myxoedema: in 5% of patients due to localized accumulation of
mucopolysaccharides forming circumscribed patches at the pretibial skin
3-Loss of weight
4-Tremors
5-Left ventricular hypertrophy and tachycardia
6-Diffuse lymphoid hyperplasia of lymphoid organs as thyroid and spleen
7-Blood: lymphocytosis and neutropenia
4. The microscopic types of thyroid adenoma
I. Follicular Adenoma:
1- Normo-follicular: normal sized follicles
2- Macro-follicular (colloid adenoma): large sized follicles distended with colloid
3- Micro-follicular (foetal or embryonic adenoma): very small follicles
4- Hurthle cell adenoma: follicles lined by large polyhedral eosinophilic cells having
abundant pink granular cytoplasm (Hurthle cells)
•All follicular adenomas are surrounded by complete intact fibrous capsules of
varying thickness with no vascular invasion
•The normal thyroid parenchyma around the adenoma is compressed
- 152 -
•Absent capsular and vascular invasions differentiate follicular adenoma from well
differentiated follicular carcinoma
II. Hyalinising Trabecular Adenoma:

Trabecular structures lined by follicular epithelium separated by typical hyaline stroma
5. Types of thyroid carcinoma & Discuss their spread
I. Types:
1- Papillary carcinoma 2-Follicular carcinoma
Age: Age:
May arise at any age including Usually arises in elderly.
children and young adults.
Microscopy: Microscopy:
- the malignant cells form cystic -Follicles lined by malignant cells
spaces arranged in papillary form showing dark nuclei.
with central thin vascular core -in less differentiated forms:
covered by multiple layers of mitoses are mainly detected.
malignant columnar epithelial -well differentiated forms:
cells with clear nuclei resemble follicular adenoma
grossly and microscopically
- the tumor is associated with
- Diagnosis of malignancy is made
calcified bodies (psammoma
when there is capsular and/or
bodies)
vascular invasion.
Distant spread: Distant Spread:

Mainly by lymphatic. mainly by blood (common to
Blood spread is very rare & late. lung and bone)
Prognosis: Prognosis:
The tumor has the best Poor
prognosis among all types of
thyroid carcinoma.
3-Hurthle cell carcinoma:

Characterized by malignant eosinophilic cells
- 153 -
4- Anaplastic carcinoma:
Composed of malignant spindle or giant cells
5- Medullary carcinoma:
• Arises from Para-follicular cells (C cells)
• malignant polyhedral cells separated by stroma containing amyloid
• may be associated with Para-neoplastic syndromes (carcinoid or Cushing
syndrome)
• prognosis is better than follicular carcinoma.
II. Spread of thyroid carcinomas:
1-Direct to:
Neck structures: as recurrent laryngeal nerve producing horsiness of voice
• Larynx & Trachea: leading to stridor or asphyxia
• Oesophagus: producing dysphagia
2-Lymphatic to:
Cervical lymph nodes
3-Blood to:
(BLB) bone, lung & brain
Early→ in follicular carcinoma
Rare or very late → in papillary carcinoma
6. Papillary carcinoma
See above
7. Pituitary hypo-function (2008)
I. Causes:
1-Idiopathic
2-Primary tumors compressing or destroying the pituitary as craniopharyngioma or
chromophobe adenoma
3-Secondary Tumors (metastases) destroy the pituitary
4-Tuberculoma or Sarcoidosis destroying the pituitary
5-Pituitary necrosis which maybe:
a) Ischemic necrosis (following post-partum hemorrhage)
b) Toxic necrosis (in case of diphtheria)
- 154 -
II. Effects:
One of the following syndromes:
1) In infants (pituitary infantilism):
↓GH → dwarfism & hypo-gonadism
2) At puberty (Frolich’s syndrome):
Obesity & hypo-gonadism
3) In adults (Simmonds’s disease):
Loss of weight, amenorrhea and infertility
E N U M E R AT E
1. Vascular lesions of diabetes mellitus
I. Micro-angiopathy:
Thickening of capillary basement membrane →
Serious effects:
• Lowered immunity: due to defective exudation in response to infection
• nephropathy: affected glomerular capillaries leak plasma protein → Nephrotic
syndrome
• neuropathy
II. Hyaline atherosclerosis:

Hyalinosis of walls of arterioles
III. Atherosclerosis & Super-imposed thrombotic lesions:
Manifested by:
• Angina pectoris
• Myocardial infarction
• Diabetic gangrene
• Cerebral ischemia
• Renal ischemia
- 155 -
2. Renal lesions of diabetes mellitus
The lesions cause ((diabetic nephropathy))

1- Hyaline atherosclerosis of afferent & efferent arterioles
2- Diffuse or Nodular glomerulo-sclerosis:
Thickening of glomerular capillaries basement membrane due to micro-angiopathy
→ Nephrotic syndrome
The nodular type is known as Kimmelsteil-Wilson disease
3- Atherosclerosis of renal artery
4- Interstitial nephritis or pyelonephritis due to infection
5- Vacuolization of tubules due to glycogen accumulation
6- Renal failure.
- 156 -
Chapter Sixteen |
Diseases of the nervous system
GIVE AN ACCOUNT ON
1. Pathological features & complications of Meningococcal meningitis:
The disease is caused by meningiococci, which are transmitted by droplets, mainly in

children.
The organism causes naso-pharyngitis, followed by septicemia & affection of meninges
by blood spread.
I. Pathology:
1- Grossly:
• The pia and arachnoid membranes are thick, congested & covered with purulent
exudate.
• The ventricles are dilated and together with the subarachnoid space contain
turbid CSF.
• The choroid plexus is congested.
2- Microscopically:
The affected meninges show dilated capillaries, several polymorphs, pus cells,
macrophages as well as excess fibrin.
3- CSF:
If withdrawn for analysis:
• It comes out with increased tension.
•Contains many neutrophils & pus cells.
• High protein content.
• Low sugar.
•Culture will show the causative organism.
- 157 -
II. Complications: (‫)ﻣﻤﻜﻦ ﺳﺆال ﻟﻮﺣﺪه‬

• Arterial thrombosis leading to cerebral infarction.
• Thrombophlebitis producing pyemia.
• Adrenal hemorrhage and acute adrenal insufficiency due to septicemia.
• Fibrosis if the patient survives, resulting in:
a) Hydrocephalus.
b) Cranial nerve paralysis.
2. The causes of Cerebral hemorrhage:
Two types of cerebral hemorrhage:

I. Massive cerebral hemorrhage (stroke) and the causes are:
1- Hypertension (80% of cases).
2- Traumatic.
3- Hemorrhage inside tumors.
4- Ruptured cerebral aneurysm.
5- Blood diseases as purpura, leukaemia. . Etc.
II. Punctate or petechial hemorrhage and the causes are:
1- Infections as encephalitis.
2- Trauma.
3- Severe anoxia.
4- Blood diseases.
3. The microscopic picture of Meningioma:
The microscopic picture of WHO GRADE I Meningioma:

There are several types of Meningioma:
I. Meningothelial meningioma:
The tumor consists of concentric whorls of proliferated meningothelial cells which are
Oval cells with indistinct cell borders, pale cytoplasm & regular round nuclei. . The cells
are separated by fibro-vascular stroma.
II. Psammomatous meningioma:

It is meningothelial type in which some of the cell whorls show central hyalinosis &
calcification. . These calcific spherules are called Psammoma bodies.
III. Fibroblastic meningioma:

It resembles fibroma.
IV. Transitional meningioma:
- 158 -
Mixture of meningothelial (or psammomatous) and fibroblastic types
V. Other types:
Microcytic, secretory, angiomatous, metaplastic inflammatory meningioma
4. Astrocytoma (Astrocytic tumors) & what are the effects of intracranial tumors:
Astrocytoma is the most common primary tumor of CNS, and there are several types:
I. Pilocytic astrocytoma WHO Grade I:

This is the only astrocytic tumor with good news, considered benign, it usually affect
children and occurs mainly in cerebellum.
1- Grossly:
It appears as circumscribed cystic mass with a solid mural nodule.
2- Microscopically:
It consists of bipolar astrocyte.
II. Low grade astrocytoma WHO Grade II (Diffuse astrocytoma):

The tumor is more common in adults and usually affects the cerebral hemispheres.
1- Grossly:
It appears as an ill-defined infiltrative whitish growth.
2- Microscopically:
It shows moderate cellularity with moderate cellular atypia. The cells are either
fibrillary astrocytes (more common) or protoplasmic astrocytes.
III. Anaplastic Astrocytoma WHO Grade III:

It usually affects the cerebral hemispheres of adults.
1- Grossly:
Appears as an infiltrative growth
2- Microscopically:
A highly cellular growth composed of pleomorphic astrocytes with mitotic activity,
but no necrosis.
IV. Glioblastoma multiform WHO Grade IV:

A highly malignant tumor, more common of adults, cerebral hemispheres is the most
frequent site.
- 159 -
1- Grossly:
Infiltrative growth, usually large-sized, showing hemorrhage necrosis & cysts.
2- Microscopically:
High cellularity with marked cell anaplasia, cell necrosis and vascular endothelial
proliferation it is the most malignant primary brain tumor.
N.B: Gemistiocytic astrocytoma:

It is a variant of high grade astrocytoma (grade III, rarely II)
Microscopically:
Consist of large astrocytes with abundant pink cytoplasm (gemistiocytes) &
atypical nuclei showing Mitosis.
• Effects of intracranial tumors:

1- Increased intracranial tension leading to headache, vomiting, blurred vision, tremors,
and brain herniation.
2- Local effects depend on tumor location e.g. Paralysis.
5. Intracranial hemorrhage:
Depending on the anatomical site of hemorrhage, it is divided into meningeal &

intracerebral hemorrhage:
I. Meningeal hemorrhage:
1- Extradural hemorrhage (Epidural hematoma):

Due to traumatic injury of the middle meningeal artery, the blood clotted rapidly
leading to compression of the brain, increased intracranial pressure & herniation.
2- Subdural hemorrhage:
Due to traumatic injury of veins crossing the subdural space, the venous blood
accumulates slowly with organization later on.
3- Subarachnoid hemorrhage:
Due to:
a) rupture of aneurysm of cerebral artery.
b) Extension from underlying cerebral hemorrhage.
c) Hemorrhagic blood diseases as leukaemia, purpura, Etc.
- 160 -
II. Cerebral hemorrhage:
II.I Massive cerebral hemorrhage (stroke):

Rapidly fatal: due to:
1- hypertension (80% of cases).
2- Traumatic.
3- Hemorrhage inside tumors.
4- Ruptured cerebral aneurysm. e) Blood diseases as purpura, leukaemia, Etc.
Pathology:
Massive extravasation of the blood usually within cerebral hemispheres may
extend to ventricles or subarachnoid space, associated with compression on the
adjacent parenchyma.
II.II Punctate or Petechial hemorrhage:

Small hemorrhagic spots due to:
1- Infections as encephalitis.
2- Trauma.
3- Severe anoxia.
4- Blood diseases.
6. Peripheral neuritis:
I. Definition:
This is inflammation and degeneration of peripheral nerves.
II. Causes:
1- Diabetes mellitus: one of the most common causes.
2- Chronic alcoholism.
3- Chronic lead poisoning.
4- Beriberi.
5- Leprosy.
6- Toxemia as diphtheria.
7- Acute post-infective polyneuritis: follows some infective diseases as measles
&influenza or after vaccination and is thought to be of allergic nature.
8- Ischemia as in cases of poly-arteritis nodosa.
9- Infections as measles.
10- Traumatic as in case of disc prolapsed.
7. Etiology & gross of brain abscess:
I. Aetiology:
- 161 -
• Bacteria:
Large variety of pyogenic bacteria as staphylococci, pneumococci, E-coli,
streptococci, mixed infection with more than one organism may occur.
• Routes of infection:
Cerebral abscess occur as a complication of other diseases:
1- Direct spread:
a) Chronic suppurative infection of middle ear, mastoid ear abscess & Para-nasal
abscess may be associated with erosion of the thin bony plates producing
temporal lobe, cerebellar and frontal lobe abscesses respectively.
b) Infection following a skull fractures.
2- Blood spread:
a) From suppurative lung diseases as lung abscess, bronchiectasis & empyema.
b) Pyemic abscesses may develop due to septic emboli e.g. derived from acute
infective endocarditis. These abscesses are multiple & small.
II. Gross picture:

• The abscess appears as a swelling having liquefied centre filled with pus.
•The surrounding brain shows oedema.
• If the abscess is not treated it becomes surrounded by a fibrogliotic wall (chronic
abscess).
8. Meningioma:
Dif.:
It is a relatively common tumor arising from dura or leptomeninges, most examples
occur in adults, females are more commonly affected, most cases are benign (WHO
Grade I) but some are WHO Grade II or WHO Grade III.
I. WHO Grade I. Meningioma:

This is the benign tumor:
• Grossly:
A globular capsulated firm greyish mass, the cut surface may show whorly
appearance & calcific foci. The tumor may compress the brain or spinal cord.
• Microscopically:
There are several types of Meningioma:
- 162 -
1- Meningothelial meningioma: the tumor consists of concentric whorls of

proliferated meningothelial cells which are Oval cells with indistinct cell
borders, pale cytoplasm & regular round nuclei. The cells are separated by
fibro-vascular stroma.
2- Psammomatous meningioma: its meningothelial type in which some of the
cell whorls show central hyalinosis & calcification. These calcific spherules are
called Psammoma bodies.
3- Fibroblastic meningioma: it resembles fibroma.
4- Transitional meningioma: A mixture of meningothelial (or psammomatous)
and fibroblastic types.
5- Other types:
Microcytic, secretory, angiomatous, metaplastic inflammatory meningioma
II. WHO Grade II Meningioma:

This is an aggressive tumor with high incidence of recurrence after surgical excision.
It includes:
1- Atypical meningioma.
2- Clear cell meningioma.
3- Rhabdoid meningioma.
III. WHO Grade III Meningioma:

This is an aggressive malignant tumor with high incidence of recurrence after surgical
excision.
It includes:
1- Anaplastic.
2- Papillary meningioma.
3- Chordoid meningioma.
- 163 -

Complete Final Pathology

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Complete Final Pathology

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Lymph Notes in Pathology |

Diseases of lower respiratory system 9

Diseases of the liver 75

Diseases of gall bladder, pancreas & peritonium 80

Disease of the urinary system 86

Male genital system 101

Diseases of the female genital system 107

Diseases of the breast 122

Diseases of bones and Joints 128

Diseases of lymphoid tissue 141

Haemopoeitic disorders 147

Diseases of the endocrine glands 150

Diseases of the nervous system 157

GIVE AN ACCOUNT ON EACH OF THE FOLLOWING:

II. Chronic rhinitis:

1. Swollen epithelial cells.

An atopic disease caused by inhalation of certain antigens as pollens → allergic

II. Microscopically (The polyp consists of):

Definition and etiology:

Pathological features of rhinoscleroma:

Definition and etiology:

II. Severe toxaemia that may lead to:

II. General causes:

II. Follicular “Suppurative”:

II. Lymphatic spread:

III. Blood spread:

IV. Hypersensitivity reactions:

As rheumatic fever and glomerulonephritis.

V. Chronic non-specific tonsillitis.

II. Aural polyp:

III. Chronic suppurative otitis media, this may lead to:

I. Squamous cell papilloma of larynx:

I.I. Papilloma of adults:

I.II. Papilloma of children:

II. Squamous cell carcinoma of larynx: (category A)

2. Supraglottic (35%) and infraglottic (<5%):

Direct and by lymphatics to cervical lymph nodes. Blood spread is late.

1. Four types of lung abscess.

1. Aspiration lung abscess.

1. Chest wall deformity (Barrel-shaped chest).

1. Lung Abscess may complicated by lung gangrene.

- Direct spread → empyema, pericarditis, and mediastinitis.

1. Pathological features of lobar pneumonia-gray hepatization.

- Alveolar inflammation (congested capillaries, neutrophils, pus cells & fibrin).

I. Excessive elastase (protease) activity.

I. Excessive elastase (protease) activity:

III. Chronic bronchitis, helping factor due to:

II. The pulmonary capillaries are compressed.

III. Elastic tissue stains show reduced elastic tissue.

II. The chest wall:

II. Bronchial obstruction:

Long standing obstruction by foreign body, tumor,... etc, leads to:

III. Congenital lesions:

I. Rupture: leads to:

II. Lung gangrene.

1. Direct → empyema, pericarditis & mediastinitis.

IV. Chronic abscess:

II. Stage of red hepatization:

III. Stage of gray hepatization:

IV. Stage of resolution:

Gross: both lungs particularly lower lobes show:

11. Bronchiectasis (definition, pathogenesis, microscopic picture, and

Aetiology and pathogenesis: