BIOM3002 Lecture Notes - Lecture 3: Lobar Pneumonia, Squamous Metaplasia, Lung Abscess
26 May 2018
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HISTOPATHOLOGY LECTURE THREE
Respiratory pathology:
1. Pneumonia, abscesses
2. Causes and features pulmonary embolism
3. Obstructive and restrictive lung diseases [bullous emphysema
with air trapping; asbestosis with lung fibrosis]
4. Smoking and lung cancer [squamous metaplasia; squamous cell
carcinoma; mesothelioma and asbestosis]. CYTOKINAL GF
MESSAGE AS MACROPHAGES CAN'T REMOVE ASBESTOS.
Defence mechanisms against pulmonary disease:
Physical:
A) filtering within upper airways [cilia on bronchial
epithelia cells]
B) reflexes including coughing
C) muco-ciliary escalator [goblet and ciliary cells]
D) alveolar phagocytic inflammatory cells [macrophages] reside
in lung therefore rapid-acting; esinophilic and large when
active
Cellular: Alveolar immunologic mechanisms including IgA
Pneumonia:
o Lung inflammation caused by bacterial/viral infection
o Air sacs fill with neutrophils, oedema, fibrinogen, pus –
may become solid
o Acute inflammation may affect all lung tissue
[BRONCHOPNEUMONIA] or only one lobe [LOBAR PNEUMONIA]
Abscess:
o Localised neutrophils, pus and necrosis in tissues, usually
= acute inflammation [heat, redness, swelling and oedema]
and frequently caused by bacteria
o Either needs to be removed by phagocytes or rebuilt by
fibrosis
o Sometimes = cysts with a CT border if body can't rebuild
Infections of the lung – pneumonias:
o Most common lung infection
o Lungs most common site human infections
o Streptococcus pneumonia most common cause
o Infection and inflammation = central processes
o Alveoli = filled with inflammatory exudate and lung becomes
solid
Bronchopneumonia:
o Focal areas consolidation throughout lobes
find more resources at oneclass.com
find more resources at oneclass.com
Lobar pneumonia:
o Affects whole lobes
Histology pneumonia general:
o Alveolar pores of Kohn allow disease transmission
o Alveoli more distinct when infected as BVs dilated
o Higher power view = dilated, distinct capillaries,
neutrophils [mostly] and histocytes [un-activated
macrophages] + fibrin
Pattern of infection depends on:
o Virulence of bacteria
o Extent of infection [focal vs whole lobe]
o Hosts defence
Bronchopneumonia:
o Common
o Often extension of bronchitis
o Opportunistic infections of young, old, immunocompromised
o May become confluent and then hard to distinguish from lobar
pneumonia
Lobar pneumonia:
o Rare due to antibiotics however resistance strains are
problematic
o Highly virulent bacterial infection that can infect even the
healthiest individuals
Pneumonia complications:
1. Some types of bacteria lead to necrosis – may form abscess
o Local inflammation within an organ
o Can lead to ulcer
o Bacterial infection, necrosis, localised collection acute
inflammatory cells – usually neutrophils
2. Emphysema: infection spreads to pleural cavity,
lung expansino restricted again
3. Organisation of exudate – lung solidifies
4. Dissemination of infection: heart valves, brain,
pericardium, kidneys, spleen, joints
Ulcer:
o Inflammation in epithelial surface
o Necrotic base
o Inflammatory cells [acute and chronic]
o Putting down granulation [collagen, vessels, fibroblasts,
macrophages] [rebuilding tissue]
o Epithelial layer can be regenerated
find more resources at oneclass.com
find more resources at oneclass.com
