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Y1B4 (RESP & RAU) 📙 > Pathology 🩺 > Flashcards

Pathology 🩺 Flashcards

1
Q

What are the upper respiratory tract infections?

A

(1) Common cold (Acute coryza)
(2) Rhinoscleroma
(3) Diphtheria

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2
Q

What is the Pathology of common cold?

A
  • Acute catarrhal “Inflammation of the mucous membrane” inflammation caused by rhinovirus with few neutrophils.
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3
Q

What is the fate of common cold?

A
  1. Subsides after few days with regeneration of the damaged epithelium.
  2. Secondary bacterial infection — suppurative inflammation (increase number of neutrophils). “‏سائل أخضر أو أصفر”
  3. Spread of infection to:
    a) middle ear (otitis media).
    b) lower respiratory tract (bronchitis, bronchopneumonia).
  4. Chronicity especially in maxillary sinus “Due to congestion with fluid” (due to upward direction of drainage — easy for secretion to retain).
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4
Q

What is the Pathology of rhinoscleroma “Chronic inflammation” ?

A
  • destructive infective granuloma caused by Klebsiella Rhinoscleromatis.
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5
Q

What is the primary site of rhinoscleroma?

A

Nose

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6
Q

What are the characteristics of rhinoscleroma?

A
  1. The primary site is the nose:
    ✓ enlarged and hard.
    ✓ Its mucous membrane is thickened and granular —progresses to a hard large mass filling the nasal cavity.
  2. Inflammation may extend to paranasal sinuses, nasopharynx, oropharynx, larynx and trachea.
  3. It destructs the soft tissue but bony structures limit its spread.
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7
Q

What is the M/E of Rhinoscleroma?

A

l. Surface epithelium shows areas of hyperplasia or
squamous metaplasia. “To survive”

  1. Subepithelial tissue shows:
    ❖Mickulicz cells (hydropic degeneration of macrophages). They are large rounded cells having well definedborders, abundant clear or foamy cytoplasm. The nucleus is small flattened, deeply stained and eccentric.

❖Russel bodies (hyaline change of plasma cells). These are ovoid or rounded eosinophilic bodies, sometimes having pyknotic eccentric nuclei.

❖Granulation tissue & fibrosis.

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8
Q

What is the fate and complications of rhinoscleroma?

A
  1. Nasal obstruction.
  2. Nasal deformity.
  3. Spread of inflammation to paranasal sinuses, nasopharynx, oropharynx, larynx and trachea.
  4. Epistaxis. “Rupture of vessels”
  5. Squamous cell carcinoma (on top of squamous metaplasia). “Pre-cancerous”
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9
Q

What is the definition of diphtheria?

A
  • It is an acute infectious disease caused by corynebacterium diphtheriae, occurs in non- immunized children between 2-5 years of age but may occur in adult. via blood
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10
Q

What is the method of infection by diphtheria?

A

droplet infection.

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11
Q

What is the pathology of diphtheria?

A

Via exotoxin:

  1. Locally: pseudomembranous inflammation.
  2. Reach distant organs via blood leading to degeneration of parenchymatous organs.
  3. The draining cervical lymph nodes show lymphoid hyperplasia.
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12
Q

What are the complications of diphtheria?

A
  1. Respiratory system — Epistaxis “Like rhinoscleroma” & Aspiration bronchopneumonia. “Due to a transport of part of pseudomembranous inflammation”
  2. Parenchymatous organs — degeneration (Cloudy swelling, fatty change) and necrosis.
  3. C.V.S.—Acute heart failure. “Due to acute myocarditis”
  4. Nervous system — Temporary nerve paralysis & Peripheral neuritis.
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13
Q

What are the infections of the lower respiratory tract?

A

Pneumonitis
Lobar pneumonia
Bronchopneumonia

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14
Q

What is the definition of pneumonitis?

A

It is the inflammation of lung

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15
Q

What are the causes of pneumonitis?

“Bacteria, atypical pneumonitis, granuloma and loffler’s pneumonia”

A

1) Bacterial:
✓ Lobar pneumonia.
✓ Bronchopneumonia.

2) Primary Atypical Pneumonitis:
It is an acute interstitial inflammation confined to alveolar
septa without intra-alveolar exudate. Caused by:
✓ Viruses: as influenza, parainfluenza, measles chicken pox and small pox. “Don’t put Me IN the BOX I can’t breathe!”

✓ Mycoplasma pneumonia.

✓ Undefined agent.

3) Loeffler’s Pnueumonia:
It is pneumonia with eosinophilia. It is due to parasitic infestations e.g. ascaris, ankylostoma and Bilharziasis (verminous pneumonia). “ask uncle bill”

4) Granuloma:
as T.B., sarcoidosis, leprosy, actinomycosis, moniliasis. “

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16
Q

What is the definition of lobar pneumonia?

A
  • Acute bacterial infection involving at least an entire lobe of lung.
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17
Q

What are the causes of lobar pneumonia?

A

strept. pneumoniae in 95 % of cases. “Dangerous”

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18
Q

What is the method of infection of lobar pneumonia?

A

By inhalation (droplet infection). “Like diphtheria”

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19
Q

What is the pathogenesis of lobar pneumonia?

A

A. Pneumococci are inhaled to reach alveoli.

B. In alveoli, it produces an inflammatory reaction with excess fluid exudate.

C. This fluid exudate pass from one alveolus to another through inter- alveolar pores to involve the whole lobe and the bacteria reach the pleura.

D. The fluid together with the cellular exudate expel air away from the alveoli producing a firm airless lobe leading to consolidation (hepatization) of the affected lobe.

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20
Q

What is the type of inflammation caused by lobar pneumonia?

A

Sero-fibrinous

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21
Q

What are the stages of Sero-fibrinous inflammation of the Lung by lobar pneumonia?

A

Stage of congestion
Stage of red hepatization
Stage of gray hepatization
Stage of resolution

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22
Q

What is the duration of congestion, red hepatization, gray hepatization and resolution respectively?

A

1st day

2nd - 4th day

5th - 8th day

9th day till 21

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23
Q

What is the N/E of congestion, red hepatization, gray hepatization respectively?

A

Enlarged
Red “VD”
Wet sponge
Exudes frothy fluid “some air”

Enlarged
Red
Consolidated (Hepatized)
Dry, Red “air expelled”
S.F Pleurisy Enlarged
Enlarged

Gray
Consolidated (Hepatized)
Dry, Gray “increased fibrin”
S.F Pleurisy
Enlarged

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24
Q

What is the M/E of congestion, red hepatization, gray hepatization respectively?

A

Congested
Thickened
-Bacteria.
-Fluid exudate

Congested
Thickened
-Bacteria
-Fibrin
-RBCs
-Few neutrophils

Less congested
Thinned & compressed by the distended alveolar spaces
-Dead bacteria
-Shrunken fibrin
-Hemolyzed RBCs
-Numerous PMNL
-Macrophages

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25
Q

What are the characteristics of stage of resolution?

A
  • Resolution occurs due to absence of necrosis with phagocytosis of cellular debris by macrophages to restore the normal aeration of alveoli & normal lung structure except pleurisy which organizes to form adhesions.
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26
Q

What are the complications of lobar pneumonia?

A
  1. Pulmonary: Fibrosis due to organization of alveolar exudate. “Due to decreased work of macrophages”
  2. Extra-pulmonary: (Spread of infection):
    • Direct to pleura: Fibrous thickening and adhesion.
    • Lymphatic spread: pericarditis, Mediastinitis, osteomyelitis of chest wall bones.
    • Blood spread meningitis, arthritis, bacteraemia and septicaemia.
  3. Due to toxaemia: Toxic myocarditis and acute heart failure.
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27
Q

What is the clinical course of lobar pneumonia?

A

7-9 days and terminates by crisis (sudden improvement).

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28
Q

What is the definition of bronchopneumonia?

A
  • Acute bacterial infection of the bronchioles and the surrounding alveoli leading to patchy consolidation.
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29
Q

What is the iteology of bronchopneumonia?

A

Many micro-organisms are responsible most commonly:

1) staphylococcus aureus.

2) streptococcus pyogens,

3) pneumococcus.

4) haemophilus influenza

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30
Q

What is the mode of infection of bronchopneumonia?

A

by inhalation.

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31
Q

What are the types of bronchopneumonia?

A

1) Primary bronchopneumonia

2) Secondary bronchopneumonia

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32
Q

What causes primary bronchopneumonia and in which type of people does it occur?

A
  • Due to primary exogenous invaders.
  • Occurs in extremes of age (infancy, children and old age).
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33
Q

What Causes secondary bronchopneumonia and what are its types?

A
  • Due to secondary endogenous invaders which complicate other diseases. It may be: (PIHT)
  1. Post infective: Complicates respiratory tract infection as influenza.
  2. Inhalation: Due to inhalation of infected material.
  3. Hypostatic: Complicates pulmonary oedema of heart failure.
  4. Terminal: Complicates severe diseases as cancer or coma and is usually fatal. “Already very weak immunity”
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34
Q

What is the Pathology of bronchopneumonia?

A

Acute supparative inflammation

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35
Q

What is N/E of bronchopneumonia?

A

1) Multiple patches of consolidation ± suppuration centered around the bronchioles & distributed through several lung lobes or one lobe.

2) Areas between the patches are normal.

3) In severe cases patches fuse together forming large consolidated area called confluent bronchopneumonia.

4) Pleurisy is not a marked feature, as the patches do not usually contact the pleura.

5) Suppurative patches heal by fibrosis.

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36
Q

What is the M/E of bronchopneumonia?

A

1) The affected bronchioles show picture of acute suppurative inflammation:
✓ The lumen is filled with pus and shedded epithelium.
✓ Epithelial lining is ulcerated.
✓ Wall infiltrated by excessive number of neutrophils & pus cells.

(2) The attached alveoli:
- Alveolar spaces are filled with pus rich in neutrophils and pus cells.
- Inter-alveolar septa are acutely inflamed.

(3) The patches are either:
❖ early non-suppurative patches,
❖ Late suppurative patches, OR healed fibrotic patches.

(4) Lung Tissue in between the patches appear normal.

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37
Q

What are the complications of bronchopneumonia?

A

A. Pulmonary: Fibrosis, pulmonary hypertension and right-sided heart failure. “Not common in lobar pneumonia due to resolution:

B. Extra-pulmonary: Spread of infection: “As lobar pneumonia”

**Direct : to surroundings.
**Lymphatic spread: pericarditis, Mediastinitis, osteomyelitis of chest wall bones.
**Blood spread meningitis, arthritis, bacteraemia and septicaemia.

C. Due to toxaemia: Toxic myocarditis and acute heart failure.

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38
Q

What is the clinical course of bronchopneumonia?

A

2 - 3 weeks and terminates by lysis. “Longer”

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39
Q

Compare between lobar pneumonia and bronchopneumonia according to:

Definition
Etiology (organism - route)
Pathology (N/E - M/E)
Fate
Course

A
  • Def:
  • Acute sero-fibrinous inflammation Bronchopneumonia
  • Acute suppurative inflammation
  • Aetiology: (Organism - Route)
  • Pneumococci (95%).
  • Primary exogenous infection.
  • Staph, Strept, H influenza.
  • Primary & secondary infections.
  • Pathology
  • N/E:
  • 4 stages.
  • Diffuse lesion not related to bronchiole
  • No pus on pressure.
  • Fibrinous pleurisy is marked.
  • No stages.
    -Patchy lesion related to bronchiole
  • pus exudes on pressure.
  • Usually absent.

-M/E:
- Diffuse lesion.
- Alveolar spaces contain fibrin, neutrophils, RBCs & macrophages.
- No bronchiolitis.
- Pleurisy.

  • Patchy around bronchioles
  • Contains pus cells, RBCs & macrophages.
  • Bronchiolitis occurs.
  • No pleurisy.
  • Fate:
  • Resolution is common.
  • Fibrosis is rare.
  • Resolution is rare.
  • Fibrosis is common.
  • Course:
  • 7-9 days and ends by crisis.
  • 2-3 weeks and ends by lysis.
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40
Q

What is the definition of chronic obstructive pulmonary diseases (COPD)? “‏أمراض الانسداد الرئوي المزمن”

A
  • A group of pulmonary diseases characterized by Resistance to airflow due to partial or complete obstruction at any level.
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41
Q

What are the types of COPD?

A

➢ Chronic bronchitis.
➢ Bronchial asthma.
➢ Emphysema.
➢ Bronchiectasis

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42
Q

What is chronic bronchitis?

A
  • It is persistent productive cough (cough with sputum) For consecutive three months is for at least consecutive two years.

‏”Three consecutive months per year”

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43
Q

What are the causes of chronic bronchitis?

A

Due to chronic irritation of the bronchial mucosa by:

1- Cigarette smoking.
2- Atmospheric pollution “By chemicals for examples”
3- Chronic inflammation of upper respiratory tract, tonsils or mouth.

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44
Q

What is the Pathology or incidence of chronic bronchitis?

A

Occur in middle-aged men

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45
Q

What is N/E of chronic bronchitis?

A

Bronchial mucosa appears thick, opaque and covered by excess mucous.

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46
Q

What is the M/E of chronic bronchitis?

A

Bronchi: “Defensive Response”

  • Mucous gland hyperplasia “to inc mucous secretion” and decreased number of ciliated cells. “Replaced by goblet cells:

-Squamous metaplasia

-chronic inflammatory cell infiltrations.

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47
Q

What are the complications of chronic bronchitis?

A

1- Centrilobular emphysema.

2- Bronchopneumonia.

3- Bronchogenic carcinoma. “Due to metaplasia”

4- Chronic hypoxaemia resulting in persistent pulmonary vasoconstriction, pulmonary hypertension

5- Cardiac failure.

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48
Q

What is the definition of bronchial asthma?

A
  • A common disease characterized by recurrent attacks of widespread bronchoconstriction, in response to various stimuli.
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49
Q

How is bronchial asthma clinically manifested? “WBC”

A
  • Clinically, it is manifested by recurrent episodes of wheezing, breathlessness, and cough that is at least partly reversible, either spontaneously or with treatment.
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50
Q

What is the condition of the patients of bronchial asthma in between atracks?

A
  • Between the attacks, patients may be virtually asymptomatic
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51
Q

What are the triggering factors for bronchial asthma?

A

❑ Domestic dust mites
❑ Cockroach
❑ Animal with fur

❑ Air pollution
❑ Tobacco smoke

❑ Pollen
❑ Respiratory (viral) infections
❑ Occupational irritants

❑ Chemical irritants
❑ Drugs ( aspirin, beta blockers)

❑ Strong emotional expressions

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52
Q

What are the types of asthma and what is the significance of this distinction?

A
  • There are two types of asthma,

• Atopic ( with Family history of Atopy)

• Non atopic (without Family history of Atopy)

  • This distinction is useful from the point of pathophysiology, but In clinical practice it’s not always possible to classify asthma.
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53
Q

What is the incidence of extrinsic (immunological, atopic, allergic) asthma?

A

10% of cases, Occur In children and young

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54
Q

What are the characteristics of extrinsic asthma?

A
  • occur in 10% of cases. Occur In children and young. A positive family history is present. The attacks are provoked by type I hypersensitivity reaction to inhaled allergens such as house dust, animal dandruffs, plant pollens, fungi, ….etc
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55
Q

What are the characteristics of intrinsic (non immunological, non topic, non allergic) asthma?

A

o 90 % of cases.

o Any age, mainly in late adults. No history of atopic disease.

o It is triggered by hyperirritability of bronchial tree by infection , exposure to cold, physical excercise, anxiety, emotions, asprin and inhaled irritants… etc.

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56
Q

What is the N/E of bronchial asthma?

A

1) Bronchi and bronchioles: “due to histamine”
-Hyperaemic oedematous mucosa, Thick walled
and narrow lumen plugged with mucus.

2) Lung:
-Diffuse hyper-inflation with Patchy collapse due to complete obliteration of some bronchioles by mucus

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57
Q

What is the M/E of bronchial asthma?

A

Patchy necrosis of epithelium “By eosinophils”

Sub-mucosal glandular hyperplasia

Hypertrophy of bronchial smooth muscle “due to over-work”

Eosinophils, mast cells; lymphocyte

Mucous plugs, Whorled mucous plugs (Curschmann’s spirals)

Debris of eosinophils (Charcot-Leyden crystals

“PHHEEW”

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58
Q

What are the fate and complications of bronchial asthma?

A

l - Chronic bronchitis.

2- Emphysema, pulmonary hypertension and Rt. sided heart failure.

3- Status asthmaticus: persistant attacks for days or weaks. It is fatal due to respiratory failure.

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59
Q

What is the definition of emphysema?

A
  • Permanent dilatation of air spaces distal “after” to the terminal bronchioles accompanied by damage of respiratory bronchioles, alveolar ducts and alveoli (respiratory acinus).
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60
Q

What is the incidence of emphysema?

A
  • The commonest chronic lung disease. It occurs more in males from 40-60 years of age.
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61
Q

What are the types of emphysema?

A

A- Centriacinar (Centrilobular)
B- Panacinar (Panlobular)

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62
Q

What is the pathogenesis of centriacinar emphysema?

A
  • It is related to cigarette smoking and it is explained by the following theories:

1- ELASTASE - ANTIELASTASE IMBALANCE THEORY Smoking weakens the walls of air spaces by increasing elastase and inhibiting antielastase

2-DIRECT DAMAGE THEORY: The walls of air spaces are directly injured by toxic substances of cigarette smoking

3) CHRONIC BRONCHITIS THEORY:
a- Smoking recruits neutrophils and macrophages and stimulates the release of elastase “one of the Proteolytic enzymes found inside” from them

b- It increases mucus secretion leading to mucus plugs which partially obstruct the bronchi and terminal bronchioles. During expiration the air is entrapped and increases gradually the intraluminal pressure.

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63
Q

what is the definition of Cyntriacinar emphysema?

A
  • It involves respiratory bronchioles (central part of acinus)
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64
Q

What is the definition of panacinar emphysema?

A
  • It involves the whole acinus and occurs more in old females.
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65
Q

What is the pathogenesis of panacinar emphysema?

A
  • Related to inherited deficiency of antielastase (alpha 1 antitrypsin) in the patient’s blood. Therefore the action of elastase secreted from neutrophils and macrophages becomes unopposed.
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66
Q

What is the N/E of centriacinar emphysema?

A
  • Upper zones of the lung lobes are first affected, The lungs are moderately “only the bronchioles” enlarged, C/S:- Enlarged air spaces.
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67
Q

What is the N/E of panacinar emphysema?

A

1) Barrel shaped chest: The chest wall takes a fixed exaggerated inspiration position:

a- The anteroposterior diameter increases to equal the transverse. The sternum is pushed forward.

b- The ribs, costal cartilages and the intercostal spaces are horizontal.

2 ) Lungs:
Lower zones of lung lobes are first affected. “Increased blood causes increased neutrophils and consequently increased elastase”

❑ The lungs are voluminous and very light. “Air”

❑ They are pale “thin septum” and dry “air” .

❑ The surface is smooth and presents the indentations of ribs. “Due to pressure”

❑ Lungs have a feathery feeling and pit on pressure (due to loss of elastic tissue).

❑ Large bullae project on the surface in the poorly supported parts (along apices, anterior margin and free edge of base). ‘زي كيس شفاف كدا” 🫥

❑ A bulla is an emphysematous space of more than 1 cm in diameter, it is semitranslucent with paper – thinned
walls.

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68
Q

What is the M/E of centrilobular emphysema?

A

Dilated respiratory bronchioles with normal A.D. and alveoli.

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69
Q

What is the M/E of panacinar emphysema?

A

1) Alveoli are:
Few in number “as they fuse” , increased in size, distorted in shape.

2) Interalveolar septa:
❑ Thin and in advanced stages, alveolar septa rupture.
❑ The interalveolar capillaries are compressed by dilated air spaces.

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70
Q

What are the complications of emphysema?

A

1) Respiratory system:
❑ Ch. bronchitis. “And chronic bronchitis cause emphysema as well”
❑ Interstitial emphysema.
❑ Spontaneous pneumothorax “rupture of Bullae”
❑ Respiratory failure.

2) C. V. S.:
❑ pulmonary hypertension and right sided heart failure.

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71
Q

What are other types of emphysema?

A

I- Obstructive Hyperinflation
II- Compensatory Hyperinflation
III- Senile (Atrophic) hyperintlation
IV- Interstitial Emphysema: It is the escape of alveolar air into the interstitial tissue of the lung.

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72
Q

What is the definition of bronchiectasis?

A
  • Permanent (irreversible) dilatation of medium sized bronchi and bronchioles “before RESP. Bronchioles” caused by chronic suppurative inflammation in their walls and surrounding lung tissue.
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73
Q

What is the incidence of bronchiectasis?

A
  • It is frequent before the age of 20 years in males more than females. It can occur in adults.
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74
Q

What is the pathogenesis of bronchiectasis?

A
  • For bronchiectasis to occur
    (1) Weak bronchial wall (Chronic pyogenic infection)

(2) Forces for dilatation which may be:
a- Pushing forces from inside ( bronchial obstruction) “the force of air”

b- Pulling forces from outside. “Fibrosis”

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75
Q

What is the N/E of bronchiectasis?

A

1- Bilateral and basal.
2- Dilated medium and smaller sized bronchi and bronchioles that are filled with pus.
3- Their lining are thick
4- Their walls show fibrosis.

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76
Q

What is the M/E of bronchiectasis?

A

1) The affected bronchi show chronic suppurative inflammation.
a- Lumen: reveals shedded epithelial cells, inflammatory cells and R.B.C’s.
b- Mucosa: Extensive ulceration
c- Wall: is infilterated by inflammatory cells.

2) Lungs show areas of collapse and fibrosis and areas of compensatory emphysema

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77
Q

What is the definition of tuberculosis?

A
  • chronic infective granuloma affecting nearly all body “In secondary infections” systems mainly the lungs.

“Regenerating mess of histiocytes due to tuberculosis infection”

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78
Q

What are the predisposing factors for tuberculosis?

A

A. Environmental
• Low socioeconomic standard.
• Bad general hygiene.
• Contact with tuberculous persons.
• Overcrowding.
• Environmental pollution.

B. Personal factors
• Negroes (more than white persons)
• Malnutrition
• Debilitating diseases (as D.M)
• Immune deficiency states

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79
Q

What is the causative agent of tuberculosis and what are its characters?

A
  • T.B. bacilli are aerobic, acid- fast, non- motile, not produce exotoxins, and carried by macrophages.
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80
Q

What are the substances that enter in the structure of TB bacilli?

A
  • Carbohydrate, lipid and protein (tuberculoprotien or PPD).
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81
Q

What are the types of TB Bacilli?

A
  • Human type causes infection by inhalation./Bovine type causes infection by ingestion.
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82
Q

What are the characteristics of primary tuberculosis? (Childhood type)

A
  • Occur in young ages, non- immunized persons. Source of infection is exogenous. About 5% of infected persons develop significant disease. “While the rest are releavied”
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83
Q

What are the methods of infection by primary tuberculosis?

A

1) Inhalation.
2) Ingestion
3) Direct contact.

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84
Q

What are the sites of primary TB complex? “Like pulmonary TB”

A

1- Lung. “inhalation”
2- Intestine “ingestion”
3- Tonsils “ingestion”
4- Skin “contact”
5- Nose (rare). inhalation”

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85
Q

What is the reaction of the body against TB bacilli?

A
  • Proliferative reaction (tubercle formation)
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86
Q

What is the pathogenesis of proliferative reaction against tuberculosis?

A

I) At 1 st:The bacilli are taken by the macrophages. The organisms multiply in macrophages, which are unable to kill the organism

2)Then The native macrophages present the (purified protein derivative PPD) on its surface to native helper T cells. Macrophages release interleukin 12 (IL-12) which activates the helper T lymphocytes to secrete the following

1- Interferone gama (INF): responsible for immunity and delayed “3-4 days” hypersensitivity with granuloma formation. This is achieved by activation of native and blood monocytes and results in more secretion of IL- 12 “a cycle” with increased ability for expression of the PPD, phagocytosis and killing of bacilli.

2- 2-Tumor necrotizing factor (TNF- ) which causes: Increase blood flow to the area of inflammation. Attraction of lymphocytes and blood monocytes to area of infection

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87
Q

What is the N/E of tubercle?

A
  • In 3 weeks, the tubercle is visible 1-3 mm size, with central yellow caseation “dead cells in the center” and its periphery is grey.
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88
Q

What is the M/E off do tubercle?

A
  • Central caseating material (sturctureless eosinophilic material with no cellular details (H &E) Ephithelioid cells, macrophages, Langhan’s giant cells, lymphocytes and peripheral fibroblastic reaction surround the caseation. “To limit spread”
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89
Q

What is the favorable site for TB and why?

A
  • lungs are a Favorable site for TB (easy inhalation and aeration).

“Aerobic bacteria”

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90
Q

What does primary pulmonary tuberculosis or primary pulmonary complex consist of?

A

Childhood type consists of 3 parts:

1- Parenchymatous lesion (Ghon’s focus): “usually in The right”
- Is a caseous lesion 1-2cm. in diameter beneath the pleura in the lower part of upper lobe or upper part of middle lobe 1-2 cm. from pleural cavity, grayish yellow in color.

2- Tuberculous lymphangitis

3- Tuberculous lymphadenitis

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91
Q

What is the fate of primary tuberculosis?

A
  • Good fate: Healing
  • Bad fate: Spread:

Local spread: to pleura causing TB Pleurisy

Lymphatic: to peri and paratracheal lymph nodes& mediastinal structures.

Blood spread:: produce miliary tuberculosis

Natural passages….less common than secondary…it leads to the development of tuberculous bronchopneumonia and pneumonia “bronchi”

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92
Q

What is the N/E of miliary tuberculosis?

A
  • The lesion appear as multiple scattered uniform small size (3mm) tubercles separated from each other by normal tissue and not surrounded by area of congestion “if so, then pyramid abscess” and present on outer and cut surface of organs.
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93
Q

What is the M/E of miliary tuberculosis?

A

-Poorly developed tubercle (No fibrous capsule, absent giant cell)

-central caeseation

-Distribution related to blood vessels

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94
Q

What is the source of secondary pulmonary TB?

A
  • the organism may be acquired exogenously or from reactivation of a healed primary complex.
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95
Q

Where does secondary tuberculosis take place?

A
  • It usually occurs in adults.
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96
Q

What does the hypersensitivity reaction in secondary pulmonary tuberculosis cause? “Not delayed”

A

excessive tissue destruction and extensive caseation.

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97
Q

Is there any nodal affection in secondary tuberculosis and why?

A
  • No nodal affection as the organism is destroyed in the necrotic tissue.
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98
Q

What are the organs affected by secondary tuberculosis?

A
  • Organs most commonly affected are:

Kidney - Suprarenal gland - Fallopian tube - Epididymis. - Brain and meninges - Bone and joints.

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99
Q

What is the N/E of secondary tuberculosis?

A

• An apical lesion (Assmann focus) begins as a small caseating tuberculous granuloma.

• In most cases, destruction of the lung leads to cavitations.

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100
Q

What is the M/E of secondary tuberculosis?

A
  • There’s a central area of caseation that is surrounded by granulomatous inflammatory reaction.
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101
Q

What are the fate and complications of secondary tuberculosis?
“Like primary but there is no lymphatic spread”

A

A. Regression (good fate)

B. progressive lesion (Bad Fate)
1- Local tissue Distruction
- Blood vessels…hemorrhage
- Bronchi..open to the pleura leading to pneumothorax and pyopneumothorax.
- Reactive systemic amyloidosis.

2- Pulmonary fibrosis…pulmonary hypertension ..right sided heart failure (cor pulmonale).

3- Spread…..*Local to the pleura (pleurisy) *Bronchial…TB pneumonia and bronchopneumonia *Blood…..isolated organ TB or miliary TB “more common”

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102
Q

What happens to the apical lesions of secondary tuberculosis in cases of good immunity?

A
  • With good immunity, healing of the apical lesion occurs and a dense fibrous capsule surrounds a central area of caseation
  • Calcification often occurs, and a (latent tuberculosis) develops which can be reactivated if the patient’s immunity is lowered.
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103
Q

What is the definition of tuberculoma?

A
  • It is a localized mass of caseating tuberculous reaction surrounded by fibrous tissue.
104
Q

What is tuberculoma mistaken for?

A
  • It may reach a large size (to be mistaken for a tumor)
105
Q

Where does tuberculoma occur?

A
  • It can occur at any organ (lung, kidney, brain…)
106
Q

What is the clinical classification of glomerular diseases?

A

1- Nephrotic syndrome. “Problem if filtration slits —> protenuria & severe edema”

2- Nephritic syndrome. “Problem in mesangial cells —> oligourua, hypertension & mild edema”

3- Acute renal failure.

4- Chronic renal failure.

107
Q

What is the pathological classification of Glomerular diseases?

A

Primary and secondary

108
Q

What are primary glomerular diseases?

“Arise from glomeruli”

A
  1. Minimal Change Disease (MCD)
  2. Focal Segmental Glomerulosclerosis (FSGS)
  3. Membranous Nephropathy (MN)
  4. Membrano-proliferative Glomerulonephritis (MPGN)
  5. Acute Post-Streptococcal Glomerulonephritis (APSGN)
  6. Rapidly progressive (Crescentic) Glomerulonephritis
109
Q

What are secondary glomerular diseases?

“Only cause nephrotic syndrome”

A
  1. SLE
  2. DM
  3. Amyloidosis
110
Q

What is a diagnosis of glomerular diseases? (Renal biopsy)

A

1- Light microscopy: Cellularity, Extracellular matrix “of mesangial cells” , basement membrane. Can use some special stains (PAS stain, Masson trichrome, Silver for sclerosis and basement membrane)

2- Immunofluorescence microscopy (deposits of immune complexes). “Colored —> green” “as 99% of causes of renal problems are immunologic”

3- Electron microscopy “the most Acc” (deposits of immune complexes, foot processes of podocytes) “not colored”

111
Q

What does each of the following terms mean?

• Focal:
• Diffuse:
• Segmental:
• Global:
• Mesangial proliferation:
• Sclerosis:

A

• Focal: affect some glomeruli only.
• Diffuse: affect all glomeruli.
• Segmental: affect part of the glomerulus.
• Global: affect the whole glomerulus.
• Mesangial proliferation: more than 2 cells/area. “At high power”
• Sclerosis: Fibrosis of the glomeruli (increased Mesangial matrix).

112
Q

What are the Glomerular diseases causing nephrotic syndrome?

A

• Primary:
- Minimal change disease (commonest cause in children).
- Focal segmental glomerulosclerosis.
- Membranous “BM” nephropathy (commonest cause in adults).
- Membranoproliferative “BM & Scleroses” glomerulonephritis

• Secondary:
- Systemic lupus erthymatosus.
- Amyloidosis.
- Diabetic nephropathy.

113
Q

What is the incidence of minimal change disease? (Foot process disease, lipoid nephrosis, nil disease)

“Due to normal shape of glomerulus under LM”

A

• The most common cause of the nephrotic syndrome in children (peak 2-3 years old)

114
Q

What are the causes of minimal change disease?

A

• 90% are idiopathic.

• May be secondary:-
- Hodgkin’s Disease.
- HIV.
- Atopy.
- NSAIDs.

115
Q

What is a selectivity of minimal change disease?

A

• Proteinuria is usually selective (albumin only).

116
Q

What is the fate of minimal change disease?

A

• Usually resolve completely. “By anti-inflammatory”
“Even though there is no proof that the cause is immunological!”

• Rarely can progress to: FSGS.

117
Q

What is a complment level in minimal change disease?

A

Normal “no itis”

118
Q

How is minimal change disease diagnosed?

A

Diagnosis: Renal biopsy:

  • Light microscopy: Normal.
  • Immunofluorescence microscopy: Normal (No
    deposits of immune complexes).
  • Electron microscopy: Effacement (fusion) of foot
    processes of podocytes.
119
Q

What is the pathophysiology of minimal change disease?

A

1- Effacement of foot processes of Podocytes (loss of negative charge of foot processes).

2- Widening of slit diaphragm.

120
Q

What is the incidence of Focal segmental glomerulosclerosis?

A

• Accounts for 10-15% of nephrotic syndrome.

• More commonly seen in young adults (20-30s).

121
Q

What is the cause of Focal segmental glomerulosclerosis?

A

• Majority of cases are idiopathic.

• May be secondary :
- HIV.
- Hepatitis B,C.
- Heroin addict.
- Diabetes mellitus.
- Reflux nephropathy.
- Sickle cell anemia.

122
Q

What is the selectivity of Focal segmental glomerulosclerosis?

A

• Non-selective proteinuria.

123
Q

What is the complement level of Focal segmental glomerulosclerosis?

A

Normal

124
Q

What is the diagnosis of Focal segmental glomerulosclerosis?

A

Diagnosis: Renal biopsy:
1- Light microscopy: sclerotic process involving only some of the glomeruli and among the affected glomeruli, only a portion of the glomerular tuft. “Sclerosis to some parts of the glomeruli”

2- Immunofluorescence microscopy: Deposits of immune complexes (Mesangial).

3- Electron microscopy: Effacement (fusion ) of foot processes of podocytes + Deposits of immune complexes (Mesangial).

125
Q

What is the incidence of membranous glomernephropathy?

A

• The most common cause of nephrotic syndrome in adults (most common in middle-aged men).

126
Q

What is the cause of membranous glomernephropathy?

A

• Majority of cases are idiopathic

• May be secondary :
- infections e.g. Hepatitis B,C and HIV. - Diabetes mellitus.
- SLE (Systemic lupus erythematosus). - Cancer: Colon, breast, lung.

127
Q

What is the selectivity of membranous glomernephropathy?

A

• Nonselective proteinuria.

128
Q

What is the complement level of membranous glomernephropathy?

A

Normal

129
Q

What is the diagnosis of membranous glomernephropathy?

A

Diagnosis: Renal biopsy:

  1. Light microscopy: Thickening of basement membranes. “Membranous” By silver stain (Spikes and domes).
  2. Immunofluorescence microscopy: Deposits of immune complexes (IgG, C3).
  3. Electron microscopy: Subepithelial immune-complex deposits.
130
Q

What is the selectivity of membranoproliferative glomeronephritis?

A

• Nonselective proteinuria.

131
Q

What is the cause of membranoproliferative glomeronephritis?

A

• May be idiopathic mainly in children and young adults (8-30 years).

• May be secondary mainly in adults ( > 30 years).
- infections e.g. Hepatitis B,C and HIV. - SLE (Systemic lupus erythematosus). - Cancer: Melanoma.

132
Q

What is the complement level of membranoproliferative glomeronephritis?

A
  • Characterized by reduced complement level.
133
Q

What can membranoproliferative glomeronephritis cause?

A
  • Can cause either nephrotic or nephritic syndrome.
134
Q

What is the diagnosis of membranoproliferative glomeronephritis?

“Same as membranous nephropathy but for the mesangial proliferation”

A

• Diagnosis : Renal biopsy:

1- Light microscopy: Thickening of basement membranes (tram track appearance) + proliferation of mesangial cells (> 2 cells/ area).

2- Immunofluorescence microscopy : Deposits of immune complexes (IgG, C3)

3- Electron microscopy: Subendothelial immune-complex deposits.

135
Q

What are the characteristics of poststreptococcal glomerulonephritis?

“Acute diffuse focal proliferation glomerniphritis”

“Btw it happens due attack against antigens similar to that of strept which are found in kidney and heart producing ASPGN and rheumatic fever respiectively”

A

• Glomeruli are globally and diffusely enlarged and hypercellular due to:
- neutrophils
- proliferation of Mesangial cells
- proliferation of endothelial cells

136
Q

What is another name for poststreptococcal glomerulonephritis?

A

Also called ‘exudative’ glomerulonephritis.

137
Q

What is the state of glomeruli in poststreptococcal glomerulonephritis after months?

“Btw it is the most common cause of nephritic syndrome in children”

A

Returns to normal

138
Q

What is the resultant of swelling of endothelial cells and presence of inflammatory cells?

A

obstructs capillary lumina leading to oliguria. “Due to decreased GFR”

139
Q

What is the definition of Rapidly progressive (crescentic) glomerulonephritis?

“The most dangerous”

A
  • This form of GN represents a clinicopathologic syndrome in which rapid and progressive decline in renal function is associated with severe oliguria and anuria, usually resulting in irreversible renal failure in weeks or months. “Transplantation, dialysis or …. death”
140
Q

What are the characteristics of Rapidly progressive (crescentic) glomerulonephritis?

A
  • It is characterized by extensive proliferation of the cells in the Bowman’s space with conspicious crescent formation.
141
Q

What are the symptoms of Rapidly progressive (crescentic) glomerulonephritis?

A
  • Hematuria is a common finding, but proteinuria or hyprtension and edema may or may not be present.

“Due to destruction of BM”

142
Q

What is the diagnosis of Rapidly progressive (crescentic) glomerulonephritis?

A

Diagnosis : Renal biopsy:

1- Light microscopy: Crescent formation (proliferation
of epithelial cells “parietal” of bowman’s capsule). “No glomerular space”

2- Immunofluorescence microscopy: No deposits of
immune complexes. “Some have btw”

3- Electron microscopy: Effacement (fusion ) of foot
processes of podocytes

143
Q

What are the Glomerular diseases causing nephritic syndrome?

“Acute - more dangerous than nephrotic syndrome”

A
  • Acute poststreptococcal glomerulonephritis.
  • Membranoproliferative glomerulonephritis.
  • Rapidly progressive glomerulonephritis (crescentic glomerulonephritis).
144
Q

What is the definition of pyelonephritis?

“Pus in the Interstitium & tubules”

A
  • It is a suppurative bacterial infection of renal tubules and interstitium.
145
Q

What are the microorganism is causing pyelonephritis?

A
  • Mostly E-coli or mixed with other bacteria.
146
Q

What are the predisposing factors for pyelonephritis?

“Female - obstruction - contamination”

A

1- Female Gender because of:

a. Short urethra. “Easy ascent for bacteria”

b. Urethra is close to the anus (source of gram negative bacilli like E.Coli) as well as vagina.

c. Female hormones (like estrogen and progesterone) relax the smooth muscles in the urethra causing stasis which allows bacterial overgrowth.

d. In pregnancy the uterus compresses the bladder.

“C & d lead to stasis”

2- Obstruction of urinary flow such as: (Obstruction Stasis bacterial growth)

a. Urethral obstruction in benign prostatic hyperplasia “BPH” (most common cause in men especially those >50 years)

b. Stones

c. Tumors

3- Instrumentalization : Mainly catheters inserted into the bladder which introduce infection

“‏خلي بالك القسطرة تكون متعمقة كويس”

4- Surgery in the kidney or urinary tract “ no sterialization”

5- Diabetes mellitus “due to hyperglycemia”

6- Immunosuppression and Immunodeficiency

147
Q

What is the mood of infection by pyelonephritis?

“Outside and inside”

UTI in children by VUR
UTI in Male by BPH

A

1- Ascending: by external entry of organisms through the urethra into the bladder then ureters (vesicoureteral reflux) (VUR) “‏عكس التيار” then kidney (which is the most common cause of urinary tract infections in children)

2- Hematogenous: (very dangerous) from another focus of infection (e.g: endocarditis)through the blood the bacteria will reach the kidney. Usually by Staphylococcus Aureus

3- From the neighboring organs through the communicating lymphatics.

148
Q

What are the clinical manifestations of pyelonephritis?

“Small painful suppurative bloody contaminated urine”

A

1- Urinary frequency: void small amounts of urine at frequent intervals.

2- Dysuria: Painful, burning sensation on urination

3- Pyuria: large numbers of neutrophils in the urine

4- Haematuria: blood in the urine

5- Bacteriuria: presence of bacteria in urine. It must be distinguished from contamination of urine specimen by external flora.

149
Q

What does the presence of neutrophil cast indicate?

“Neutrophils but not in casts may indicate any bacterial infection”

A

Pyelonephritis

150
Q

Compare between acute pyelonephritis and chronic pyelonephritis “fibrosis” Acc to: “2S & 2C”

-Size
-surface
-Capsule

-Cut surface
Outlines
Mucosa
Contents

A

Size : Increased - Decreased

surface: Suppurative patchy foci surrounded by hyperemia - Irregular coarsely granular due to
underlying coarse irregular scarring.

Capsule: Strips easily - Adherent with decortication “due to fibrosis”

Cut surface Calyces and pelvis:
• outlines: Distorted - Deformed by scarring
• Mucosa: Hyperemic - Rough thick, mildly hyperemic
• Contents: Full of pus - Some pus

151
Q

Compare between acute pyelonephritis and chronic pyelonephritis according to:

Glomeruli
Tubules
Interstitium
Blood vessels

A

Glomeruli:

  • Periglomerular fibrosis. Some totally sclerotic glomeruli.

Tubules:

-Neutrophil cast
- Groups of atrophic tubules (thyriodization i.e. dilated and lined by flattened epithelium and contain hyaline casts picture simulating thyroid follicles) Some tubules contain neutrphil casts.

Interstitium:

  • Focal infiltration with acute inflammatory cells.
  • Focal fibrosis and chronic suppurative inflammation.

Blood vessels:

  • Hypertensive changes “Thickening in walls”
152
Q

What is the fate of acute pyelonephritis?

A
  • Recovery
  • Acute renal failure.
  • Chronic pyelonephritis
153
Q

What is the fate of chronic pyelonephritis?

A
  • Secondary hypertension “Thickened blood vessels dec RBF which Increase renin”
  • Chronic renal failure
154
Q

What is the definition of cystitis?

A
  • Inflammation of urinary bladder
155
Q

What are the predisposing factors for cystitis?

Same as pyelonephritis + bilharziasis”

A
  • Obstruction, diabetes mellitus, local lesions (stones, Bilharsiasis and tumors)
156
Q

What are the organism is causing cystitis?

A
  • E-Coli, pyogenic cocci and specific organism as TB.
157
Q

What is the mood of infection by cystitis?

“Like pyelonephritis + descending”

A
  • Ascending, descending, hematogenous, lymphatics or nearby infection.
158
Q

What is the N/E of cystitis?

A
  • Thick wall due to inflammation and fibrosis.
159
Q

What is the M/E of cystitis?

A

1- Acute inflammation: catarrhal, purulent or membranous. “CPM”
2- Chronic inflammation: Non specific and specific.
“TB - Bilharziasis”

160
Q

What are the complications of cystitis?

A

-Ascending infection leading to Ureteritis and Pyelonephritis.

-Local effects: Gangrene, stones and leukoplakia (whitish patches in the mucosa due to squamous metaplasia)
“Due to inflammation”

161
Q

What are the causes of Urinary tract obstruction?

A
  1. Urethral obstruction
  2. Urinary bladder obstruction
  3. Ureteric obstruction
  4. Renal pelvis obstruction
162
Q

What are the causes of urethral obstruction?

A

• Congenital:
-Phymosis (Congenital stenosis of prepuce opening),
- Stricture.

• Acquired:
- In the wall: Stricture (post traumatic instrumentation or inflammatory).

  • In the lumen: Calculi.
  • From outside: Enlarged prostate.
163
Q

What are the causes of urinary bladder obstruction?

A
  • Organic: Stones, tumors obstructing the bladder neck or ureteric orifices . Bladder neck fibrosis e.g. due to fibrosis , prostatic hyperplasia….
  • Functional: Neurogenic disturbances of bladder control due to spinal cord lesion.
164
Q

What are the causes of ureteric obstruction?

A

1- From outside:
- Tumors, enlarged nodes, hematoma or fibrous bands.
- Periureteral inflammation e.g. appendicitis.

2- In the wall:
- Ptosed kidney or floating kidney due to exhaustion of supporting fat leading to kink the ureter.
- Tumors.
- Fibrosis.

3- In the lumen: Stones, Ureteritis cystica.

165
Q

What are the causes of renal pelvis obstruction?

A
  • Stones and tumors in the renal pelvis.
166
Q

What are the effects of urinary tract obstruction?

A
  • Sudden acute obstruction cause reflex anuria.
  • Incomplete gradual obstruction or complete intermittent obstruction leading to:

A- Dilatation of urinary tract infection. Above the obstruction:
- Kidney → hydronephrosis.
- Ureter → hydroureter.
- Bladder → dilatation, hypertrophy and diverticulum formation.

B- Infection:- Pyelonephritis, pyonephrosis, pyoureter and cystitis.

C- Urinary calculi.

167
Q

What is hydronephrosis?

A
  • It is dilatation of calyces and renal pelvis with pressure atrophy of renal parenchyma due to lower down obstruction.
168
Q

What is the gross appearance of hydronephrosis?

A
  • Size Increased. “Swelling”
  • Outer surface: Lobulated.
  • Cut section: Cortex is atrophic and forms thin walled sac filled with fluid and communicating with each other and with the renal pelvis
169
Q

What is the microscopic appearance of hydronephrosis?

A
  • Atrophic tubules and glomeruli.
170
Q

What are the complications of hydronephrosis?

A
  • Secondary infection , hypertension “Na & Water Retention” and chronic renal failure.
171
Q

What is the definition of pyonephrosis?

A
  • It is a chronic suppurative inflammation of the renal pelvis, calyces and interstitium with obstruction .The kidney is converted to a bag of pus.
172
Q

What are the causes of pyonephrosis?

A

• Pyelonephritis with obstruction.

• Secondary infected hydronephrosis

173
Q

What is the gross appearance of pyonephrosis?

A

-Size: increase

  • Capsule: Thick and adherent with decortication. “Due to fibrosis”
  • Outer surface: Irregular due to underlying locules of pus.
  • Cut surface: Thin atrophic cortex, dilated calyces communicating with each other and with dilated pelvis forming locules of pus.
174
Q

What are the effects of urinary tract obstruction on the urinary bladder?

A

1- Dilatation.

2- Compensatory hypertrophy of the muscles with thick prominent trabeculae separated by depressions. “To compress the returning urine”

3- Herniation of the mucosa over the depressions leading to false diverticulae.

4- Failure of compensatory mechanisms leading to huge bladder dilatation with thin wall.

175
Q

What is bladder diverticulate?

A
  • It is local dilatation producing a pouch-like projection.
176
Q

What are the types of bladder diverticulate?

A

1- Congenital: True diverticulum. Its wall is formed of the whole thickness of the urinary bladder.

2- Acquired: It is a false diverticulum. Its wall is formed of the mucosa only.

177
Q

What is the pathogenesis of diverticulum information?

A
  • Herniation of the mucosa over depressions between the hypertrophied muscle bundles (trabeculations) resulted due to the effect of obstruction .
178
Q

What are the complications of bladder diverticulate?

A
  • Stagnation, infection, stones, ulceration, perforation and malignancy
179
Q

What are the tumors of the kidney?

A

1- Benign Tumors→ Very rare
a. Renal Adenoma / Tubuloadenoma
b. Angiomyolipoma
c. Oncocytoma

2-Malignant tumors:

180
Q

What are the main characteristic of renal adenoma?

“Adenoma —> related to the glands as they have the same type of cells”

A
  • small Pale nodule on the renal cortex
181
Q

What is the M/E of renal adenoma?

A
  • Benign tubular cells that can appear as Papilloma.
182
Q

What is the prognosis of renal adenoma (Tubulo-adenoma)?

A
  • It is not critical (LEAVE ME ALONE lesion)
    Renal adenomas increase in frequency with age, and are asymptomatic, usually found at autopsy.
183
Q

What is the definition of angiomyolipoma?

“Bigger”

A
  • Angio = vascular , myo = smooth muscle cells ,
    lipoma= lypomatous lesion.
184
Q

What is the N/E of angiomyolipoma?

A
  • It can be large and bilateral→ compresses the kidney
185
Q

What is characteristic for angiomyolipoma?

A
  • It is very vascular→ can cause hemorrhage.
186
Q

What is the N/E of oncocytoma?

“Like first but bigger”

A
  • Similar to tubuloadenoma (but much bigger in size).
  • can be mistaken for RCC “as begnin tumors are very rare”
187
Q

What is M/E oncocytoma?

A
  • benign cells are called Oncocytes (reddish granular cells which are rich in mitochindria)
188
Q

What is the main characteristic about oncocytoma?

A
  • Large tumor with a central scar which could be seen in imaging.
189
Q

What is the most common kidney tumor?

A
  • Renal adenocarcinoma (Hypernephroma).
190
Q

What is the origin of renal cell carcinoma?

A
  • Renal tubules. “Especially PCT”
191
Q

What is the epidemology of renal cell carcinoma?

A

-It often affects male patients who are between 50 and 70 year. -It occurs in two ways:

1- Inherited→ 10%→ Absent VHL (von Hippel-Lindau) tumor suppressor gene.
2- Sporadic→ 90%

192
Q

What is the clinical presentation of renal cell carcinoma?

“‏دم بكمية كبيرة”

A

Renal cell carcinoma patients are usually present with:

a. Macroscopic hematuria→ the most common presentation. “In the form of clots - painless”

b. Flank pain, which is a lateral pain between the last rib and the iliac crest. “Wag3 elgnab - due to compression”

c. Abdominal mass.

d. Hyper tension: This tumor sometimes increases renin secretion.

e. Weight loss: Sudden weight loss is generally on of the most common signs of malignancies.

f. Pyrexia of unexplained cause. “Fever”

g. Polycythemia : This tumor has a paraneoplastic syndrome of Erythropoietin secretion which will stimulate RBC production(erythropoiesis) .

h. And sometimes –unfortunately- the patient doesn’t notice anything until he presents with metastatic symptoms ie:
i. Severe headache→ Metastasis to the brain.
ii. Pathological fractures→ Metastasis to the bones.

193
Q

What is the N/E of renal cell carcinoma?

A
  • Arises from any part of the kidney. “As tubules are everywhere”
  • It is pseudocapsulated. “Due to compression of tissues by growing tumor”
  • Cut surface shows variable colors:
    . Golden yellow due to excess lipid contents of the cells. . . Brownish red due to excess vascularity and hemorrhage. . Whitish due to bands.and patches of fibrous tissue.
  • Cysts containing serous, mucinous, hemorrhagic or necrotic material may be seen.
194
Q

What is the M/E of renal cell carcinoma?

A
  • Cell arrangment
  • Stroma
  • Cells
195
Q

What is the cell arrangement of RCC?

A
  • Cells are arranged either in tubules, papillae or papillary cystadenocarcinoma pattern.
196
Q

What are the charachetreistcs of the stroma in RCC?

A
  • Delicate, thin vascular.
197
Q

What are the cells in RCC?

A
  • The cells are either:
  • Clear cells: This is the commonest. They are large, uniform, rounded or polyhedral with well defined border, clear abundant cytoplasm (due to its content of lipids and glycogen). The nucleus is small, rounded and central.
  • Tall columnar
  • Cuboidal: with granular cytoplasm.
  • Spindle cells
198
Q

How does renal cell carcinoma spread?

A
  • Local: To the renal pelvis, capsule and surrounding tissue.
  • Blood: The cells frequently form thrombus-like masses into renal vein tributaries and inferior vena cava.
  • Lymphatics: To the lumber and para-aortic lymph nodes.
  • Cannon ball appearance if it gives metastasis to her lung
199
Q

What is the origin of nephroblastoma?

A
  • Embyonic tumor arises from persisting immature cells of kidney rudiments called nephrogenic rests.
200
Q

What are nephrogenic rests?

A
  • They are foci of persistent nephrogenic cells resembling those of developing kidney.
201
Q

What is the shape of nephrogenic rests?

A
  • They are small tubular structures composed of cuboidal epithelium with darkly stained nuclei.
202
Q

What does the presence of nephrogenic rests indicate?

A
  • Presence of such nephrogenic nests in the other grossly uninvolved kidney is the cause of development of Wilm’s tumor later on in this kidney .
  • So, the tumor may arise bilaterally in the same time or later on.
203
Q

What is epidemiology of nephroblastoma?

A

Age: Common in children between 2-10 years.

  • It is the most common primary tumor and abdominal tumor in children.
204
Q

What is the clinical presentation of nephroblastoma?

A
  • Most common presentation is with a big abdominal mass that could be obviously noticed even by his family.
  • The child usually fails to thrive, he is immunosuppressed and his growth is delayed
  • He can also be present with HTN (Nephroblastoma is one of the rare causes of hypertension in children).
205
Q

What is the gross appearance of nephroblastoma?

A

-May be bilateral.
- It remains enclosed within the kidney capsule.
- It is soft and fleshy.
- Cut surface is homogeneous grey.

206
Q

What is the microscopic picture of nephroblastoma?

A

It is an adeno-sarcoma:

  • Sarcomatous elements: Short, spindle
    or rounded embryonal dark cells, striated muscles, cartilage, bone, myxomatous tissue.
  • Carcinomatous elements: Acini, imperfect tubules
    and glomerulus –like structures.
207
Q

What is the spread of nephroblastoma?

A

Local: To the capsule and surrounding tissues

Lymphatics: To the lumbar and para aortic lymph nodes.

Blood: Rapid spread.

208
Q

What are the tumors of the urinary bladder?

A
  • Benign
    1. Epithelial: Transitional cell papilloma.
    2. Non epithelial: Leiomyoma, fibroma, lipoma.
  • Malignant
209
Q

In what age do malignant tumor of the bladder occur?

A
  • Most of the patients are above 50 year old.
210
Q

What are the predisposing factors for malignant urinary bladder tumors?

“BASIT”

A

1- UrinaryBilharziasis

2- villous papilloma

3- Workers in some industries e.g. aniline dyes “‏صبغة صناعية”, rubber and benzidine “‏عوادم السيارات”

4- Cigarette smoking

5-Prolonged high doses of analgesics.

211
Q

What is the clinical presentation of malignant urinary bladder tumor?

A
  • The most common presentation of bladder tumors is (GROSS PAINLESS HEMATURIA).

“Thus, when a patient is complaining about passing blood and blood clots in his urine, put in your mind both renal cell carcinoma and bladder tumors”

212
Q

What is the gross appearance of malignant urinary bladder tumor?

A
  • It may form a fungating mass or malignant ulcer or diffuse infiltrating tumor .
  • In addition; the transitional cell carcinoma may have a papillary villous pattern
213
Q

What are the histopathological types of malignant bladder tumors?

A

1- Transitional cell carcinoma
2-Squamous cell carcinoma
3-Adenocarcinoma
4- Anaplasticcarcinoma

214
Q

What is the M/E of transitional cell carcinoma?

A
  • Transitional cell carcinoma in situ
  • Papillary transitional cell carcinoma:
  • Papillary and infiltrating transitional cell carcinoma
215
Q

What is the shape of transitional cell carcinoma in situ?

A
  • Replacement of normal urothelium by highly atypical cells having the criteria of malignancy which include: Loss of normal polarity and arrangement of the normal transitional epithelium, pleomorphism, hyperchromatism, frequent mitotic figures and increased nuclear cytoplasmic ratio. There is no invasion of the basement membrane.
216
Q

What is the shape of papillary transitional cell carcinoma?

A
  • The tumour is arranged in papillae with thin vascular cores not infiltrating the muscles or subepithelial tissue.
217
Q

What is the shape of popular and infiltrating transitional cell carcinoma?

A
  • The tumour forms solid sheets infiltrating the subepithelial tissue with or without invasion of the muscles.
218
Q

From where does squamous cell carcinoma arise?

A
  • It arises on top of squamous metaplasia
219
Q

What is the shape of squamous cell carcinoma?

A
  • Sheets of malignant squamous cells with variables degrees of keratinization and cell nests formation.
  • The more differentiated tumors show more cell nests.
220
Q

What is the shape of adenocarcinoma?

A
  • Malignant Glands in different grades of differentiation forming irregular glands
221
Q

From where does adeno carcinoma rise?

A
  • It arises on top of glandular metaplasia or remnants of urachus at the apex of urinary bladder.
222
Q

What is signet ring adenocarcinoma?

A
  • the cells may have a signet ring appearance in a background of mucin.
223
Q

What is anaplastic carcinoma?

A
  • Tumour cells lose any pattern of differentiation
224
Q

What is the incidence of Bilharizial carcinoma?

A
  • Common in Egypt. Males are affected more than females. At younger age.
225
Q

What is the M/E of Bilharizial carcinoma?

A
  • squamous cell carcinoma mainly and to lesser extent adenocarcinoma.
226
Q

What is the pathogenesis of Bilharzial carcinoma?

A
  • Chronic bilharzial cystitis leading to squamous and glandular metaplasia and predisposes to Gm-ve cystitis.
  • Bacteria break down dietary nitrites and nitrates secreted in urine forming the carcinogenic material nitrosamines which acts as initiator of carcinoma.
227
Q

What is the spread of carcinoma of the urinary bladder?

A

Local: To the wall of bladder and surroundings

Lymphatic: To pelvic lymph nodes.

Blood: By the systemic circulation to the lungs then bones and other organs.

228
Q

What are the benign tumors of the nose and paranasal sinuses?

A

A. Epithelial:-
- Squamous cell papilloma & Transitional cell papilloma.

B. Mesenchymal: Osteoma - Chondroma
- Fibroma - Capillary hemangioma.

229
Q

What are the malignant tumors of nose and paranasal sinuses?

A

A. Epithelial:-
- Squamous cell carcinoma & Transitional cell carcinoma.

B. Mesenchymal: Sarcoma - Lymphoma.

230
Q

What are benign tumors of nasopharynx?

A

Nasopharyngeal Fibroma “ Juvenile Angiofibroma”.

231
Q

What is the incidence of nasopharyngeal fibroma “juvenile fibroma”?

A

Uncommon - Male children.

232
Q

What is the origin of nasopharyngeal fibroma?

A

From the fibrous tissue of periosteum.

233
Q

What is the N/E of nasopharyngeal fibroma?

A
  • Non-capsulated greyish pink highly vascular mass projecting into the nasopharynx.
  • It may extend into the Nasal cavity - Cheek - Orbit.
  • It may cause bone destruction by pressure atrophy.
234
Q

What is the M/E of nasopharyngeal fibroma?

A
  • Small vascular spaces set in poorly cellular fibrous tissue.
235
Q

What are the complications of nasopharyngeal fibroma?

A

Bleeding (Epistaxis).

236
Q

What are malignant nasopharyngeal tumors?

A
  1. Squamous cell carcinoma.
  2. Adenocarcinoma: Related to wood dust (Furniture workers).
  3. Anaplastic carcinoma (Related to Epstein Barr virus).
237
Q

What are the tumors of the tonsils?

A
  • Benign: Squamous cell papilloma.
  • Malignant: Squamous cell carcinoma - Lymphoma.
238
Q

What are benign tumors of the larynx?

A

Squamous Cell Papilloma

239
Q

Compare between adult squamous cell papilloma and juvenile papillomatosis acc to:-

Incidence
Age
Etiology
N/E
M/E
Prognosis

A

Incidence: Commonest - Less common

Age: Adult - Children

Etiology: Chronic irritation - Human Papilloma Virus

N/E:
- single, On the vocal cord (Glottic), Small sessile soft mass
- Multiple, On and outside vocal cord, Small pedunculated soft mass

M/E: Squamous cell papilloma

Prognosis:
-No recurrence after removal & May turn malignant
- Recurrence, No malignant transformation & Spontaneous cure at puberty

240
Q

What are malignant tumors of the larynx?

A

Squamous Cell Carcinoma

241
Q

What is the incidence of squamous cell carcinoma of the larynx?

A

Common laryngeal tumor.

242
Q

What are pre-cancerous lesions for squamous cell carcinoma of the larynx?

A

Squamous cell papilloma (Adult) - Leukoplakia.

243
Q

What is the pathology of squamous cell carcinoma of the larynx?

A

1) Verrucous carcinoma

2) Classic invasive squamous cell carcinoma

244
Q

What are the characteristics of verrucous carcinoma?

A
  • Uncommon low grade papillary squamous cell carcinoma.
  • Superficially invasive and has a relatively good prognosis.
245
Q

What are the types of classic invasive squamous cell carcinoma of the larynx?

A

Intrinsic - Extrinsic

246
Q

Compare between intrinsic and extrinsic types of classic invasive squamous cell carcinoma of the larynx according to:-

Incidence
Sex
Age
N/E
M/E
Radiosensitivity
Spread
Prognosis

A

Incidence: 80% - 20%

Sex: Male - Female

Age: Above 50 years - Below 50 years

N/E:
- From vocal cords, Fungating - Ulcerating
Infiltrating
- Outside the vocal cords, Infiltrating - Ulcerating
Fungating

M/E: Well differentiated SCC - Undifferentiated SCC

Radiosensitivity: Radiosensitive

Spread:
1) Local: To the surroundings
2) Lymphatic: To cervical LNs
3) Blood: Late - Disseminates extensively

Prognosis:
- Good due to:-
1) Early diagnosis (Early hoarseness of voice)
2) Slowly growing
3) Well differentiated
4) Easily removed due to Fungating growth pattern

  • Bad due to:-
    1) Late diagnosis (Dysphagia then laryngeal signs &symptoms)
    2) Rapidly growing
    3) Undifferentiated
    4) Difficult removal due to Infiltrating growth pattern
247
Q

What are the benign tumors of the lung?

A
  1. Epithelial: Squamous cell papilloma.
  2. Mesenchymal: Lipoma (Subpleural) - Fibroma - leiomyoma.
  3. Adenochondroma (Lung hamartoma): It’s a hamartoma consists of mixture of mature cartilage with cleft-like spaces ling by flat or respiratory epithelium - Fat - Fibrous tissue - Blood vessels.
248
Q

What are locally malignant tumors of the lung?

A

Bronchial Carcinoid tumor (Bronchial Adenoma)

249
Q

What is the origin of bronchial adenoma?

A
  • Arises from neuro-endocrine cells in the bronchial mucosa.
250
Q

What is the incidence of bronchial adenoma?

A
  • Female more than males - 40 years - 1-5% of lung tumors.
251
Q

What is the Pathology of Bronchial Adenoma?

A

it’s APUDoma. It’s a locally malignant or slowly growing malignant tumor that occasionally metastasizes.

252
Q

What is the N/E of bronchial adenoma?

A
  • Usually it grows inside the bronchus as a polypoid mass.
  • it may grow outside the bronchus if both directions “Dumbbell shaped tumor”.
  • About 30% metastasize to hilar LNs and occasionally to distant sites (liver).
253
Q

What is the M/E of bronchial adenoma?

A
  • It consists of groups of small uniform ounded cells having deeply stained nuclei with little mitosis.
  • These groups are separated by delicate
    stroma.
254
Q

What are the complications of bronchial adenoma?

A
  1. Hemoptysis.
  2. Bronchial obstruction leading to bronchiectasis, collapse etc.
  3. Frank malignancy.
  4. Carcinoid syndrome: Tumor cells secrete bioactive substances “ Serotonin (5HT) + Histamine” which pass to circulation causing a syndrome composed
255
Q

What are the symptoms of carcinoid syndrome?

A
  • Tumor cells secrete bioactive substances “ Serotonin (5HT) + Histamine” which pass to circulation causing a syndrome composed of:

a) Flushing of the face (Due to VD).
b) Diarrhea and bronchospasm (Due to stimulation of smooth muscles).
c) Tricuspid and Pulmonary valve stenosis (Fibroblastic proliferation).
d) Tryptophan deficiency and Pellagra.

Y1B4 (RESP & RAU) 📙 (8 decks)

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