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
Q
Foreign body type
A
- 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
Q
Silicone associated
A
- 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
Q
Examples of non-infective granulomas
A
- 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
Q
Factors involved in promoting healing and repair
A
- Phase of acute inflammation
- Granulation tissue formation
- Local angiogenesis - new vessels grow
- Fibrosis and scar formation
29
Q
Granulation tissue formation
A
- 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
Q
Fibrosis and scar formation
A
- Phagocytosis of fibrin
- Myofibroblasts move in and lay down collagen
- Contraction of scar
31
Q
Overall favoured wound healing
A
- Cleanliness
- Apposition of edges (no haematoma)
- Sound nutrition: wound healing is a catabolic process
- Metabolic stability and normality
- Normal inflammatory and coagulation mechanisms
32
Q
Angiogenesis
A
- New vessels form capillary buds
- Vascular Endothelial Growth Factor (VEGF) released by hypoxic cells stimulates proliferation
- Enzyme blood supply to enter damaged tissue
33
Q
Nature of Process of Angiogenesis
A
- 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
Q
Impaired wound healing
A
- Dirty, gaping wound, large haematoma
- Poorly nourished, lack of vitamins C, A
- Abnormal CHO metabolism, diabetes, corticosteroid therapy
- Inhibition of angiogenesis
35
Q
Fracture healing 1
A
- 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
Q
Fracture healing 2. New bone
A
- 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
