7. healing Flashcards
chronic inflammation mediated by
Mediated by macrophages, lymphocytes, and plasma cells
chronic inflammation characterized by three simultaneously ongoing components
It is characterized by three simultaneously ongoing components, in varying combinations:
1. Active inflammation
2. Tissue destruction
3. Attempts at repair
macrophages activated by
classical by microbial products
alternative by il13 and il4
Granulomatous inflammation
Characterized by granuloma, which is a microscopic aggregation of epithelioid histiocytes (activated macrophages), usually surrounded by giant cells, a rim of lymphocytes and plasma cells
Type of granuloma
Noncaseating granulomas
caseating
Noncaseating granulomas
lack central necrosis.
Common etiologies include
reaction to foreign material,
sarcoidosis,
beryllium exposure,
Crohn disease,
Leprosy and
at scratch disease
Caseating granulomas
exhibit central necrosis and are characteristic of
tuberculosis,
fungal infections and
Syphilis gumma
Infectious granulomas
Bacterial: tuberculosis, leprosy, syphilis, cat scratch disease and lymphogranuloma venerum(Chlamydia)
Fungal: histoplasmosis, cryptococcosis, coccidiodomycosis, blastomycosis
Helminthic: schistosomiasis
Protozoal: leishmaniasis, toxoplasmosis
Noninfectious or immune granulomas
Usually are noncaseating granulomas
Sarcoidosis, primary biliary cirrhosis and hypersensitivity pneumonitis
Types of Multinucleate giant cells
langhans - nuclei around periphery of cell
- in TB
foreign body type - nuclei scattered around
Morphologic features of chronic inflammation
Chronic abscess e.g. Empyema
Sinus e.g. Tuberculous lymphadenitis
Fistula e.g. Fistula in ano
Ulcer e.g. skin or gastric peptic ulcer
Fibrosis e.g. urethral or esophageal stricture
termination of acute inflammatory response
neutrophils short half life
stop signals switch pro to anti inflammatory
macrophages release anti inflammatory cytokines TGF-B and il-10
neural impulse cholinergic
Neutrophils synthesize precursors of active lipoxins and pass these to platelets, where they are converted to mature lipoxins.
Tissue Repair
refers to the restoration of tissue architecture and function after an injury
tissue repair consists of two processes
- tissue regeneration and
- fibrous organization (scar formation)
Liver regeneration by
TNF and IL-6 G0 to G1
HGF and EGF progression through the rest of the cell cycle
FGF and TGF-α are mitogenic for hepatocytes
Key Players in Healing and Repair
- Cells – Macrophages, lymphocytes, platelets, endothelial cells, fibroblasts etc.
- Cytokines, Growth factors, Enzymes
- Extracellular matrix: Structural proteins (eg. collagens), Adhesive glycoproteins (eg. cadherins) Proteoglycans and Hyaluronan
ECM Exists in Two Different Forms
- Interstitial matrix
- Basement membrane
…………..are found in the granulation tissue and are important for the contraction of wounds and the prevention of dehiscence
Myofibroblasts
functions of growth factors 3
- Cell cycle activation (by direct stimulation or removal of blocks that inhibit cell cycle)
- Prevention of apoptosis
- Enhanced synthesis of cellular proteins
Phases of healing
1 the inflammatory phase;
2 the proliferative phase;
3 the remodeling phase (maturing phase).
Granulation tissue
replace lost tissue and template for scar production
The process of healing through granulation tissue formation is called
organization
Fetal cutaneous wounds heal without scar why?
TGF β isoforms (non-fibrogenic),
lack of osteopontin, &
the absence of a TH2 response
Primary union and secondary union
Primary union(healing by first intention) is seen in incised wounds with opposed edges (clean and uninfected wound).
Secondary union(healing by secondary intention) is seen in open wounds with separated edges, extensiveloss of cells and large defects.
Regaining Wound Strength is result of
Is a result of type III collagen is replaced by type I collagen,
excess collagen synthesis,
cross-linking of collagen and
↑↑ fiber size
There are three main steps in bone repair
- Procallus (soft tissue callus) formation
- Osseous callus formation
- Remodelling
- Osseous callus formation
Healing of muscle
if muscle sheath intact - heals
eg zenker in typhoid
if muscle muscle sheath not intact - scar
eg volkman ischemic contraction
Cardiac muscle healing
: Replaced by the permanent scar tissue
cns healing
Neuroglial cells only show proliferation called gliosis.
pns healing
Proliferation of Schwann cells and fibrils from distal ends is seen in response to injury.
1 mm per day
Painful nodule “pseudotumor” results from
a failure of the outgrowing axons to find their distal
Factors that retard wound healing
local and systemic factors
local and systemic factors
Local; Decreased blood supply, Denervation, Local infection, Foreign body, Mechanical stress, Large amounts of haemorrhage and necrosis
Systemic; Old age, Malnutrition, Anemia, Obesity, Drugs (steroids), Systemic infection, Genetic disorders, eg, Marfan syndrome and Ehlers–Danlos disease, Diabetes mellitus, Uremia and Vitamin and trace metal (zinc and copper) deficiency
Abnormality in Wound Healing
Deficient scar formation
Excessive formation of the repair components and contraction
Atrophic /hypotrophic scar (sunken)
Implantation cyst
Pigment changes: depigmented (vitiligo) /hyperpigmented
