View
230
Download
2
Category
Tags:
Preview:
Citation preview
PULMONARY TUBERCULOSISPULMONARY TUBERCULOSIS
ByBy Dr. Abdelaty ShawkyDr. Abdelaty Shawky
Assistant professor of pathologyAssistant professor of pathology
1
* Definition: chronic infective granuloma affecting nearly all body systems but mainly the lungs.
* Predisposing factors:a) Environmental: low socioeconomic level, bad general hygiene, overcrowding.b) Personal factors: cases of low resistance e.g. malnutrition – AIDS - D.M.
2
* Causative Agents: T.B. bacilli
* Structure o f T.B. bacilli:
Tuberculoprotein core covered by glycolipid.
* Types of TB Bacilli:
• Human type: transmitted from human to human by
droplet infection.
• Bovine type: transmitted from cows to human by
ingestion of infected milk.
3
* Types of T.B:
I. Primary (1ry) T.B.II. Secondary (2ry) T.B.
4
Primary tuberculosisPrimary tuberculosis(childhood type)(childhood type)
* Age:- Occurs in young persons < 3 years, who are: non immunized, and infected for the first time.* Sites:
1. Lung. 2. Nose. 2. Intestine. 3. Tonsil. 4. Skin.
5
* Methods of infection: 1. Inhalation 2. Ingestion 3. Direct contact.
* Tissue reaction (Reaction of the body against T.B bacilli): proliferative (tubercle formation).
6
*Pathogenesis of tubercle (T.B granuloma) formation:
A. In the first 24 hours:
•Carbohydrate coat of the bacilli recruits neutrophils, which
fails to kill it.
•Bacilli are taken by surface macrophages to the deep parts
of the tissues, draining lymphatics & L.Ns.
•Macrophages process the bacilli releasing the purified
protein derivative PPD, then express it on the surface
carried on MHC class II molecules.
7
B. After 10-15 days:
- T.B granuloma is formed as follow;
•Macrophages secrete IL-12 which activate the naïve CD+4 T
lymphocytes to T helper (TH1) cells.
•TH1 cells release lymphokines:
1. INF-y (interferon Gama) leads to macrophage
activation.
2. IL-2 (interleukin-2) leads to lymphocyte proliferation.
3. TNF (tumor necrosis factor) & lymphotoxins8
• The accumulated macrophages undergo a
morphologic transformation into epitheial-like cells
(epithelioid cells). Some epithelioid cells coalesce to
each other to form langhan’s giant cells. Collections of
epithelioid cells, langhans giant cells and a collar of
lymphocytes is termed (non-caseating tubercle).
9
C. After 2-3 weeks:
•The tubercles undergo central caseation necrosis (very
rare with 1ry T.B), the causes are:
1. Relative central ischemia.
2. Lymphotoxins.
3. Proteolytic enzymes of neutrophils.
10
* Gross picture of tubercle:
Small, 1-3 mm, with central yellow caseation and
grey periphery.
* Microscopic picture of tubercle: Central caseating material (structureless, eosinophilic
material, epithelioid cells, macrophages, Langhan’s giant
cells, lymphocytes and peripheral fibroblastic reaction.
11
Non-caseating tubercles
12
Pulmonary TuberculosisPulmonary Tuberculosis
13
Lung is a favorable site for T.B. (easy inhalation and
aeration).
Types:Types:
1. 1ry pulmonary T.B.
2. 2ry pulmonary T.B.
14
1ry pulmonary T.B1ry pulmonary T.B
15
* Age:
• Children.
* Mode of infection:
• Droplet infection.
* Lesions:
• More in the right lung than the left lung.
• 1ry pulomnary complex (Ghon’s triad).
16
Primary pulmonary complex (Ghon’s triad)
Consists of 3 parts:
1. Parenchymatous lesion (Ghon’s focus):
- Tubercles which develop at the lower parts of upper
lung lobes or upper parts of lower lung lobes,
subpleural.
- Consists of non-caseating and caseating tubercles.
1. Tuberculous lymphangitis.
2. Tuberculous lymphadenitis.
17
18
GhonGhon’’s focuss focus
19
* Fate:* Fate:
A. Good fate: A. Good fate:
- Healing by fibrosis and dystrophic calcification.
- Formation of a dormant T.B focus.
B. Bad fate: B. Bad fate: Spread.
1. Local.
2. Lymphatic.
3. Hematogenous
4. Natural passage: through the lumen of bronchi20
2ry2ry PULMONARY T.B PULMONARY T.B
21
* Age: adults who are infected or vaccinated before.
* Mode of Infection:
1. Reactivation of dormant focus.
2. Exogenous by inhalation.
* Lesions:
• It is only caseating tuberclous reaction (Assman’s focus or
Simon’s focus) develop at the apical portion of the lung.
• No complex formation.
22
Apical pulmonary T.BApical pulmonary T.B
23
24
25
* The Fate of 2ry pulmonary T.B:* The Fate of 2ry pulmonary T.B:
A. Good fate: A. Good fate:
- Regression and healing. In cases of good immunity.
B. Bad Fate: B. Bad Fate:
- Progression and spread in cases of poor immunity.
1. Cavitary Tuberculosis
2. Chronic fibrocaseous pulmonary tuberculosis
3. Acute tuberculous bronchopneumonia & acute
caseous pneumonia.26
ThanksThanks
27
Recommended