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Pathology A > chronic inflammation > Flashcards

chronic inflammation Flashcards

1
Q

What is chronic inflammation? like what are its characteristics ya know?

A
  • prolonged beyond weeks
  • active inflammation, tissue destruction and repair
  • persist until stimulus eradicated
  • can be injurious
  • affect tissue cannot resolve, but undergo healing
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2
Q

what are the 3 causes of chronic inflammation

A

unresolved acute inflammation, prolonged exposure to toxic agents and immune mediated responses

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3
Q

describe how unresolved acute inflammation leads to chronic inflammation using osteomyelitis

A
  • persistent bone marrow infection
  • chronic inflammatory cells stimulate bone resorption and despoit bone tissue
  • can be fixed with antibiotics and surgery
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4
Q

describe how prolonged exposure to toxic agents can lead to chronic inflammation in terms of prosthetics

A

wear particles released from degradation

- granulaomatous inflammation where clustered t cells activate macrophages and transform into epithelial-like cells

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5
Q

describe immune mediated reaction rheumatoid arthritis

A
  • own cells = foreign
  • t cells activate macrophages and cytokines
  • stimulate synovial cells
  • pannus formation = destroy cartilage and lose joint space
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6
Q

what are the main features of chronic inflammation

A

mononuclear cell infiltration
tissue destruction
attempted healing and replacing damage tissue with ct

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7
Q

what are the systemic effects of chronic inflammation

A 
arthralgia and myalgia 
fever 
leukopenia 
chronic fatigue + mood disorders 
GI complications
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8
Q

what is the most dominant cell type in chronic inflammation

A

macrophages

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9
Q

how are macrophages activated

A

signals from t helper cells (lymphocytes)

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10
Q

what is the function of macrophages

A

chemical mediators, killing bacteria and cells, remove EV debris, fibrin, foregin particles, granulomatous inflammation

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11
Q

what is the lifespan of macrophages and describe their maturation

A 
in blood (monocyte) = 1 day 
in tissue = months -> years 
maturation mediated by growth factors, cytokines, adhesion molecules, cellular interactions
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12
Q

what are the positives and negatives of macrophage activity

A 
positives = increases lysosomal effects and reactive oxygen species which is toxic to microbes. also helps fibroblast proliferation and stimulates angiogenesis 
negatives = products are responsible for tissue injury and dissolution of EC matrix
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13
Q

what is granulomatous inflammation

A

a focal collection of macrophages, epitheliods, and multinucleated giant cells that have amassed an indigestible substance
its a protective response that leads to tissue necrsosis because of the secretory cells

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14
Q

what is a mn giant cell and what are the different types

A

its a fusion of macrophages
langhans = nuclei arranged peripherally
foreign body = indigestible material within the cytoplasm

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15
Q

what are the steps of granulomatous inflammation

A

injury -> inability to digest agent -> acute failure -> persistent injury -> macrophage recruitment -> giant cell formation -> cell mediated response => granuoma

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16
Q

features of lymphocytes

A 
proliferate bone marrow + tissues 
long lined 
some present normally 
antigen activated
release mac act ctokines 
pos feedback loops
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17
Q

features of plasma cells

A

humoral
terminally differentiated B cells
1 kind of antibody produced
common lymphoid progenitor

18
Q

features of fibroblasts

A

secrete EC matrix components

for immune and wound healing

19
Q

feature of endothelial cells

A

angiogenesis

20
Q

features of eosinophils

A

IgE mediated reactions

granules are toxic proteins

21
Q

what are the outcomes of chronic inflammation

A

if you remove stimulus = repair through fibrosis and scar formation
but healed tissue is not parenchymal tissue
often loses function
if stimulus not removed = poor prognosis, dependant on causative agent

22
Q

what are the aims of wound healing

A

remove damaged tissue
fill gap caused by tissue destruction
restore structural continuity and function if possible

23
Q

what does regenerative healing mean and what are the possibilities for labile, stable and permanent cells

A

replaced with parenchymal tissue
labile = can regenerate quickly
stable = can regenerate slowly
permanent = cannot regenerate

24
Q

name the 3 phases of wound healing

A

reactive, reparative, remodelling

25
Q

describe the reactive phase of wound healing

A

haemostasis and vascular spasm
platelet coagulation and clot formation
inflammation, decrase pathogens, cells migration + vasodilation (signs of acute inflam)

26
Q

describe the reparative phase of wound healing

A 
epithelialisation = grows under the clot, separating clot and underlying tissue = bridge between wound edges 
granulation = fibroblasts, myofibs (like fibroblasts w/contractile potential), macs, collagen, caps, lymphatic vessels
27
Q

describe the remodelling phase of wound healing

A

macrophages, scar formation, realignment of tissue

28
Q

describe primary intention healing

A

wound with close edges
fibroblasts and granulation tissue
closure = 1 week
return function with minimal scarring

29
Q

describe secondary intention healing

A 
wound with far edges 
healing from bottom up 
loss cells and tissue 
inflammation is intense 
carries lots of necrotic debris and exudate 
increased granulation tissue fills until the epithelia regenerates increased collagen synthesis 
wound contraction is frequent 
scar tissue replaces normal tissue
30
Q

what is the function of granulation tissue

A

to protect against microbial invasion and further injury

fills base up with new tissue and vasculature and replaces necrosis until that is replaced with scarring

31
Q

what are the components of granulation tissue

A

new, thin blood vessels

fibroblasts, keratinocytes, endothelial cells, inflammatory cells phagocytose dead tissue

32
Q

what are the sequential changes of granulation tissue

A
  • vascular (new caps, macs, support cells that replace area of tissue damage)
  • fibrovascular (fibroblasts, caps, macs)
  • fibrous (fibroblasts -> collagen = align and deposit increase contraction)
33
Q

stages of regenerative healing in a fracture

A

haematoma -> granulation tissue -> soft calus -> hard callus -> remodelling

34
Q

describe the haematoma an granulation tissue stage of regenerative healing

A

happens at time of fracture and severs bv and preiosteum
leads to blood clot
invastion of fibsm macs, oclasts + obblasts
invasion turns the clot into soft fibrous mass of GT

35
Q

describe the soft callus stage of regenerative fracture healing

A

angiogenesis
collagen within GT
chondroblasts => patches of firbrocartilage
GT gets stronger but is still malleable

36
Q

describe the hard callus stage in regenerative fracture healing

A

oblasts produce bone ring around fracture site
joining ends together
makes sure broken bone is immobilised and prevents reinjury or misalignment

37
Q

describe remodelling phase of regenerative fracture healing

A

hard calus = 3-4 months
oclasts dissolve broken bone fragments
oblasts deposit spongy bone

38
Q

describe the reactive phase of nonregenerative MI healing in terms of hours

A

6-12 = myocytes die, no macroscopic changes, high eosinophilia
12-24 hours = high eosinophilia + myocyte necrosis
24-72 = high neutrophils infiltrating tissue and removing necrotic myocytes, nuclei fade from cells (karyolsis)

39
Q

describe the reparative phase of non-regenerative healing in MI

A

3 days post MI = fibroblasts + endothelial cells infiltrate injury
weeks after = GT

40
Q

describe remodelling phase of nonregenerative MI healing

A

6-8 weeks = healed myocaridum
fibs lay collagen
infalm cells drain via lymps
mature scar

41
Q

local factors taht influence healing

A 
infection
mechanical
foreign bodies
vascular supply
size, location, type

Pathology A (26 decks)

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