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PoD > ChronInflam > Flashcards

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
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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
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3
Q

Cells types involved in chronic inflammation

A
  • Lymphocytes
  • Plasma cells
  • Macrophages
  • Fibroblasts
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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
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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
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6
Q

B Cells

A
  • Differentiate to plasma cells
  • Facilitate immune response and have an immune memory
  • Collaborate with macrophages: antigen presenting cells
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7
Q

Plasma cells

A
  • Differentiated B cell
  • Antibody production
  • Intermediate size
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8
Q

Macrophages

A
  • Remove debris
  • Role in immune system, antigen presenting cell
  • Bone marrow, blood tissues
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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
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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
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11
Q

Fibroblasts

A
  • Motile cells
  • Metabolically active
  • Make and assemble structural proteins: collagens and various other types
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12
Q

Causes of primary chronic inflammation

A
  • Material resistant to digestion
  • Exogenous substance
  • Endogenous substances
  • Granulomatous inflammation common in all of these
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13
Q

Material resistant to digestion

A
  • Mycobacteria, Brucella, viruses

- Cell wall resistant to enzymes

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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

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15
Q

Endogenous substances

A
  • Necrotic tissue, keratin, hair

- Similar concept as exogenous, you can’t get phagocytosed

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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
  1. Phase of acute inflammation
  2. Granulation tissue formation
  3. Local angiogenesis - new vessels grow
  4. 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

PoD (33 decks)

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