Inflammation

Broadly steps of inflammation are:

Recognition of pathogen/injurous agent
---> recruitment of WBC to the area which then get activated
---> eliminate the pathogen
----> inflammation gets switched off and repair
1. Vascular response
Main component   Dilatation of blood vessels --> ↑blood flow
 ↑permeability of vessels --> plasma protein & WBC leave
Patterns circulation
Morphologic patterns  Leucocyte emigrate into damaged area --> get activated &
Serous Inflammation remove offending agent
Fibrinous Inflammation
Suppurative/ Purulent Inflammation 1. Cellular response
 Are all caused by chemical mediators
 Inactive endothelium gets activated --> allow adhesion
Outcomes? neutrophils
1. Complete resolution  Inactive neutrophils gets activated --> for phagocytosis, bacterial
2. Healing by connective tissue killing & generation of inflammatory mediators
replacement (fibrosis)  Neutrophils develop ability to actively move in a directional
3. Progression--> Chronic inflammation fashion from vessels towards area of damage
margination--> rolling--> adhesion--> migration

In inflammation there are chemical mediators that play a role

Granulomatous inflammation: Distinctive pattern of chronic inflammation.
Seen in TB, Syphilis, Leprosy, Sarcoidosis, Crohns Disease
Characterised by collection of epithelioid histiocytes (macrophages
which are transformed into epithelium like cells) surrounded by
collar of mononuclear leukocytes, principally lymphocytes and
plasma cells.
Types of granuloma: Foreign body granuloma (talc, suture)
Immune granuloma (caused by agents capable of inducing a cell mediated response)
 Growth disorders
Mechanisms of adaptation:
Hypertrophy-- Increase in size, usually has a increased functional demand;
eg.body builders, ventricular hypertrophy

Atrophy--reduce cell size, assoc with decrease function e.g is disuse atrophy
in immobilisation in fracture cast. testes atrophies in old age. Sometimes
cells can reduce in number due to physiological process and this is involution
e.g thymus involutes in adolescence, myometrium involutes post partum.

Hyperplasia- increase in cell number; can be physiological as in breast

development during puberty, BPH.

Metaplasia - change from one mature cell type to the another

eg. Barretts esophagus, Smoking
Necrosis Nuclear changes – Karyolysis ( basophilia of chromatin fades dt loss of DNA)
Pkynosis (nuclear shrinkage & ↑ basophilia dt chromatin condensation)
Karyorrhexis (fragmentation)

Coagulative necrosis Liquefactive necrosis

Denatured proteins & enzymes Digestion of dead cells  liquid viscous mass.
Seen in ischemia. Seen in focal bacterial/fungal infections.
Eg: wedge shaped kidney infarct Necrotic material is creamy yellow – pus
Seen in hypoxic injury of CNS
Caseous necrosis Fibrinoid necrosis
TB Seen in immune reactions involving blood vessels (vasculitis)
Granuloma--- Ag-Ab complexes deposited
Cheese like necrosis surrounded by epithelioid cells, Pink amorphous material – fibrin like
lymphocytes, histiocytes and Langerhans type of
multinucleated giant cells
Fat necrosis
Gangrenous necrosis Not a specific pattern
Not a specific pattern Usually applied to damaged fat
Usually applied to limb  loss of blood supply Ac pancreatitis

Apoptosis:
Is a mechanism of programmed cell death
Is a normal cellular process that eliminates cells which are no longer needed, no longer viable or are
potentially harmful
Causes: Physiological OR Pathological
Embyogenesis DT DNA damage
Involution of hormone dependent tissue Improper folded proteins &
- hormone withdrawal Cell death in certain infections
Cell loss in proliferating cell population
- immature lymphocytes in bone marrow & thymus
Neoplasia
 Characteristics of cancer
Evasion of apoptosis
Limitless replicative potential
Sustained angiogenesis
Ability to invade and metastasize

Grading of a cancer is based on the

degree of differentiation

Staging of cancers is based on the size

of the primary lesion, its extent of
spread

Modes of spread of malignant neoplasms/METASTASIS

There are four main modes of tumour spread:

▪Local invasion/Direct spread. Invasive tumours tend to spread into surrounding tissues by the most direct route.
Examples include carcinoma of the breast invading overlying skin or deeply into underlying muscle and carcinoma of
the cervix invading rectum or bladder.
▪Lymphatic spread. Tumours may spread via lymphatic vessels draining the site of the primary tumour. Neoplastic cells
are conducted to local lymph nodes where they may form secondary tumours, e.g. breast cancer spreading to lymph
nodes in the axilla or carcinoma of the tongue spreading to lymph nodes in the neck.
▪Vascular spread. Tumours can spread via the veins draining the primary site. Gut tumours tend to spread via the portal
vein to the liver where secondary tumours are very common. In the systemic circulation, neoplastic cells may be
trapped in the lung to form pulmonary metastases.
▪Transcoelomic spread. Certain tumours can spread directly across coelomic spaces, for example across the peritoneal
or pleural cavities. Carcinoma of the ovary may spread transcoelomically to produce large numbers of metastatic
deposits on the peritoneal surfaces.