Inflammation & Repair

Explanation :
Granulomatous inflammation is a form of chronic inflammation characterized by collections of activated macrophages, often with T lymphocytes, and sometimes associated with necrosis.
Granuloma formation is a cellular attempt to contain an offending agent that is difficult to eradicate. In this attempt there is often strong activation of T lymphocytes leading to macrophage activation, which can cause injury to normal tissues.
Epitheloid cell predominant.

Reference: Davidson 23rd, Page: 72 , Box : 4.4

Dominant cellular player in chronic inflammation is macrophage

ESR is increased disproportionately to CRP in Bacterial endocarditis

Explanation :
Acute phase proteins :
CRP,Ceruloplasmin,Cryoglobulin
Serum amyloid A protein 
Fibrinogen
Ceruloplasmin
Heptoglobin
Ferritin
Lactoferrin

The richest source of histamine is mast cell

Explanation :
Chronic inflammation is characterized by the
following:
• Infiltration with mononuclear cells, which include macrophages, lymphocytes, and plasma cells.
• Tissue destruction, induced by the persistent offending agent or by the inflammatory cells.
• Attempts at healing by connective tissue replacement of damaged tissue, accomplished by angiogenesis (proliferation of small blood vessels) and, in particular, fibrosis.

Keloid is excess production of scar tissue that is out of proportion to the wound

Explanation :
Acute inflammatory exudates :
Contains neutrophil
Rich in Fibrinogen 
Have protective function
Due to change in blood vessels

Explanation :
Purulent inflammation is characterized by the production of pus, an exudate consisting of neutrophils, the liquefied debris of necrotic cells, and edema fluid. The most frequent cause of purulent (also called suppurative) inflammation is infection with bacteria that cause liquefactive tissue necrosis, such as staphylococci; these pathogens are referred to as pyogenic (pus-producing) bacteria.
A common example of an acute suppurative inflammation is acute appendicitis.

Explanation -
Immediately after an injury the narrow incisional space is filled with clotted blood containing fibrin and blood cells. 

Within 24 hours, Neutrophil appear at the margin of the incision moving towards the fibrin clot.

Explanation -
Preformed chemical mediators :
Histamine 
Serotonin
Lysosomal enzyme 

[Robbins 9th 98]

Explanation :
Local factor influence wound healing -
Local blood supply
Denervation
Local infection
Foreign body
Haematoma
Necrotic tissue
Mechanical stress
Protection ( dressing)
Surgical techniques
Types of tissues

Explanation :
Causetive agents of pain in acute inflammation :
Prostaglandin 
Bradykinin
Increased K+
Decreased pH
Tissue reaction
5-HT/ serotonin

Leukocyte migration through endothelium is called diapedesis

Beneficial effect of inflammation is control of infection

Explanation :
C-reactive protein (CRP) is a protein made by the liver.
The level of CRP increases when there's inflammation in the body.
Synthesis upregulated by TNF.

Complication of wound healing due to deficient scar formation is wound dehiscence

Main source of TNF is macrophage

[Robbins 9th 90]

Explanation :
Source of serotonin in acute inflammation -
Platelet 
Neuroendocrine cell

Predominant acute inflammatory cell in first 24 hours is neutrophil

Exuberant scars that recur after excision are called desmoids

Explanation: In Pregnancy, old age and multiple myeloma, isolated elevation of ESR not CRP.

[Robbins 9th 71]

Ref. Robbins 9th p-93

Explanation :
Effects of complement in acute inflammation :
Vasodilation 
Increased vascular permeability 
Phagocytosis
MAC
Chemotaxis
Leucocyte adhesion

Explanation -
Granulation tissue found in :
Wound
Ulcer
Sinus tract
Pyogenic granuloma 
Fistula
Wall of abscess
Granulation tissue absent in :
All types of granulomatous inflammation except pyogenic granuloma 
Scar
Necrosis
Organizing haematoma
Congestion.

Explanation :
Inflammatory arthritis -
Morning stiffness  - present 
Joint pain - Worse after rest and improved after movement 
Temperature - Raised
Joint effusion - Present
Joint crepitation  - Absent

Explanation 
Acute inflammatory oedema is due to -
Increased vascular permeability by endothelial cell contraction
Increased capillary hydrostatic pressure 
Breakdown of large molecules of tissue proteins
Increased fluidity of the tissue ground substance. 

[Robbins 9th 71]

Granulation tissue easily bleeds on touch due to rupture of new capillaries

Emigration of leukocyte to the site of injury is called chemotaxis

Vit A essential for epithelialization, Vit C essential for collagen synthesise , VitD easential for bone formation

Cause of redness in acute inflammation is increase in blood flow

The process of coating a particle to target it for ingestion is called opsonization

Explanation :
Contraction of endothelial cells resulting in opening of interendothelial gaps is the most common mechanism of vascular leakage. It is elicited by histamine, bradykinin, leukotrienes, and other chemical mediators. 

Explanation :
Sites of moist gangrene -
Intestine is the commonest sites
Mouth
Pressure area
Vulva
Scrotum
Anterior abdominal wall
Thigh

Dominant leukocyte in pus is neutrophil

Arachidonic acid derived mediators are called eicosanoids