Pathology Flashcards

1
Q

Give an account on the types of intracranial hemorrhage

A

Extradural: Rapid accumulation of blood between skull & dura due to acute severe trauma severing MMA

Subdural: Mild traumatic injury to veins crossing subdural space produces chronic venous blood accumulation

Intracerebral: may disrupt or compress adjacent brain tissue, leading to neurological dysfunction. Can increase ICP and cause cerebral herniation

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2
Q

Enumerate the causes of Hydrocephalus and discuss its types

A

a) Obstruction in the normal flow of CSF
b) Problems with resorption of CSF into the venous system
c) Excessive production of CSF.

Communicating: The whole ventricular system is dilated caused by impaired absorption of CSF. The most common causes are post hemorrhagic or post-inflammatory changes

Non communicating: hydrocephalus develops from a block in CSF pathways.

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3
Q

Increased intracranial tension (3, last one has 5 subgroup)

A

An increase in the amount of CSF.

Cerebral edema.

Space occupying lesions:
* Tumors
* Hemorrhage
* Hematoma
* Infarction (with Hemorrhage &edema)
* Infections (localized abscess).

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4
Q

Causes of cerebral infarction

A

Cerebral artery occlusion due to thrombus or embolus

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5
Q

Complications of acute meningitis (4)

A

1- Spread of infection to the brain: brain abscess.

2- Phlebitis may cause venous occlusion and hemorrhagic infarction of the brain.

3- Septicemia resulting in DIC and suprarenal hemorrhage leading to acute adrenal insufficiency

4- Fibrosis in the subarachnoid space leads to:
- Obstructive hydrocephalus.
- Cranial nerve palsies (paralysis).
- Epilepsy

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6
Q

Route of spread of Brain abscess

A

o Septic emboli: from acute bacterial endocarditis produce multiple pyaemic abscesses

o Hematogenous spread: from chronic pulmonary infections.

o Direct spread: from otitis media which produces mastoiditis and infection is transmitted to the temporal lobe. In paranasal sinusitis a frontal lobe abscess occurs.

o Trauma: producing an abscess at site of injury.

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7
Q

Complications of brain tumors (5)

A

1- Increased intracranial pressure:
* Pressure on vital centers due to medullary herniation.
* Brain atrophy which is responsible for paralysis or dementia.

2- Invasion and brain tissue destruction.
3- Cerebral edema.
4- Irritation effects in the form of seizures or epileptic fits.
5- Obstructive hydrocephalus.

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8
Q

Etiology & pathogenesis of Hashimoto’s thyroiditis

A

Ø It is an autoimmune disease directed against thyroid antigens.

Ø Autoimmune injury is mediated by circulating Abs to thyroglobulin & thyroid peroxidase.

Ø Thyroid autoimmunity is accompanied by:-
1-progressive follicular cell loss.
2-fibrosis.

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9
Q

Etiology & pathogenesis of Subacute thyroiditis

A

a) It is attributed to a viral infection or post viral inflammatory process, resulting in cytotoxic T-cell-mediated follicular epithelial damage.

b) Because the immune response is virus initiated, it is self-limited.

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10
Q

Grave’s disease (definition and pathogenesis)

A

Definition: It is an autoimmune disorder characterized by thyrotoxicosis. (thyroid storm)

A) Production of autoantibodies to TSH receptor :

1- Thyroid stimulating immunoglobulin (TSI) à binds to the (TSH ) receptor and mimics the action of TSH, leading to T3 and T4 release.

2- Thyroid Growth Stimulating I.G (TGI) is directed against (TSH ) receptor but these autoantibodies induce thyroid follicular epithelium proliferation.

B) T-cell mediated autoimmunity: Ophthalmopathy.

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11
Q

Definition and complications of goiter

A

is a non-inflammatory, non-neoplastic enlargement of the thyroid gland.

  1. Cosmetic effects of a large neck mass.
  2. Airway obstruction .
  3. Dysphagia .
  4. A hyper functioning nodule may develop within a long-standing goiter resulting in hyperthyroidism.
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12
Q

Follicular adenoma (Gross and microscopic)

A

Gross: Solitary, spherical,& average about 3 cm in diameter, encapsulated, gray-white to red-brown

well demarcated from the surrounding parenchyma. with fibrosis, hemorrhage, or calcification

Microscopic : Follicles: Compact, small lined by cubical calls, surrounded by a fibrous capsule .

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13
Q

Complications of diabetes

A

Microangiopathy: Retinopathy, nephropathy, neuropathy

Hyaline atherosclerosis

Accelerated atherosclerosis—>angina pectoris, myocardial infarction, diabetic gangrene

Increase susceptibility to infections due to lowering of immunity

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14
Q

Enumerate the thyroid tumors

A

Follicular adenoma
Follicular carcinoma
Papillary carcinoma
Anaplastic carcinoma
Medullary carcinoma

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15
Q

Define lymphadenopathy

A

Enlargement of lymph nodes secondary to disease. It may be localized in one group or generalized

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16
Q

Causes of lymphadenopathy (7)

A
  1. Reactive lymphoid hyperplasia.
  2. Lymphadenitis: Acute /chronic inflammatory inflammation.
  3. Sarcoidosis.
  4. Lymphoma: Primary neoplasm of lymphoid tissue.
  5. Metastasis: Metastatic carcinoma in lymph nodes (more common than lymphoma)
  6. Blood diseases; mainly leukemia.
  7. Some metabolic storage disease.
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17
Q

Enumerate Types of lymphoid Hyperplasia

A

Reactive lymphoid hyperplasia:
follicular hyperplasia
paracortical hyperplasia
reticular hyperplasia

Lymphadenitis: acute and chronic lymphadenitis

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18
Q

Enumerate Types of RS cells

A

Classic RS
Mononuclear variant
Lacunar variant
Lymphohistiocytic variant

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19
Q

Enumerate subtypes of Hodgkin’s Lymphoma

A

1- Classical Hodgkin lymphoma:
Nodular sclerosis type
Mixed cellularity type
Lymphocyte-rich type
Lymphocyte-depletion type

2-Nodular lymphocyte predominant type

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20
Q

comparison between low and high grade non Hodgkin’s lymphoma

A
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21
Q

Complications of Plasma cell tumors 7

A
  1. Pathological fracture.
  2. Replacement of the marrow by tumor cells, resulting in pancytopenia
  3. Hypercalcemia, and metastatic calcification
  4. Increased levels of Immunoglobulins (secreted by plasma cells) in the blood and/or in the urine causing renal failure
  5. Amyloidosis: Deposition of secreted abnormal protein in the tissues
  6. Renal changes : secondary to blockage of tubules and pyelonephritis
  7. Spread: direct & early blood producing plasma cell leukemia.
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22
Q

Causes of splenomegaly (5)

A
  1. Inflammations & Infections:
    * Bacterial: TB
    * Parasitic: Malaria -Bilharziasis.
    * Viral: Infectious mononucleosis.
  2. Circulatory disturbances:
    * Rt. Sided Heart failure & systemic venous congestion (CVC).
    * Portal hypertension.
    * Recent infarction.
  3. Blood disorders:
    * Leukemia-polycythemia.
    * Hemolytic anemia-thrombocytopenia.
  4. Tumors: Lymphoma & Leukemia.
  5. Metabolic disorders:
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23
Q

causes of bone fracture (2, last one has 4)

A

A. Traumatic.

B. Pathological:
1. Osteomyelitis.
2. Osteoporosis.
3. Tumors: primary and secondary tumors.
4. Bone cyst.

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24
Q

Factors delaying healing of fractures

A
  1. Inadequate immobilization: slows tissue union. If this continues, movement will prevent bone formation and collagen will be laid down instead giving rise to fibrous union and false joint at fracture site.
  2. Soft tissue interposition: will prevent healing and if not removed will lead to non-union.
  3. Infection: will delay healing.
  4. Pre-existing bone disease: If the bone is broken due to a disease in the bone, it is called pathological fracture. Example of pathological fracture is fracture due to metastatic carcinoma.
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25
Q

Complications of osteomyelitis

A
  1. Spread of infection: Direct spread causing arthritis, myositis and neuritis; or blood spread as toxemia, septicemia, and pyemia.
  2. Pathologic fracture.
  3. Amyloidosis.
  4. Malignancy: Squamous cell carcinoma in the sinus tract, bone osteosarcoma.
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26
Q

What is Pott’s disease and enumerate its characteristics

A

It is vertebral tuberculosis

Characterized by:
Kyphosis
Cold abscess
Paraplegia

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27
Q

Compare between Osteoid osteoma and osteoblastoma

A

-Osteoid Osteoma: Benign bone tumor that commonly occurs in the shafts of long bones of adolescents and young adults, who complain of persistent pain, worse at night, often relieved by aspirin.

-Osteoblastoma: is uncommon solitary tumor that involves vertebrae and, to a lesser extent, the long bones of the extremities. It is similar to osteoid osteoma histologically, but is larger and not accompanied by nocturnal pain

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28
Q

Osteochondroma

A

It affects patients under 20 years and both sexes are affected. Osteochondromas commonly develop in the metaphyseal region (near the growth plate) of long bones, especially near the knee.

Gross: Lesions are mushroom-shaped surface protrusions, covered by a cap of hyaline cartilage with surface perichondrium.

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29
Q

Gross and microscopic of Fibrous dysplasia

A

Gross: Lesions are well-circumscribed, intramedullary masses that are tan-white, gritty, and variable in size.

Microscopic: Lesions are composed of curvilinear trabeculae of woven bone with no osteoblastic rim (likened to Chinese letters) separated by richly vascularized fibrous stroma. Mature lamellar bone is not formed and lesions do not enlarge after puberty. This suggests that the lesion represents an arrest of bone maturation at the woven bone stage.

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30
Q

Define Rheumatoid Arthritis and discuss the pathogenesis. Enumerate the extraarticular manifestations

A

Definition: Chronic systemic inflammatory disease of autoimmune origin that principally attacks joints, producing a non-suppurative proliferative synovitis that progresses to joint destruction and ankylosis. Most patients have an increased level of anti Ig antibody (rheumatoid factor)

a. Rheumatoid skin nodules over bony prominences.

b. Heart: Rheumatoid nodule in valves & pericardium with a lympho-plasmacytic & histiocytic infiltrate.

c. Lung rheumatoid nodules.

d. Arteritis but may also cause phlebitis.

e. Lymphadenopathy & splenomegaly

f. Amyloidosis.

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31
Q

Define Tenosynovial giant cell tumor and discuss its types

A

group of closely related benign neoplasms involving synovial membranes, tendon sheaths, and bursae.

1- Diffuse type: typically presenting in the knee (80%) with pain, “locking”, and swelling; range of motion is decreased and aggressive lesions erode into the bone and adjacent soft tissue.

2- Localized type (giant cell tumor of the tendon sheath):, commonly manifesting as a solitary painless mass involving the tendon sheaths of the wrist and fingers.

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32
Q
  • Gross picture of melanocytic Nevus and melanoma
A

-Most nevi arise in childhood and adolescence. Common melanocytic nevi are tan to brown, uniformly pigmented small papules. After many years, nevi gradually lose their pigmentation, decrease in size and disappear.

-Melanomas have an irregular border and marked variation in pigmentation including shades of black, brown, red and dark blue. They are usually larger than nevi. Tumor development shows two phases: radial (in situ not metastatic yet) and vertical growth phase (metastatic)

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33
Q

Define fibromatosis and discuss its two types of

A

A group of fibroblastic proliferation which are cytologically benign but grow in an infiltrative fashion , and can recur after surgical excision but do not metastasize.

a. Superficial fibromatoses: Palmar fibromatosis, in the palmar fascia, Plantar fibromatoses, Penile fibromatosis (Peyronie disease).

b. Deep fibromatoses: Abdominal desmoid tumor, arises from the rectus abdominis muscle in post- partum women or in scars of abdominal surgery.
*Extra-abdominal desmoid arises from the shoulder or pelvic girdle muscles.
*Retroperitoneal fibromatosis.

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34
Q

Enumerate vascular tumors and tumor like conditions. 7

A

VASCULAR ECTASIA
HEMANGIOMAS
LYMPHANGIOMAS
GLOMUS TUMOR
HEMANGIOENDOTHELIOMA
KAPOSI SARCOMA
ANGIOSARCOMA

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35
Q

Discuss the pathological stages of lobar pneumonia

A

Congestion (24h): The lung is edematous, red and heavy. The capillaries are hyperemic and the alveoli are filled in protein rich exudates

Red hepatization (few days): The lung is red, solid and airless, and consistency resembles fresh liver. The alveoli shows fibrin and massive accumulation of polymorphs and macrophages.

Grey hepatization (few days): The lung is gray show more accumulation of fibrin § Lysis of red blood cells.

Resolution (8-10 days):The lung returns to normal. Liquefaction and absorption of the exudate, and enzymatic digestion of inflammatory debris

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36
Q

Mention 4 complications of lobar pneumonia

A

1 - failure of resolution—–> Carnification

2- Toxemia: on 9th day acute heart failure due to toxic myocarditis

3- Spread: Direct or by blood

4- Post pneumatic lung abscess

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37
Q

Discuss the morphology of bronchopneumonia (septic bronchopneumonia)

A

Gross: Usually bilateral lower lobe affection
* Patchy areas of yellow consolidation.
* Pleurisy.
* Enlarged hilar lymph nodes (lymphadenitis).

Microscopic:
§ Suppurative exudation filling bronchi, bronchioles, and alveoli.
§ Alveoli: The alveoli are full of pus

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38
Q

Predisposing factors of bronchopneumonia

A
  • It occurs most commonly in extreme of age: infants and old age.
  • Commonly in patients with debilitating diseases such as : diabetes, cancer and cardiac failure.
  • It may complicate viral infections as viral bronchitis.
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39
Q

Complications of bronchopneumonia 7

A

1) Death, especially in debilitated patients.

2) Post pneumonic lung abscess & gangrene.

3) Spread: to the pleura causing pericarditis, mediastinitis.

4) Toxemia causing toxic myocarditis.

5) Septicemia causing meningitis, arthritis, osteomyelitis and infective endocarditis.

6) Fibrosis is common, due to tissue destruction by suppuration.

7) Bronchiectasis: healing of bronchial walls by fibrosis, results in weakened walls and permanent dilatation of the lumen

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40
Q

Discuss the types of abscesses (5)

A

Aspiration lung abscess: due to blood or vomitous or foreign body. These locations represent the more direct course for the aspirated material from the trachea. The abscess wall is irregular and congested. The lining is shreddy yellow and the contents of cavity is yellow pus.

Post pneumonic abscess: in lobar or bronchopneumonia

Bronchial obstruction with bronchogenic carcinoma: aspiration of blood and tumor fragments contribute to the development of lung abscess.

Pyemic abscess: Septic emboli from septic thrombophlebitis of systemic veins.

Direct traumatic punctures or spread of infection from adjacent Organs.

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41
Q

Fate and complications of acute lung abscess (6)

A

1) Small size: Resolve with proper treatment

2) Rupture into a bronchus: results in hemoptysis & cough of purulent sputum

3) Rupture into a pleural cavity: results in empyema and pyopneumothorax.

4) Lung gangrene: ( the cavity is irregular with a necrotic lining but black in color & has a foul odor).

5) Embolization of septic material to the brain results in meningitis and brain abscess.

6) Chronic lung abscess: Well-defined cavity with a thick fibrous wall. The lining is smooth & the contents are inspissiated (thick pus).

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42
Q

Enumerate obstructive lung diseases and restrictive lung diseases.

A

1) Emphysema.
2) Chronic bronchitis.
3) Bronchiectasis.
4) Bronchial asthma.

1) Chest wall disorders in the presence of normal lungs.
Eg. : severe obesity, diseases of the pleura,

2) Chronic interstitial lung diseases:
Eg . pneumoconiosis and interstitial fibrosis.

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43
Q

Define emphysema and give an account on their types

A

Permanent over distention of air spaces distal to the terminal bronchioles, with destruction of their walls

Centriacinar: The lesions are more common and severe in the upper lobes. This type is common in cigarette smokers & coal workers

Panacinar: Occurs more commonly in the lower lung zones. It is the type of emphysema that occurs with alpha 1 antitrypsin deficiency.

Distal acinar: It occurs adjacent to areas of pulmonary scarring. It is usually in the upper half of the lung, and forms multiple adjacent dilated air spaces, some forming bullae.

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44
Q

Enumerate the complications of emphysema (3)

A

1) Pulmonary hypertension and right sided heart failure

2) Respiratory failure from defective ventilation, perfusion & diffusion of gases

3) Rupture bullae containing air into pleura producing pneumothorax

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45
Q

Define chronic bronchitis

A

Chronic bronchitis is defined clinically as persistent productive cough for at least 3 consecutive months, for 2 consecutive years.

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46
Q

Define bronchial asthma and enumerate its types

A

It is a chronic inflammatory disorder of the airways, characterized by paroxysmal reversible bronchospasm due to smooth muscle hyper-reactivity and increased mucus production

Atopic (allergic) asthma: it is caused by a type I hypersensitivity reaction (Ig E- mediated) triggered by environmental antigens

Non-atopic asthma: Hyper-reactivity of airways can be triggered by respiratory tract infections, chemical irritants

Aspirin induced asthma: exact mechanism unknown

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47
Q

Discuss the gross picture of bronchial asthma

A

Lungs are overinflated

Bronchial wall is thick, swollen & red.

Bronchial lumen contains large amounts of thick mucus plugs

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48
Q

Discuss the microscopic picture of bronchial asthma

A

Bronchial lumen: Occlusion of bronchi and bronchioles by mucus plugs which contain whorls of shed epithelium known as Curschmann spirals.
Numerous eosinophils are also present.

Bronchial wall
§ mucous gland hypertrophy.
§ smooth muscle hypertrophy,
§ thickening of basement membrane

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49
Q

Discuss the etiology of Bronchiectasis

A

1) Congenital:
-Kartagener’s syndrome: Structural abnormalities of the cilia impair mucus clearance in the airways resulting in persistent infections

-cystic fibrosis: A hereditary disease associated with thick mucus in exocrine glands, respiratory, gastrointestinal and reproductive tracts.

2- Septic bronchopneumonia particularly in children.

3- Bronchial obstruction (e.g., by tumor or foreign body).

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50
Q

Discuss the pathogenesis (mechanism) of Bronchiectasis

A

Two processes are involved: obstruction and chronic persistent infection.

In septic bronchopneumonia: Severe persistent suppurative inflammation in bronchi or bronchioles
causes:
- loss of cough reflex and accumulation of secretions,
- inflammation of the wall and weakening of the wall by fibrosis

In case of obstruction: caused by foreign body or lung cancer:
- There is accumulation of secretions which favor infection,
- Infection damages the bronchial walls leading to their weakening
- The obstruction causes collapse of lung parenchyma , and the week bronchial wall are exposed to the negative intrathoracic pressure with each inspiration leading to its dilatation.

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51
Q

Discuss the gross picture of Bronchiectasis

A

Medium sized bronchi & bronchioles: Airways can be dilated up to four times the normal size.

The bronchi appear thickened, with suppuration of their lining.

The pleura is thickened , fibrotic with adhesions

-There ;are 3 types of dilatation

Saccular dilatation: involves a part of the circumference of a segment sac like dilatation
Fusiform dilatation involves the whole circumference of a segment of the bronchus
Cylindrical :dilatation involves the whole circumference of the whole length of the bronchus.

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52
Q

Give an account on the microscopic picture of bronchiectasis

A

Bronchi
§ Lumen: filled with pus & blood.
§ Lining respiratory epithelium shows areas of ulceration.
§ Wall shows intense acute and chronic inflammatory cells and fibrosis.

Alveoli
§ Adjacent alveoli undergo fibrosis.
§ Patches of compensatory emphysema

Pleura
§ Fibrosis and adhesions.

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53
Q

Enumerate the complications of bronchiectasis 6

A

a. Hemoptysis with,yellowish red sputum (pus + blood).

b. Lung abscess- gangrene.

c. Spread of infection (see septic bronchopneumonia).

d. Bilateral lung fibrosis , pulmonary hypertension & right sided heart failure (cor pulmonale).

e. Secondary amyloidosis (chronic destructive condition).

f. Squamous metaplasia (due to chronic irritation) which may lead to squamous cell carcinoma.

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54
Q

Define atelectasis and give its types

A

Atelectasis is failure of expansion of the lung or collapse of previously inflated lung, affecting part or all of one lung,

Resorption atelectasis :Occurs with complete airway obstruction e.g. mucus plugs postoperatively or with bronchial ashma, and foreign bodies in children causing collapse of alveolia.

Compression atelectasis :Is associated with accumulation of fluid, blood or air in the pleural cavity, which compress and collapse the lung.

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55
Q

Enumerate microscopic types of lung carcinoma

A
  1. Squamous cell carcinoma.
  2. Adenocarcinoma.
  3. Large cell carcinoma.
  4. Small cell carcinoma.
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56
Q

complications of lung cancer

A

A) Spread:
Direct:
-to the pericardium, mediastinum and esophagus.
- Pleural seeding especially in adenocarcinoma.

Lymphatic: To the hilar and mediastinal lymph node.
.
Blood spread: To the brain, bones, liver, adrenals or other lung.

B) Hemoptysis.

C) Obstruction leading to collapse, secondary infection, bronchiectasis or lung abscess.

D) Paraneoplastic syndrome: 3-10% of patients with lung cancer develop clinical paraneoplastic syndrome due to secretion of polypeptide hormones.
-It presents in one or more of the following forms:
Hypercalcemia.
Cushing syndrome.
Myasthenia gravis.
Excess ADH.

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57
Q

Gross and microscopic picture of mesothelioma

A

Mesothelioma is usually unilateral, starting as small nodules on the visceral pleura and extends to cover the whole lung and obliterate the pleural cavity. The tumor is yellowish white.

Microscopic:

Epithelioid type: Cuboidal cells forming papillae and acini (looks like adenocarcinoma)

Sarcomatoid type” sheets of spindle malignant cells (looks like sarcoma)

Mixed type (biphasic): Epithelial + sarcomatous

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58
Q

Enumerate: Four causes of endometrial hyperplasia.

A

Prolonged estrogen stimulation
Estrogen secreting tumors
Prolonged estrogen therapy
Obesity

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59
Q

Four causes of uterine bleeding caused by local organic lesion

A

Pregnancy disorders: abortion

Benign tumors: endometrial polyp

Malignant tumors: carcinoma of endometrium

Inflammations: endometritis

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60
Q

Causes of dysfunctional uterine bleeding 4

A

Anovulatory cycle
Endocrine disorders
Estrogen producing ovarian tumors
Inadequate Luteal phase

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61
Q

Predisposing factors of uterine cervical carcinoma.4

A
  1. Early age of sexual activity
  2. Females with multiple sexual partners
  3. Male partner with multiple previous sexual partners
  4. Chronic cervicitis
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62
Q

Complications of endometriosis 3

A

Dysmenorrhea: Painful menstruation due to intrapelvic bleeding.

Dyspareunia: painful intercourse

Infertility: Adhesions around the tubes

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63
Q

Complications of puerperal sepsis. 4

A

severe toxemia and septicemia

Spread of infection to the tubes -> salpingtis.

spread of infection to peritoneum –> peritonitis

Healing of infected tubes–> fibrosis and infertility

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64
Q

Mention differences between partial and complete hydatiform moles.

A

Complete: diploid, fertilization of empty ovum by two sperm, fetal parts absent and rarely progress to carcinoma

Partial: triploid, fertilization of ovum by two sperms, fetal part present and very rarely progress to carcinoma

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65
Q

Give an account on duct ectasia (periductal mastitis) (definition, etiology, gross and microscopic pictures).

A

marked dilatation of mammary ducts containing inspissated Secretions

unknown etiology

Gross: firm tender greyish white mass with large dilated ducts

Micro: dilated ducts contain foamy macrophages and are surrounded by granulomatous inflammation

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66
Q

Complications of puerperal sepsis. 5

A
  1. Severe toxemia and septicemia.
  2. Septic thrombophelipitis may cause pyemia.
  3. Spread of infection to the parametrium, and tubes causing salpingitis.
  4. Spread of infection to peritoneum may cause localized (in the pelvis) or diffuse peritonitis.
  5. Healing of salpingitis causes fibrosis and infertility.
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67
Q

Complications of uterine leiomyomas. 3

A
  1. Uterine bleeding.
  2. Infertility
  3. Multiple leiomyomas may cause marked uterine enlargement and pressure on nearby organs and pelvic veins.
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68
Q

Complications of pelvic inflammatory disease 4

A
  1. Spread of infection to the peritoneum; peritonitis.
  2. Toxemia.
  3. Chronic PID and chronic tubo-ovarian abscess.
  4. Infertility.
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69
Q

Complications of ovarian mucinous cystadenoma. 3

A
  1. Pressure effects on nearby organs.
  2. Torsion of the pedicle causing, hemorrhage, shock.
  3. Malignant change.
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70
Q

Complications of vesicular (Hydatidiform) mole 3

A
  1. Bleeding
  2. 10% of complete mole are invasive
  3. 2-3% give rise to choriocarcinoma.
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71
Q
  • Three theories explaining endometriosis
    and
    *Four common sites of endometriosis
A
  1. The regurgitation theory: (more accepted).
    Proposes menstrual backflow through the fallopian tubes with subsequent implantation.
  2. The metaplastic theory: Proposes endometrial metaplasia of serosal cells covering ovaries or fallopian tubes.
  3. Lymphatic :Used to explain extra pelvic endometriosis.

Sites: Pelvic structures, ovaries, Peritoneal cavities and fallopian tubes

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72
Q

Cause of acute salpingitis.

A

Inflammation of fallopian tube, most commonly sexually transmitted due to chlamydia and gonorrhea.

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73
Q
  • Types of benign ovarian surface epithelial tumors and describe one of them.
A

serous cystadenoma
mucinous cystadenoma

Serous cystadenoma is often unilocular. The outer surface and the lining are smooth. The inner surface may show papillary projections

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74
Q
  • Types of ovarian teratoma and describe the most common form
A

Benign, Malignant and specialized teratoma.

Benign teratoma shows mature ectodermal, endodermal and mesodermal structures such as teeth and hair.

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75
Q

Define Endometriosis.

A

It is the presence of endometrial glands and stroma in a location outside the inner lining of the uterus.

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76
Q

Define Adenomyosis.

A

It is a down growth of endometrium and its entrapment deep within the myometrium

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77
Q

Define Dysfunctional uterine bleeding

A

It is abnormal uterine bleeding caused by hormonal dysfunction without organic (anatomic) cause

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78
Q

Gross and microscopic picture of chronic non-specific cervicitis.

A

There is eversion of the ectocervix with hyperemia, edema and granular surface. Nabothian cysts may be visible as pearly white vesicles.

Microscopic: The cervix shows inflammatory cellular infiltrate; rich in plasma cells, lymphocytes and histiocytes, with fibrosis.

  • Often some of the mucous glands are obstructed and dilate to form mucus- filled cysts called Nabothian cysts (follicles).
  • The surface epithelium may show squamous metaplasia.
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79
Q

Pathology and complications of Female Gonorrheal infection. 6

A
  1. Urethritis: Hyperemic mucosa covered by purulent exudate.
  2. Paraurethritis: inflammation of paraurethral glands.
  3. Bartholin gland inflammation: This may lead to abscess (Bartholin abscess). Obstruction of the gland duct may lead to cyst formation (Bartholin cyst).
  4. Cervicitis (see before).
  5. Vaginitis and endometritis (rare).
  6. Salpingitis
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80
Q

Microscopic picture and grading of cervical intra-epithelial neoplasia (CIN).

A

It shows proliferated squamous epithelium with cellular atypia and loss of polarity, without basement membrane invasion.

CIN 1 (mild dysplasia): Cellular atyia in lower 1/3 of epithelium

CIN 2 (moderate dysplasia): Cellular atypia in lower 2/3 of epithelium

CIN 3 (severe dysplasia): Cellular atypia involves the full epithelial thickness without surface maturation.

81
Q

Gross picture of endometriosis.

A
  • Endometriosis contains functional endometrium which undergoes cyclic bleeding, so they appear as red brown foci or nodules.
  • In the ovaries blood filled cysts are formed. By time the blood becomes brown in color and are called chocolate cysts.
  • Organization of the blood occurs leading to fibrosis and adhesions around the fallopian tubes, and ovaries.
82
Q

Gross and microscopic picture of adenomyosis.

A

Gross: Enlarged uterus with thick myometrium showing trabeculations and haemorrhagic foci.

Microscopic: The myometrium shows foci of endometrial glands and stroma with hemorrhage

83
Q

Microscopic types of endometrial hyperplasia.

A
  1. Non-atypical hyperplasia:
    * An increase in the gland-to-stroma ratio.
    * The glands show variation in size and shape and may be crowded with back- to- back glands. Cystic change may be present.
    * The glands are lined with tall columnar cells which show stratification.
  2. Atypical hyperplasia:
    * The glands are commonly back-to-back and often have complex outlines due to branching of the glands.
    * Individual cells are rounded and lose the normal perpendicular orientation to the basement membrane. In addition, the nuclei have open chromatin and nuclear atypia.
84
Q

Types of endometrial carcinoma.

A

a. Endometrioid type (80%) which resembles the normal endometrial glands.
■ It is the most common and arises in the setting of endometrial hyperplasia.
■ This type associated with (1) obesity, (2) diabetes (3) hypertension, (4) infertility, and (5) unopposed estrogen stimulation.
■ It occurs around the menopause.

b. Serous type of endometrial carcinoma (20%) arises in the setting of endometrial atrophy in older menopausal women.

85
Q

Enumerate Non-neoplastic ovarian cysts. 5

A
  1. Follicular cysts
  2. Polycystic ovaries
  3. Corpus luteum cyst
  4. Theca-lutein cysts
  5. Chocolate cysts
86
Q

Ectopic pregnancy (Definition, sites, predisposing factors).

A
  • Ectopic pregnancy is fetal implantation at any site other than normal intrauterine cavity.
  • The most common site is within the fallopian tubes (about 90%), other sites include ovary and abdominal cavity.
  • Most important predisposing factor is prior pelvic inflammatory disease resulting in fallopian tube scaring or fibrosis.
87
Q

Give an account on ovarian granulosa cell tumor.

A

Gross: Well defined solid and cystic tumors and may be hemorrhagic.

Microscopic: The tumor is composed of granulosa cells which mostly have grooved nuclei. Cells are arranged in micro follicular pattern

Effects: The tumor may be functional and produce estrogen.

88
Q

Mention causes of liver abscess

A

Solitary abscess: amoebic abscess, infected hydatid cyst, cholecystitis, traumatic injury

Multiple abscesses: Amoebic abscess, pyemic abscess, actinomycosis

89
Q

5 causes of liver cirrhosis

A

Post hepatitis Cirrhosis
Alcohol/Nutritional cirrhosis
Post- Necrotic Cirrhosis
Primary biliary cirrhosis
Cirrhosis related to circulatory disorders

90
Q

5 complications of gall bladder stones

A

Predisposes to cholecystitis
Stones migrate to common bile duct and may cause obstruction
Acute pancreatitis
Distention of gall bladder
Predispose to carcinoma

91
Q

Three predisposing factors for hepatocellular carcinoma

A

Cirrhosis
Chronic viral hepatitis C
Hepatocarcinogen alfatoxins

92
Q

Three types of gall bladder stones

A

Cholesterol stones: yellowish-white; cannot be seen by X-ray

Pigmented stones: very dark and small; opaque on X-ray

Mixed stones: most common, faceted, different colors

93
Q

5 causes of hepatomegaly.

A

Inflammatory diseases
Degenerative diseases
Metabolic disorders as glycogen storage disease
Neoplastic diseases
Some types of Cirrhosis

94
Q

List Clinco-pathological syndromes of viral hepatitis

A

Acute asymptomatic infection with recovery
Acute symptomatic infection with recovery
Fulminant hepatitis
Chronic hepatitis
Carrier state

95
Q

Define acute hemorrhagic pancreatitis

A

a severe and potentially life-threatening inflammation of the pancreas characterized by the presence of hemorrhage, or bleeding, within the pancreatic tissue

96
Q

Acute viral hepatitis microscopic picture.

A
  1. Liver cell injury:
    * ballooning of hepatocytes.
    * Apoptosis of individual cells, resulting in acidophil bodies
    * Focal necrosis , leaving collapsed reticulin network behind.
    * In severe cases, necrosis occurs, commonly centrilobular, or even central-portal bridging necrosis.
  2. Cholestasis: Accumulation of bile in the liver cells and bile canaliculi Kupffer cells engulf bile and undergo hyperplasia.
  3. Portal tract inflammation: In the form of mild mononuclear cell infiltration.
97
Q

Chronic hepatitis (definition and etiology).

A

Chronic hepatitis is defined by the presence of symptomatic, biochemical, or serologic evidence of continuing or relapsing hepatic disease for more than 6 months, with histologically documented inflammation and necrosis.

Etiology:
* Viral etiology (most common): HBV (+HDV) or HCV. Mixed infection may occur.
* Autoimmune: Caused by autoantibodies as antinuclear antibodies & anti­ actin antibodies.
* Drug induced: Isoniazid, methyl dopa
Metabolic diseases as: antitrypsin deficiency.

98
Q

Microscopic picture of Chronic Viral Hepatitis

A

Microscopy:
1) Inflammation :
* Portal inflammation: Expansion of the portal tracts by chronic inflammatory cells, Bile duct walls may be inflamed
* Lobular inflammation

2) Piecemeal necrosis: This is inflammation with destruction of the liver cells at the limiting plates of liver lobules. The liver cells become detached.

3) Fibrosis: Portal fibrosis, bridging fibrosis, accompanied by regeneration nodules (cirrhosis).

4) Other Features: Steatosis of hepatocytes
* Hepatocellular dysplasia (precancerous)

99
Q

Complications of Chronic Viral Hepatitis

A
  1. Post hepatitic cirrhosis.
  2. Liver failure.
  3. Hepatocellular carcinoma.
100
Q

Enumerate Liver abscesses. 3

A

Amoebic liver abscess
Ascending cholangitic abscesses
Pyemic Abscesses

101
Q

Causes of portal hypertension 5

A

Portal vein thrombosis: Tumor and Infection

Portal tract fibrosis: Schistosomiasis, Sarcoidosis, Biliary cirrhosis

Cirrhosis

Veno-occlusive disease

Hepatic vein thrombosis

102
Q

Complications of acute cholecystitis 4

A
  1. Gangrene
  2. Perforation resulting in septic peritonitis
  3. Adhesions and fistulous tract between gall bladder and duodenum leading to passage of gall stone to the intestine. Large stones can lodge in the ileo­ cecal valve and lead to gallstone ileus.
  4. Chronic cholecystitis.
103
Q

Etiology of acute pancreatitis 6

A

Pancreatic necrosis, hemorrhage and inflammation may be due to:

1- Obstruction of ampulla of Vater by gall stone. Thus bile passes into pancreatic duct and activates trypsinogen into trypsin which digests the pancreatic tissue.

2- Excess alcohol abuse may lead to increased secretion of pancreatic juice and contraction of sphincter of oddi leading to rupture of pancreatic duct.

3- Accidental surgical injury of pancreas.

4- Hyperparathyroidism.

5- Polyarteritis nodosa.

6- Viral and bacterial infection.

104
Q

complications of chronic pancreatitis 3

A

1- Malabsorption.
2- Diabetes mellitus.
3- Pseudocysts.

105
Q

Mention the predisposing factors of gastric carcinoma

A

H.pylori gastritis; as there is sequence of events of atrophy, intestinal metaplasia and dysplasia

Smoked food and canned food have carcinogenic substances

Autoimmune gastritis type A through atrophy

Genetic factors

106
Q

Mention the microscopic picture of Crohn’s disease

A

Segmental inflammation and ulceration rich in neutrophils affecting the whole thickness of the wall

Fibrosis

107
Q

Mention the microscopic picture of ulcerative colitis

A

Active phase: Mucosal ulcers, diffuse infiltration by inflammatory cells, crypt abscess formation, degenerative changes in the surface epithelium, severe mucosal edema

Chronic phase: mucosal crypt distortion, mucosal atrophy and submucosal fibrosis, epithelial dysplasia

108
Q

Five Complications of peptic ulcer disease.

A

Bleeding from eroded vessels
Penetration into solid viscera as pancreas
Pyloric obstruction in ulcers
Perforation of peritoneal cavity
Malignant transformation does not occur

109
Q

Six causes of acute pancreatitis.

A

Obstruction of Ampulla of Vater by gall stone
Excess alcohol abuse
Accidental surgical injury
Viral infection
Bacterial infection
Hyperparathyroidism

110
Q

Six causes of acute intestinal obstruction

A

Paralytic ileus
Strangulation hernia
Adhesion of healed peritoneal inflammation following surgery
Lumen obstruction
Volvous: completely twisting of bowel loop
embolism of mesenteric artery

111
Q

Five complications of acute suppurative appendicitis

A

Rupture with septic peritonitis
Gangrene
Chronicity (Chronic appendicitis)
Pus formation
Mucocele of appendix

112
Q

Five of the pathological features gross pictures of ulcerative colitis

A

Rectosigmoid commonly affected by multiple superficial ulcers
Pseudo polyps which are small elevations
Fibrosis in prolonged disease
It involves the rectum and extends proximally retrograde to colon

113
Q

Four non neoplastic colonic polyps

A

Bilharzial polyps
Hyperplastic polyps
Pseudo polyps
Hamartomas polyps

114
Q

List the complications of gastric carcinoma 5

A

Melena
Hematemesis (bloody vomiting)
Pyloric obstruction
Anemia
Spread: direct, lymphatic spread and blood spread

115
Q

Discuss pathogenesis and gross picture of chronic duodenal ulcer (Peptic Ulcer Disease)

A

Pathogenesis: hyperacidity and failure of mucosal defense mechanism

Gross picture: peptic ulcers are four times more common in the duodenum than in the stomach. Are usually solitary, round or oval in shape. The floor is smooth and base is firm

116
Q

Define acute hemorrhagic pancreatitis

A

a severe and potentially life-threatening inflammation of the pancreas characterized by the presence of hemorrhage, or bleeding, within the pancreatic tissue

117
Q

Define ulcerative colitis

A

Ulcerative colitis is a chronic inflammatory bowel disease (IBD) characterized by inflammation and ulcers in the colon and rectum,

118
Q

Define dysentery

A

Dysentery is a term used to describe a group of gastrointestinal disorders characterized by inflammation of the intestines, particularly the colon, and accompanied by symptoms such as severe diarrhea, abdominal pain, and the presence of blood and mucus in the stool

119
Q

Define Liver cirrhosis.

A

Liver cirrhosis is a late stage of scarring (fibrosis) of the liver caused by many forms of liver diseases and conditions

120
Q

Discuss the gross picture of cirrhosis

A
  1. The liver is decreased in size and weight due to loss of liver tissue & fibrous tissue shrinkage.
  2. The surface and cut section are nodular. According to size of regeneration nodules, cirrhosis is classified
  3. The color is :
    - Yellow in cases of nutritional or alcoholic cirrhosis
    - Green in case of biliary cirrhosis.
  4. Consistency is firmer than normal, edges are sharp & retracted cut section (due to fibrosis).
121
Q

Discuss the microscopic picture of cirrhosis

A
  1. Regeneration nodules:
    - Regenerating hepatocytes are arranged in collections trying to simulate a liver lobule but the sinusoids are irregular. These masses of regenerating hepatocytes are totally surrounded by fibrous bands.
  • Liver cells proliferate haphazardly so that the liver cell plates are more than two cell thick
  • Other changes that may be observed according to the cause: necrotic foci, fatty change, hydropic changes,
  1. Fibrosis: in the form of bands of collagen encircling the regenerating nodules involving the portal areas. According to the presence or absence of inflammatory cells within the fibrous septae, cirrhosis is either active or inactive.
  2. The portal tracts are widened by the fibrosis, the inflammatory cells & show proliferating bile ducts
122
Q

Define leukoplakia

A

It is a clinical descriptive term for a white mucosal patch which cannot be attributed to any specific disease . It cannot be removed by rubbing.

Microscopically, It is squamous hyperplasia with hyperkeratosis. It is a precancerous lesion in the oral cavity.

123
Q

Define diverticular disease of colon

A

Diverticulae are acquired herniations of mucosa and submucosa into the wall of the intestine. It is a disease of old age.

124
Q

Gross picture of pleomorphic adenoma

A
  • Benign tumor with an incomplete capsule.
  • Lobulated outer surface.
  • Bluish white in color.
  • Soft, gelatinous consistency.
  • Cut section: Bulging with rounded borders & cystic areas.
125
Q

Microscopic picture of pleomorphic adenoma

A
  • Epithelial glands.
  • Myoepithelial cells in solid groups.
  • Myxoid, hyaline, (pseudocartilage) or osseous stroma.
126
Q

Esophageal varices etiology and complications

A

Etiology:
In case of liver fibrosis or cirrhosis : the blood flow through the liver is impaired leading to portal hypertension & opening of porto-systemic anastomosis.

Complications: Hematemesis- as the varices are easily traumatized by food and it can be fatal.

127
Q

Give an account of Barrett esophagus

A

■ Barrett’s esophagus is a complication of long standing GERD characterized by foci of intestinal metaplasia in the esophageal squamous mucosa.

■ By endoscopy: It appears as salmon-colored tongues replacing the pearly white squamous epithelium of the esophagus.

■ Patients with Barrett’s esophagus have a higher risk of developing esophageal adenocarcinoma than the general population.

128
Q

Complications of reflux esophagitis 5

A

Ulceration
hematemesis
melena
stricture
Barrett esophagus.

129
Q

Complications of Meckel’s diverticulum

A
  1. It may contain heterotropic gastric epithelium, which may secrete acid & pepsin resulting in peptic ulcer.
  2. Acute intestinal obstruction: Meckel’s diverticulum can result in abnormal twisting of a loop of intestine on itself (volvulus) causing acute intestinal obstruction.
  3. May get inflamed and present as acute abdomen mimicking acute appendicitis.
130
Q

Complications of bacillary dysentery and amebic Dysenetry 6

A

■ Local
1- Hemorrhage.
1- Perforation.
2- Rectal prolapse from frequent motions & straining.
3- Intussusception due to frequent motions with abnormal peristalsis.
4- Healing by fibrosis with stricture formation.

■ General toxic manifestation:
Myocarditis, arthritis, peripheral neuritis.

131
Q

Complications of Colonic carcinoma 5

A

1- Intestinal obstruction: Mechanical obstruction of lumen by tumor.

2- Intussusception

3- Hemorrhage from ulceration or tumor necrosis.

4- Perforation leads to septic peritonitis & trans-coelomic spread.

5- Spread: - Direct: Malignant fistula formation.
- Lymphatic spread.
- Blood spread mainly to the liver.

132
Q

Autoimmune gastritis pathogenesis

A
  • Destruction of parietal cells is the major pathogenic mechanism by cell mediated autoimmunity.
  • Autoantibodies to parietal cells & intrinsic factor are also present in the serum.
  • Parietal cell destruction leads to defective gastric acid secretion (achlorhydria).
  • Reduced intrinsic factor production impedes B12 absorption & causes pernicious anemia.
133
Q

Morphology (patterns) of H.Pylori gastritis

A
  1. The gastritis is predominantly antral and is associated with high acid production (which makes the mucosa of gastric body hostile to H pylori). Individuals with this pattern of gastritis are at increased risk of duodenal ulcer.
  2. Another pattern is diffuse involvement of antrum and body (pangastritis) with multifocal glandular atrophy and fibrosis, and decreased acid output. Patients with this pattern are at increased risk of gastric ulcer and carcinoma.
134
Q

complications of H.Pylori gastritis

A
  1. Severe cases usually proceed to atrophy with intestinal metaplasia which is precancerous, and can lead to adenocarcinoma.
  2. H. pylori infection is also a risk factor for peptic ulcer disease, & gastric lymphoma.
135
Q

Hirschsprung’s disease (etiology and gross).

A

Etiology: Congenital absence of the ganglionic cells in the myenteric plexus of the intestine at the recto-sigmoid junction. Peristalsis stops at the affected site resulting in functional obstruction leading to chronic intestinal obstruction.

Gross: The ganglionic segment is narrow markedly dilated colon proximal to it (Megacolon). The intestinal wall is thickened due to hypertrophy of the muscle wall.

136
Q

Gross picture of acute and chronic intestinal obstruction.

A

Acute: The proximal segment is markedly dilated, edematous wall. The mucosa is congested with loss of its folds (stretched), with accumulation of fluid & gas in the lumen . The distal segment is collapsed.

Chronic:
Proximal segment: Above obstruction there is dilatation, hypertrophy of wall. The lumen contains accumulating liguefied food & gases.
* Distal segment: Below obstruction: the segment is collapsed .

137
Q

Complications of ulcerative colitis 5

A

1- Hemorrhage.
2- Perforation & septic peritonitis.
3- Dysplasia & adenocarcinoma.
4- Amyloidosis.
5- Extra-intestinal manifestations as liver and biliary damage.

138
Q

Complications of Crohn’s disease 4

A

1- Hemorrhage.
2- Malabsorption.
3- Fistulae & healing by fibrosis with strictures. 4- 2ry amyloidosis.

139
Q

3 neoplastic colonic polyps

A
  1. adenomatous polyp
  2. papillary adenoma.
  3. Tubulo-villous adenoma.
140
Q

Predisposing factors of colonic adenocarcinoma 5

A

1- Adenomas: All adenomas. Villous adenomas are more likely to show invasion
2- Diet: high fat & low fiber
3- Ulcerative colitis with dysplasia
4- Familial adenomatous polyposis.
5- Hereditary Non-polyposis Colorectal Cancer

141
Q

Discuss the etiology of piles (hemorrhoids) 4

A

1- Portal hypertension.
2- Congenital weakness of vessel walls.
3- Obstruction of lumen by tumor in rectum.
4- Chronic right sided heart failure with systemic venous congestion

142
Q

What is meant by acute pyelonephritis? Enumerate the predisposing factors.

A

common suppurative inflammation affecting kidney and pelvis caused by bacterial infection

> Diabetes (++) susceptibility to infection
Immune suppression and immunedeficiency
short UTI

143
Q

Define Crescentic glomerulonephritis and enumerate the causes

A

> rapid progressive loss of renal function
histological formation of cresents + Severe oliguria

1- Post infectious: after acute diffuse proliferative GN in adults

2- With systemic diseases as PAN, SLE, good pasture syndrome

3- idiopathic

144
Q

Define pyonephrosis?
Mention two causes?

A

Dilatation and distension of renal pelvis and calyces with pus———> progressive atrophy of the kidney due to total complete obstruction of high urinary tract

Hydronephrosis
Chronic pyelonephritis

145
Q

List Prerenal Causes of Hematuria

A
  1. hypertension
  2. Leukemia, purpura
  3. vitK,C deficiency
  4. Anticoagulation drugs
146
Q

Enumerate six 6 post-renal causes for hematuria

A

1- Congenital bladder diverticulum
2- Trauma: catheterization
3- Bilharziasis
4- Cystitis, urethritis
5- kidney stones
6- Urinary bladder tumors

147
Q

Renal causes of hematuria

A

Renal trauma
Glomerular nephritis
Kidney stones
Renal vascular diseases

148
Q

Enumerate types of renal calculi

A
  1. calcium oxalate: > 75%
  2. triple phosphate: 10%
  3. uric acid: 6-9%
  4. cysteine stone (rare)
149
Q

Mention complications of cystitis

A
  • Ascending infection -> pyelonephritis
  • Stones
  • Chronic fibrosed contracted bladder
  • Hematuria
150
Q

Give short account on etiology and pathogenesis of acute diffuse proliferative glomerulonephritis (acute post streptococcal GN)

A

Exogenous: certain strains of B-hemolytic streptococci or Other infections: as mumps, measles, chickenpox

Endogenous: systemic lupus erythematosus (SLE)

PATHOGENESIS:
During latent period between infection and nephritis, antibodies against streptococcal antigens are formed in serum the Immune complex deposit between GBM and epithelial cells -> subepithelial granular deposits -> complement activation -> glomerular damage

151
Q

Give the clinical manifestation of Nephritic syndrome

A

Acute onset of gross hematuria hypertension, mild proteinuria, edema

152
Q

Give the clinical manifestation of Nephrotic syndrome

A

heavy proteinuria, severe edema, hyperlipidemia and lipiduria

153
Q

Define chronic pyelonephritis and give its causes

A

Chronic tubulointerstitial inflammation and scarring associated with deformity

Causes: obstruction and reflux of UTI with congenial vesicoureteral reflux.

154
Q

Enumerate four causes of urinary tract obstruction (Obstructive uropathy)

A

Congenital anomalies
Tumors
Pregnancy
Benign prostatic hypertrophy

155
Q

Define Hydronephrosis and give 3 complications

A

Dilation of the renal pelvis and calyces associated with progressive atrophy of the kidney due to partial obstruction to the outflow of urine

Secondary infection
Chronic renal failure
Hypertension

156
Q

Define pyonephrosis and give 2 causes

A

Dilation and distension of the renal pelvis and calyces with pus associated with progressive atrophy of the kidney due to total or almost complete obstruction of the outflow urine.

Hydronephrosis
Chronic pyelonephritis

157
Q

Enumerate the types of stones

A

Calcium oxalate
Triple phosphate stones
Uric acid stones
Cystine stones

158
Q

Enumerate factors (pathogenesis) that cause calculi formation in urine

A

Increase urinary concentration of the stones constituents: increased urinary concentration of calcium, increased uric acid in urine, dehydration

Change in pH of urine: infection by urea splitting organism and decrease acidity

Lack of substances in urine which inhibit precipitation of crystals

159
Q

Discuss the complications of renal calculi

A

Migration of stones from pelvicalyceal system to ureters resulting in colics and obstructive uropathy

Obstruction produces hydroureter and hydronephrosis

Infection: cystits

Squamous metaplasia, dysplasia. squamous cell carcinoma and carcinoma insitu

160
Q

Enumerate the tumors of the kidney

A

Benign tumors: Renal papillary adenoma, angiomyolipoma, oncocytoma, squamous cell papilloma

Malignant tumors: renal cell carcinoma, Wilm’s tumor, Urothelial carcinoma

161
Q

Give the causes of acute renal failure

A

Pre-renal causes: hemorrhage

Renal causes: acute diffuse GN, Acute pyelonephritis, acute tubular necrosis

Post renal causes: Sudden complete obstruction of ureter by stone

162
Q

Enumerate the causes of chronic renal failure 6

A

Chronic glomerulonephritis
Chronic bilateral pyelonephritis
Polycystic kidney disease
Bilateral hydronephrosis
Diabetes mellitus
Essential hypertension

163
Q

Enumerate the predisposing factors of carcinoma in the bladder 3

A

Schistosoma haematobium infection
Cigarette smoking
Industrial carcinogens

164
Q

Discuss the types of carcinoma found in the bladder 3

A

Urothelial carcinoma: are either papillary or non papillary. Papillary are superficial and can be removed while non papillary are more invasive and likely yo infiltrate lamina propria of bladder.

Squamous cell carcinoma: associated with chronic bladder infection and irritation

Adenocarcinoma: fungating mass that invades the bladder wall and ulcerates the mucosa

165
Q

List four renal causes of hematuria

A

Trauma
Tumors of kidney
Nephritic syndrome
Polycystic kidneys

166
Q

List complications of gonorrhea?

A

Spread: to seminal vesicles or prostate
Sexual transmission to female partner
Chronicity
Fibrosis—–> obstructive uropathy

167
Q

List the germ cell tumors of the testis?

A

Seminoma

Non seminomatous: Embryonal carcinoma, yolk sac tumor, teratoma, mixed germ cell tumors

168
Q

Define hematocele and mention 2 causes for it?

A

Def: collection of blood in tunica vaginalis

Causes: traumatic, malignancy tumors of testis, hemorrhagic blood disease

169
Q

Effects and complications of benign prostatic hyperplasia?

A

Gradual hypertrophy of bladder musculature–> diverticula and dilation of bladder

Hydroureter, hydro nephrosis

Cystic

Bladder calcunli

170
Q

List 4 complications for adult polycystic kidney disease?

A

Hematuria
secondary infections
hypertension
chronic renal failure

171
Q

List 3 causes for rapidly progressive glomerulonephritis

A

1) Post infectious; follow acute diffuse proliferative GN, especially in adults.

2) In association with systemic disease as polyarteritis nodosa (PAN), SLE & Goodpasture syndrome.

3) Idiopathic.

172
Q

List 4 systemic diseases associated with glomerular lesions

A

SLE.
Bacterial endocarditis.
Diabetic glomerulosclerosis.
Amyloidosis.

173
Q

Types and causes of acute tubular necrosis

A
  1. Toxic ATN:
    * Heavy metals
    * Organic solvents (carbon tetrachloride, chloroform)
    * Therapeutic substances: Antibiotics, anaesthetics.
    * Pesticides
  2. Ischemic ATN: Shock due to various causes as trauma, burns and infections, leading to hypoperfusion of the peritubular circulation.
174
Q

Mention 4 complications for renal stones

A
  1. Migration of stones from pelvicalyceal system to ureters resulting in colics and obstructive uropathy
  2. Obstruction produces hydroureter and hydronephrosis.
  3. Infection: cystitis, pyelonephritis, pyoureter, pyonephrosis.
  4. Injury of mucosa especially in oxalate stones resulting in hematuria.
175
Q

Define hydrocele and mention 4 causes for it

A

Definition: Accumulation of serous fluid in the tunica vaginalis.

Causes:
1. Idiopathic
2. Secondary to:
a) Inflammations of epididymis or testes e.g gonorrhea or TB.
b) Filariasis of the spermatic cord
c) Torsion of the testis
d) Tumors of testis

176
Q

Causes of acute pyelonephritis

A
  • Mostly caused by the gram-negative bacilli
  1. Ascending infection: From the lower urinary tract is the most common cause of clinical pyelonephritis.
  2. Hematogenous infection: Through the blood stream. Less common and results from seeding of the kidneys by bacteria from distant foci e.g.in the course of septicemia.
177
Q

Fate and complications of acute pyelonephritis 5

A
  1. Mild cases: Recovery.
  2. Repeated attacks may lead to chronic pyelonephritis.
  3. Pyonephrosis (if associated with obstruction)
  4. Papillary necrosis: Occurs mainly in diabetics and with urinary tract obstruction. There is necrosis of the tips of the renal pyramids. It may lead to acute renal failure.
  5. Perinephric abscess develops in severe cases
178
Q

Types and causes of cystitis

A
  1. Acute cystitis:
    * Bacterial suppurative cystitis: Caused by E.coli, Proteus, Klebsiella mostly through ascending infections. It is a common cause of acute pyelonephritis.
    * Hemorrhagic cystitis in patients treated by
    antitumor drugs
  2. Chronic cystitis:
    * Bilharzial cystitis (see general).
    * Chronic tuberculous cystitis:
    Organism spreads transluminally from tuberculous infection of kidney. Multiple ulcers with undermined edges form which heal by fibrosis and the bladder becomes thickened and contracted.
179
Q

Pathogenesis of glomerulonephritis

A

A. Immune mechanisms: Antibody mediated injury is the most common type of glomerular injury as glomerular deposits of immunoglobulins and complement are detected in more than 70% of cases.

Two forms of antibody mediated injury have been established:

  1. The antibodies react directly with intrinsic tissue antigens (Anti GBM nephritis) or planted antigens (IgA nephropathy).
  2. Deposition of circulating antigen antibody complexes in the glomeruli.

B. Non-immune Mechanisms:
1. Loss of glomerular polyanion as in minimal change disease.
2. Hemodynamic changes as in focal segmental glomerulosclerosis.

180
Q

Define rapidly progressive GN (crescentic GN) and discuss its etiology

A

It is a clinicopathologic syndrome characterized by:
-Rapid & progressive decline in renal function.
-Histologically; formation of crescents.

Etiology:
1) Post infectious; follow acute diffuse proliferative GN, especially in adults.
2) In association with systemic disease as polyarteritis nodosa (PAN), SLE & Goodpasture syndrome.
3) Idiopathic.

181
Q

Discuss the microscopic picture of rapidly progressive GN (crescent GN)

A

-The glomeruli are enlarged, hypercellular showing proliferation of endothelial, mesangial and epithelial cells as well as leucocytic infiltration. Usually there is glomerular necrosis and may be glomerular capillary thrombosis.

-Crescents are formed in the Bowman space and compressing the tufts. They are formed of proliferating parietal epithelial cells, fibrin and migrating monocytes and leucocytes.

182
Q

Discuss the fate of rapidly progressive GN (crescentic GN)

A

Course: Rapidly fatal due to:

Acute renal failure.
Hypertension.
Pulmonary hemorrhage in Goodpasture syndrome.

183
Q

Discuss the pathogenesis of urolithiasis

A
  1. Increased urinary concentration of the stone’s constituents:
    * Increased urinary concentration of calcium.
    a. This can occur in cases of hypercalcemia or b. Without hypercalcemia: attributable to defect in tubular reabsorption of calcium, or increase calcium absorption from the gut.
  • Increased uric acid in urine , with or without with hyperuricemia.
  • Increased oxalates in urine: may be primary hereditary or due to intestinal overabsorption.
  • Dehydration.
  1. Change in ph of urine
    * Infection especially by urea splitting organisms e.g.proteus vulgaris increase the ph leading to precipitation of triple phosphate stones.
    * Acidity leads to uric acid and cystine stones formation.
  2. Lack of substances in urine which inhibit precipitation of crystals, as pyrophosphates and citrates.
184
Q

Describe the morphology of urothelial carcinoma

A

a) 80% of bladder carcinomas are papillary tumors:
* They are formed of delicate fronds of vascular connective tissue core covered by urothelium.
* Most are superficial and can be treated by cystoscopic resection, with follow up for recurrence in the same area or different area of the bladder.
* When these tumors become invasive, they may superficially infiltrate the lamina propria or extend deeply into underlying muscle. The extent of invasion at the time of initial diagnosis is the most important prognostic factor.

b) 20% of tumors are solid (flat, non-papillary) and invasive at presentation and infiltrating the muscle. Such lesions are preceded by a carcinoma in situ. CIS is a flat lesion showing highly atypical cells.

185
Q

Microscopic picture of acute diffuse proliferative GN 4

A
  1. All the glomeruli are enlarged and hypercellular due to proliferation of endothelial, mesangial and epithelial cells as well as due to infiltration by neutrophils and monocytes. There may be crescent formation.
  2. The tubules show hydropic degeneration and may contain red cell and granular casts. The interstitium is edematous and may be infiltrated by neutrophils.
  3. By immunofluorescence microscopy, there are granular deposits of IgG in GBM
  4. By electron microscopy there is subepithelial electron dense deposits (humps).
186
Q

Causes of acute renal failure

A

a- Pre-renal causes: Shock with decreased renal blood flow as in hemorrhage, crush injuries,

b- Renal causes:
1- Acute diffuse GN.
2- Acute pyelonephritis.
3- Acute tubular necrosis.
4- Malignant nephrosclerosis.

c- Post- renal causes: Sudden complete obstruction of the ureter by a stone (calculous anuria)

187
Q

Clinical manifestations of glomerular disease 5

A
  1. Nephritic Syndrome: It is dominated by acute onset of gross hematuria, hypertension, mild/ moderate proteinuria, edema and oliguria. It is the presenting feature of acute post streptococcal glomerulonephritis
  2. Nephrotic Syndrome: The syndrome is fundamentally the result of excessive glomerular permeability to plasma protein and thus heavy proteinuria is its prime characteristic, hypoalbuminemia, severe edema, hyperlipidemia and lipiduria.
  3. Asymptomatic hematuria or proteinuria or combination of both.
  4. Acute renal failure (ARF): dominated by oliguria or anuria (no urine flow).
  5. Chronic renal failure (CRF): characterized by prolonged symptoms and signs of uremia.
188
Q

Urinary bladder diverticula (Def, types and complications)

A

Definition: Outpouchings of the bladder wall.

  1. Congenital diverticula: Caused by focal failure of development of the normal musculature or due to some urinary tract obstruction during fetal development. It is usually single and all the layers of the wall are present.
  2. Acquired diverticula: Mostly associated with prostatic enlargement. It is usually multiple and only formed of mucosal outpouch.

Complications:
1. Inflammation: Diverticulitis (as they are sites of urinary stasis).
2. Formation of bladder calculi.

189
Q

Non renal causes of hematuria 4

A

b. Hypertension.
c. Blood diseases e.g. leukemia and purpura.
d. Vitamin C and K deficiency.
e. Drugs as anticoagulants.

190
Q

Varicocele def and types

A

Definition: Elongation, dilation and tortuosity of pampiniform plexus of veins of the spermatic cord.

Types:
1. Primary varicocele: commonest type. Occurs in young adults. May be to defective venous valves.

  1. Secondary varicocele: due venous obstruction
191
Q

Microscopic types of breast carcinoma

A

A. Noninvasive (In situ carcinoma).
1- Lobular carcinoma in situ (LCIS)
2- Ductal carcinoma in situ (DCIS).

B. Invasive carcinoma.
1- Invasive ductal carcinoma
2- Invasive lobular carcinoma.
3- Special types (Medullary, tubular, mucinous, cribriform….).

192
Q

Paget’s disease of the breast microscopic picture

A

The epidermis is infiltrated by large-sized neoplastic cells with clear cytoplasm and large hyperchromatic nuclei. These cells are called Paget’s cells.

193
Q

Breast abscess (Etiology & morphology).

A

Etiology:
* occurs during lactation
* causative organism: staphylococcal infection
* route: cracks in nipple with bad hygiene

Gross: Diffuse, swollen, edematous, red, tender breast inflammation then localized–>acute abscess.

-If untreated –>chronic abscess may be clinically mistaken for a neoplasm

Microscopic: Infiltration by neutrophils Central cavity filled with neutrophils and secretion, surrounded by inflamed & fibrotic breast parenchyma

194
Q

Paget’s disease of the breast features and gross appearance

A

 Mammary carcinoma: Intraduct or invasive (of any pattern).

 Eczema of the nipple: due to transductal intraepidermal spread

Gross:
 The nipple is red, ulcerated and scaly

Microscopic:
 The epidermis is infiltrated by Paget’s cells

195
Q

Benign tumors of the breast. 3

A
  1. Fibroadenoma.
  2. Phylloides tumor.
  3. Duct papilloma.
196
Q

Two types of ductal carcinoma in situ (DCIS) and their microscopic appearance.

A

Comedo DICS: The ducts are enlarged and lined by several layers of high grade malignant cells with expanding central necrosis.

Non-Comedo DCIS

197
Q

Breast duct papilloma (definition & morphology)

A

 Benign neoplasm from major lactiferous ducts

serous or bloody nipple discharge

Gross:

It is polypoid intraductal mass < 3 cm, soft and Hemorrhagic.

Microscopic: Complex arborizing papillae formed of fibrovascular cores covered by Ductal epithelium & myoepithelial cells.

198
Q

Duct ectasia (Definition, etiology & morphology).

A
  • marked dilatation of mammary ducts containing inspissated Secretions
  • surrounded by chronic inflammation rich in plasma cells.
  • above the age of 40 years
  • unknown Etiology