Fibroblast

Giant cells

Lymphocyte

Thrombocyte

Histiocyte

Usually affects healthy adults

Bronchial damage will take place is there is no timely treatment

Lung fibrosis

Empyema

Complete resolution is common without treatment

Retroviruses carry viral oncogenes which through processes of reverse transcription and integration become part of infected cellular DNA which causes unregulated proliferation of the cell

Environmental factors such as ingested carcinogens or ionising radiation cause initiation (irreversible damage to DNA) and hence created mutated cells. Promotion then occurs whereby these damaged cells proliferate leading to formation of a tumour

Proto-oncogenes can suffer mutations leading them to be activated inappropriately. These oncogenes can tehn stimulate cell proliferation via a number of mechanisms such as increased expression of growth factors such as PDGF. Genes controlling apoptosis can undergo mutation which stops them from functioning properly. Cell therefore cannot be effectively destroyed resulting in accumulation of cells and therefore a tumour.

Tumour suppressor genes normally prevent uncontrolled cell proliferation. A mutant version of one copy of this gene can lead to the formation of a tumour.

Invasion into veins

Invasion into arteries

Invasion into lymphatics

Within an epithelium but not through basement membrane

Invasion into anatomcal spaces e.g. peritoneum

T4N1M0

T3N4M0

T2N4M1

T4N0M0

T4N0M1

Very few mitotic figures

Pleomorphic nuclei

Active secretions of stame type as tissue origin

Fibrous capsule surrounding tumour

Very circumscribed appearance

Tumour cells can secrete hormones such as adrenaline

Their cells are of monoclonal origin i.e. all daughter cells of a single parent cell

Their cells are all genetically identical

Normal cells would cease to grow when they come into contact with anotehr cell but tumour cells do not

Tumours >2mm in size require their own vasculature

Hilar tumour showing glandular differentiation and mucus over production

A peripheral lung tumour showing glandular differentiation mucus over production and a varyig degree of mitotic acitivity

Hilar tumour showing glandular differentiation

A peripheral lung tumour with glandular differentiation which may show signs of metastasis using cytological testing of cells taken from the tumour only

Peripheral lung tumour showing no cytokeratin staining following immunochemistry of a core lung biopsy

Amphoterecin B binds to ergosterol and may form a pore which leaks fungal intracellular contents

Acts to stimulate fungal apoptosis by stimulatin BCL-2 and BCL-XL

Amphotericin B binds to cholesterol in the plasma membrane and disruption of the plasma membrane as a result

Amphotericin B inhibits ergosterol synthesis which is an important component of the cellular membrane

Amphoterecin B stops glucan synthesis. Without glucan fungi cannot form an effective cell wall

Cryptococcus neoformans

Group A strep

Hib

Strep pneumoniae

Group B strep

Lymphatic flow increases to dilute toxins

Chemotaxis occurs in response to inflammatory mediator release

The hallmark of acute inflammation is presence of neutrophils

There are no systemic effects

Specific disease pattern of release of cytokines by inflammatory cells which orchestrates in what order new cells are stimulated to proliferate to regenerate tissue

Order in which new layers of tissue are formed to replace those lost by necrosis - preseves tissue function

Formation of new blood vessels to supply regenerating tissue with oxygen and nutrients

Replacement of specialised tissue with ECM proteins known as granulation tissue

Replacement of injured cells by proliferation of healthy cells of same type to restore function of the tissue

Hyperplasia

Dysplasia

Hypertrophy

Atrophy

Metaplasia

Cingulate

Transtentorial

Subfalcine

Tonsillar

Amoxicillin

Do nothing

Supportive therapy

Clarithromycin

Psychological counselling