ChronInflam Flashcards
1
Q
Formation of granulation tissue mechanism and function
A
- Capillaries grow
- Plasma proteins accessed
- Macrophages
- Fibroblasts lay down collagen
- Collagen replaces inflammatory exudate
- Tissue defects are patched
- Replace necrotic tissue
- Pulls together tissue
2
Q
Granulation tissue can progress to
A
- Fibrous tissue - scar
- Fibrosis as a problem: adhesion between loops of bowel following peritonitis
- Can progress to chronic inflammation
3
Q
Cells types involved in chronic inflammation
A
- Lymphocytes
- Plasma cells
- Macrophages
- Fibroblasts
4
Q
Lymphocytes
A
- Part of immune system
- Small round cells with lots of subtypes and functions
- 2 main types: T cells and B cells
- Main functions: immune response and memory
5
Q
T Cells
A
- Produce cytokines: attract and hold macrophages, excite macrophages, get other cells involved, permeability
- T-cells produce interferons: antiviral effects and attract and stimulate other cells
6
Q
B Cells
A
- Differentiate to plasma cells
- Facilitate immune response and have an immune memory
- Collaborate with macrophages: antigen presenting cells
7
Q
Plasma cells
A
- Differentiated B cell
- Antibody production
- Intermediate size
8
Q
Macrophages
A
- Remove debris
- Role in immune system, antigen presenting cell
- Bone marrow, blood tissues
9
Q
What can a macrophage become?
A
- Monocyte
- Histiocyte
- Activate macrophage
- Epitheloid cell (looks like an epithelial cell but is a macrophage)
- Giant cell
10
Q
Mechanism of macrophages
A
- Move from blood
- Take over from neutrophils
- Contain enzymes
- Produce interferons and other chemicals which destroy and influence
- Crux of chronic inflammation is if these responses tend not recede
11
Q
Fibroblasts
A
- Motile cells
- Metabolically active
- Make and assemble structural proteins: collagens and various other types
12
Q
Causes of primary chronic inflammation
A
- Material resistant to digestion
- Exogenous substance
- Endogenous substances
- Granulomatous inflammation common in all of these
13
Q
Material resistant to digestion
A
- Mycobacteria, Brucella, viruses
- Cell wall resistant to enzymes
14
Q
Exogenous substances
A
- Sutures, metal and plastic
- You don’t get an immune response as they’re sterile but you get chronic inflammation
15
Q
Endogenous substances
A
- Necrotic tissue, keratin, hair
- Similar concept as exogenous, you can’t get phagocytosed
16
Q
Clinical presentations of chronic inflammation
A
- No specific sore bit as an anatomical pointer
- Malaise and weight loss
- Loss of function
17
Q
Loss of function in chronic inflammation examples
A
- Autoimmune thyroiditis (functional gland destruction) - hypothyroidism
- Crohn’s disease (GI tract ulceration and fibrosis) - pain, diarrhoea, gut obstruction
- Leprosy (cutaneous nerve destruction) - loss of sensation, destroying the tissue
18
Q
Why do we see chronic inflammation?
A
- Arising from acute inflammation: large volume of damage, inability to remove debris, fails to resolve (super infection)
- Primary lesion: no preceding acute phase, only see chronic changes
19
Q
Adverse effects of tissue scarring
A
- After granulation tissue is characteristic of organisation
- A scar can form but this can lead to fibrosis which means there are adhesions between loops of bowel following peritonitis
- Can progress to chronic inflammation
20
Q
Granulomatous inflammation characteristics
A
- Particular kind of inflammatory response characterised by granulomas in tissues and organs
- Stimulated by indigestible antigen. E.g. macrophages can’t get rid
- Serious infections and idiopathic diseases
- Diseases important on a global scale are granulomatous inflammatory diseases
21
Q
Granulomas
A
- Aggregates of epithelioid macrophages in tissue
- May contain giant cells
- May surround dead material
- May be surrounded by lymphocytes
- Contain neutrophils, eosinophils
- May be in response to indigestible antigen
- Many are type IV hypersensitivity reactions
22
Q
Giant cells
A
Granulomas comprise of epithelioid histiocytes (aka macrophages)
- Large cytoplasm, multiple nuclei
- Several types
- Giant cells can be present even when there is no granuloma present
23
Q
Examples of types of giant cell
A
- Langhans type
- Foreign body type
- Silicone associated
24
Q
Langhans type
A
- Classically found in TB
- Peripheral rim of nuclei
- Large eosinophillic cytoplasm
25
Foreign body type
- Often associated with pyogenic granulation tissue
- Acutely inflamed
- Neutrophils, pus
- Typically you can see slits in the cell which could be acetabular particules or glass
26
Silicone associated
- Rupture silicone implants: usually but not always breast, vacuoles contain leaked silicone
- Produces granulomatous response
- Can be found around about the affected area and axillary lymph nodes
- You can also see the typical bubbles in the histology dye to the inability to dissolve`
27
Examples of non-infective granulomas
- Rheumatoid disease: tissue specific autoimmune disease
- Sarcoidosis: classical clinical picture, unknown cause, fibrosis in the lung fields
- Crohn's disease: chronic inflammatory bowel disease, unknown cause. Ulceration of mucosa, you can see the mucous disappear into granulation tissue microscopically
28
Factors involved in promoting healing and repair
1. Phase of acute inflammation
2. Granulation tissue formation
3. Local angiogenesis - new vessels grow
4. Fibrosis and scar formation
29
Granulation tissue formation
- Healing by primary intention: In surgical wounds you allow for a minimal gap, which means a small amount of granulation tissue
- Healing by secondary intention: On larger wounds, there is a lot of granulation tissue ingrowth in a lot of different directions which means there is a lot more contraction and scarring as it crosslinks.
30
Fibrosis and scar formation
- Phagocytosis of fibrin
- Myofibroblasts move in and lay down collagen
- Contraction of scar
31
Overall favoured wound healing
- Cleanliness
- Apposition of edges (no haematoma)
- Sound nutrition: wound healing is a catabolic process
- Metabolic stability and normality
- Normal inflammatory and coagulation mechanisms
32
Angiogenesis
- New vessels form capillary buds
- Vascular Endothelial Growth Factor (VEGF) released by hypoxic cells stimulates proliferation
- Enzyme blood supply to enter damaged tissue
33
Nature of Process of Angiogenesis
- Limits propagation and reinstates flow
- Malignant tumours: angiogenesisas tumour is hypoxic, stimulates tissue around it to improve blood supply
- Fibrosis and scarring in atherosclerosis: similarities with chronic inflammation
34
Impaired wound healing
- Dirty, gaping wound, large haematoma
- Poorly nourished, lack of vitamins C, A
- Abnormal CHO metabolism, diabetes, corticosteroid therapy
- Inhibition of angiogenesis
35
Fracture healing 1
- Same principle as wound healing
- Fracture and a haematoma (sub-periosteal haemorrhage)
- Bits of dead bone and soft tissue are mixed together in a bit of a mess
- Acute inflammation, organisation, granulation tissue and macrophages remove debris
- Granulation tissues contain osteoblasts as well as fibroblasts
36
Fracture healing 2. New bone
- Osteoblasts lay down woven bone
- Nodules of cartilage present
- Followed by bone remodelling: osteoclasts remove dead bone, progressive replacement of woven bone by lamellar bone, reformation of cortical and trabecular bone
