Date post: | 07-May-2015 |
Category: |
Health & Medicine |
Upload: | guruindia2012 |
View: | 144 times |
Download: | 1 times |
1
PATHOLOGY PRACTICAL
2
•LOBAR PNEUMONIA•BRONCHIECTASIS
3
4
5
6
7
1.COMMUNITY-ACQUIRED BACTERIAL ACUTE PNEUMONIAS (BACTERIAL)Streptococcus PneumoniaHaemophilus InfluenzaeMoraxella CatarrhalisStaphylococcus AureusKlebsiella PneumoniaePseudomonas AeruginosaLegionella Pneumophila
2.COMMUNITY-ACQUIRED ATYPICAL (VIRAL AND MYCOPLASMAL) PNEUMONIAS (NON-BACTERIAL)
Influenza InfectionsSevere Acute Respiratory Syndrome (SARS)
3.NOSOCOMIAL PNEUMONIA4.ASPIRATION PNEUMONIA5.LUNG ABSCESS
6.CHRONIC PNEUMONIAHistoplasmosis, MorphologyBlastomycosis, MorphologyCoccidioidomycosis, Morphology
7.PNEUMONIA IN THE IMMUNOCOMPROMISED HOST8.PULMONARY DISEASE IN HUMAN IMMUNODEFICIENCY VIRUS INFECTION
PULMONARY INFECTIONS
8
9
10
11
12
13
NORMAL
CXR
14
15
16
17
18
19
20
21
22
23
• The specimen is a slice of the left lung.• The upper lobe is relatively normal, except
for an old scar near the apex of the lung caused by tuberculosis.
• The major abnormality is that the lower lobe is uniformly consolidated (airless and solid) due to lobar pneumonia, with inflammatory cells and exuded plasma filling the airspaces.
• The shaggy material on the pleural surface is fibrin, a protein derived from fibrinogen in exuded plasma.
24
25
26
27
28
29
30
• Microscopic Appearances:
• Sections through the lower lobe show dilated, congested blood vessels in the alveolar walls.
• The alveolar spaces are filled with inflammatory cells, mainly neutrophils, and inflammatory exudate, including fibrin.
• There are large aggregates of fibrin on the pleural surface.
31
• Pneumonia is an acute inflammation of the airspaces of the lung, usually caused by bacterial infection.
• This woman died of pneumonia affecting an entire lobe of the lung, before the advent of antibiotics.
• Nowadays, it is uncommon to die in the acute stages of lobar pneumonia because Streptococcuspneumoniae ("the pneumococcal"), which is the bacterium that typically causes a lobar distribution of pneumonia, is sensitive to various antibiotics.
• However, there is an increasing incidence of pneumococcal resistance to Penicillin - usually the most effective antibiotic in this situation.
32
33
VIRAL PNEUMONIAS• Frequently “interstitial”, NOT alveolar
34
35
BRONCHIECTASIS
36
Definition • Abnormal and irreversible dilatation of bronchi
and bronchioles greater than 2.m.m. in diameter developing secondary to inflammatory weakening of the bronchial walls.
• Persistent cough with expectoration of copious amounts of foul smelling purulent sputum.
• Post infectious cases commonly develop in childhood and early adult life.
37
Aetiology
• Hereditary and congenital factors• End bronchial obstruction• Infections.
38
Infections-Micro-organisms
• Measles and Pertussis• Adeno & Influenza virus• Bacterial infection with virulent
organisms: S.aureus, Klebsiella Anaerobes
• Atypical mycobacteria• Mycoplasma• HIV• Tuberculosis• Fungi
39
IMPAIRED HOST DEFENCE
• Local causes: End bronchial obstruction• Generalized impairment:
1. Immunoglobulin deficiency
2. Primary ciliary disorders
3. Cystic fibrosis
40
41
42
• Persistent or recurrent cough with purulent sputum.
• Hemoptysis• Initiating episode: Severe pneumonia, or
insidious onset of symptoms or asymptomatic or non-productive cough – dry bronchiectasis in upper lobe,
• Dyspnoea, wheezing – widespread bronchiectasis or underlying COPD.
• Exacerbation of infection: Sputum volume increase, purulence or blood.
43
DIAGNOSIS
• Clinical• Radiology: Chest XR: May be non-specific
mild disease – normal XRC advanced disease – cysts + fluid levelsperibronchial thickening, “tram tracks”, “ring shadows”
CT Scan: Peribronchial thickening, dilated bronchioles.
• Sputum culture: Pseudomonas aeuruginosa, H.influenzae.
44
45
46
47
48