chronic inflammation

Question 1

what is the cell population in chronic inflammation

Answer 1

lymphocytes, plasma cells, macrophages

Question 2

what are the features of chronic inflammatino

Answer 2

tissue or organ damage, necrosis and loss of function (doesnt go back to how it was before)
can follow on from ongoing acute inflammation but also arises as 1y pathology
tends to be long term
leads to scarring and fibrosis

Question 3

define chronic inflammation

Answer 3

prolonged inflammatory response that involves a progressive change in the type of cells present at the site of inflammation. It is characterized by the simultaneous destruction and repair of the tissue from the inflammatory process.

Question 4

clinical presentations of chronic inflamamtion

Answer 4

• often no specific sore bit
• non-specific symptoms
• malaise and weight loss
• loss of function as tissue is damaged by chronic inflammation

Question 5

when does chronic inflammation occur

Answer 5

• arising from acute inflammation: large volume of damage, inability to remove debris, fails to resolve
• arising as a 1y lesion: only see chronic changes

Question 6

outcomes of acute inflammation (organisation)

Answer 6

granulation tissue
angiogenesis
healing and repair
fibrosis and formation of a scar

Question 7

angiogenesis

Answer 7

new vessels form capillary buds from existing vessels, VEGF released by hypoxic cells which stimulates proliferation, enzyme secretion aids the process, enable blood supply to enter the damaged tissue

Question 8

angiogenesis and organisation in thrombosis

Answer 8

limits thrombus propagation

reinstatement of flow

Question 9

angiogenesis in malignant tumours

Answer 9

angiogenesis occurs as tumour grows

anti VEGF drugs are being used to combat certain tumours as they prevent endothelial growth

Question 10

granulation tissue mechanism and function (result of acute inflammation)

Answer 10

• capillaries grow into inflammatory mass
• access of plasma proteins
• macrophages from blood (monocytes) and tissue (histiocytes)
• fibroblasts lay down collagen to replace damaged tissue
• collagen replaces inflammatory exudate
• patches tissue defects
• replaces dead or necrotic tissue
• contracts and pulls together

Question 11

acute and chronic interface

Answer 11

acute inflamamtion –> acute + chronic inflammation (exudate, neutrophils; lymphocytes plasma cells, fibroblasts, fibrosis) –> chronic inflammation

Question 12

pyogenic granulation tissue

Answer 12

acute + chronic inflamamtion

Question 13

products of granulation tissue

Answer 13

fibrous tissue - scar
fibrosis as a problem - adhesions between loops of bowel following peritonitis
can progress to chronic inflammation

Question 14

examples of scars

Answer 14

acne - chronic from acute
cholecystitis - gall bladder, walls become very thick and fibrous with lots of vasculatiry
peptic ulcer - stomach, ulcer in the gastric antrum
osteomyelitis

Question 15

primary chronic inflammation

Answer 15

• autoimmune disease
• lymphocytes, plasma cells, macrophages, fibrosis
• material resistant to digestion
• exogenous substances
• endogenous substances
• granulomatous inflammation common

Question 16

primary chronic inflammation - AI disease

Answer 16

adaptive immunity
autoantibodies directed against own cell and tissue components
damage/destroy organs, tissues, cells, cell components
thyroiditis, rheumatoid disease, pernicious anaemia, systemic lupus erythromatosis

Question 17

primary chronic inflammation - material resistant to digestion

Answer 17

mycobacteria, brucella, viruses

cell wall resistant to enzymes

Question 18

primary chronic inflammation - exogenous substances

Answer 18

sterile: sutures, metal and plastic, e.g. joint replacements, mineral crystals
dont provoke immune response

Question 19

primary chronic inflammation - endogenous substances

Answer 19

necrotic tissue, keratin, hair

cannot easily be phagocytosed

Question 20

rheumatoid disease

Answer 20

swan neck deformity, swellling and dislocation of the joints

rheumatoid nodule - chronic inflammation at extensor surfaces, usually around the elbows

Question 21

pathogenesis of chronic inflammation

Answer 21

• cells and their roles (lymphocytes, plasma cells, macrophages, fibroblasts)
• tissue components: granular tissue, collagen

Question 22

role of lymphocytes in chronic inflammation

Answer 22

B cells: differentiate to plasma cells (antibodies), facilitate immune response, act with macrophages (APC), immune memory
T cells: produce cytokines (attract, hold and activate macrophages; influence permability of nearby cells), T cells produce interferons (antiviral effects), damage and kill other cells and destroy antigen
NK cells: destroy antigens and cells

Question 23

role of plasma cells in chronic inflammation

Answer 23

antibody production

Question 24

role of macrophages in chronic inflammation

Answer 24

remove tissue debris, APC, monocyte (blood)/histiocyte (tissue); found in bone marrow, blood vessels and tissue
motile phagocytes move from blood, take over from neutrophils, contain lysozymes, produce interferons

Question 25

role of fibroblasts in chronic inflammation

Answer 25

motile cells, metabolically active, make and assemble structural proteins

Question 26

granulomatous inflammation

Answer 26

- characterised by presence of granulomas in tissues and organs (generally occur due to indigestible antigens) - many serious infectious and idiopathic diseases - NOT THE SAME AS GRANULATION TISSUE

Question 27

what are granulomas

Answer 27

aggregates of epitheliod macrophages in tissue ball of cells that may contain giant cells and may surround dead material, they can be surrounded by lymphocytes contain neutrophils (most dont) and eosinophils

Question 28

most granulomas are type...

Answer 28

IV hypersensitivity reactions (cell mediated immunity)

Question 29

giant cells

Answer 29

granulomas compromise epitheliod histiocytes possibly fusion of macrophages to form larger cells giant cells can also occur in pyogenic granulation tissue

Question 30

langhans type giant cells

Answer 30

large cells found in granulomatous conditions. They are formed by the fusion of epithelioid cells (macrophages), and contain nuclei arranged in a horseshoe-shaped pattern in the cell periphery. classically found in TB large eosinophilic cytoplasm

Question 31

foreign body type giant cells

Answer 31

``` often associated with pyogenic granulation tissue acutely inflamed neutrophils, pus organisation giant cells ```

Question 32

silicone associated giant cells

Answer 32

ruptured silicone implants usually but not always breast vacuoles contain leaked silicone leads to enlarged lymph node

Question 33

Warthin-Finkeldy type giant cells

Answer 33

- classic in measles | central cluster of nu

Question 34

infectious granulomatous diseases - relevant to global health

Answer 34

mycobacterium tuberculosis mycobacterium leprae treponema pallidum

Question 35

mycobacterium tuberculosis:

Answer 35

tuberculosis | caseous necrosis - dead tissue surrounded by macrophages, giant cells, lymphocytes)

Question 36

mycobacterium leprae

Answer 36

leprosy | treated with mutlidrug therapy, granulomatous inflammation causes peripheral nerve damage

Question 37

treponema pallidum

Answer 37

(syphilis): sensitive to benzylpenicillin; primary chancre, syphilitic gumma, snail track ulcers

Question 38

non-infective granulomas - not uncommon in global medicine

Answer 38

rheumatoid disease sarcoidosis chron's disease

Question 39

rheumatoid disease

Answer 39

tissue specific auto-immune disease, unknown cause | degenerative collagen becomes surrounded by macrophages in rheumatoid nodules

Question 40

sarcoidosis

Answer 40

disease involving abnormal collections of inflammatory cells that form lumps known as granulomas. The disease usually begins in the lungs, skin, or lymph nodes. unknown cause

Question 41

chron's disease

Answer 41

chronic inflammatory bowel disease, unknown cause

Question 42

wound healing

Answer 42

process of repair after tissue damage acute injury followed by phase of acute inflammation and granulation tissue formation (try to keep these to a minimum to reduce damage) local angiogenesis fibrosis and scar formation

Question 43

surgical healing

Answer 43

healing by primary intention minimal gap and blood clot small amount of granulation tissue small linear scar

Question 44

healing of larger defects

Answer 44

healing by secondary intention larger blood clot filling the gap, much more granulation tissue growing into the clot, contraction due to tighter collagen fibres, scarring

Question 45

sequence of events in wound healing

Answer 45

``` injury, blood clot, acute inflammation, fibrin growth factors and cytokines involved granulation tissue growth angiogenesis phagocytosis of fibrin myofibroblasts move in and lay down collagen contraction of scar re-epithelialisation ```

Question 46

favouring wound healing

Answer 46

``` cleanliness apposition of edges sound nutrition metabolic stability and normality normal inflammatory and coagulation mechanisms local mediators are important ```

Question 47

impaired wound healing

Answer 47

``` leads to infection dirty, open wound, large haematoma poorly nourished abnormal CHO metabolism, diabetes, corticosteroid therapy inhibition of angiogenesis ```

Question 48

fracture healing

Answer 48

- repair bony structures as well as soft tissue - trauma, fracture, haematoma - dead bone and soft tissue - acute inflammation, organisation, granulation tissue, macrophages remove debris granulation tissue contains osteoblasts as well as fibroblasts

Question 49

callus formation

Answer 49

osteoblasts lay down woven bone nodules or cartilage present followed by bone remodelling

Question 50

bone remodelling

Answer 50

oestoclasts remove dead bone progressive replacement of woven bone by lamellar bone reformation of cortical and trabecular bone