Tissue damage and Inflammation Flashcards

(69 cards)

1
Q

causes of tissue damage (7)

A

ishaemia / infarction
trauma
tempeerature changes
light exposure
chemical injury
dysregulated immunity
nutiritaonl damnage

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2
Q

how does ischemia cause tissue damage

A

reduced oxygen supply

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3
Q

how does trauma cause tissue damage

A

usually mechanical
zonular rupture - lens discloation
ciliary muscle disinsertion - leads to TM collapse and angle recession glaucoma

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4
Q

how does temeprature cause tissue damage

A

e.g. cryotheraphy causing adherive scar

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5
Q

how does light expsoure cause cell damage

A

UV generally leads to overproduction of free radicals by photons
Corneal epithelium damage in snow blindness
 Photoreceptor bombardment with photons

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6
Q

alkali injury

A

causes liquefactive necoriss
coagulates conjunctival blood vessels –> procealin white is due to limbal ischaemia
penetrates the corneal easliy
kills lens epithelium and causes sevre non-granulomatous iridocyilits

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7
Q

acid injury

A

causes coagulative necorsis
less desctrictuve

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8
Q

Argon laser

A

Wavelength: 485 - 514
Mechanism: photocoag
Use: coag from the chorocapillaris to the neuclear layer

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9
Q

frequency double Nd-YAG laser

A

Wavelength: 532
Mechanism: photocoag
Use: safer than argon for mac laser

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10
Q

diode laser

A

Wavelength: 810
Mechanism: photocoag
Use: ROP, retinal photocoagulation, destruciton of the CB

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11
Q

photodynamic laser therapy

A

Wavelength: 689
Mechanism: photoradical
Use: chorodial vascular pahtology e/g/ haemoagiams

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12
Q

Nd-YAG laser

A

Wavelength: 1064
Mechanism: photodisruptive
Use: YAG PC, P

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13
Q

excimer laser

A

Wavelength: 193
Mechanism: photoablation
Use: refractice surgery

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14
Q

femto laser

A

Wavelength: 1053
Mechanism: photoablation
Use: refractice surgery

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15
Q

PRP laser

A

destroys localished patches of the outer retina and RPE
reactive proliferation of RPE aorund white cirel (glial cell) = scar

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16
Q

transpupillary thermotherapy

A

IR to heat to 40degrees chorodial melanoms to bring about cell necrosis

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17
Q

acid injuriew

A

coagulative necorsis

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18
Q

alkali injuries

A

liquefactive necrosis
coagulates conjunctival blood vessels: “porcelain white” appearance
 Widespread limbal ischaemia and destruction of limbal stem cells

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19
Q

drusen

A

PAS positive structure, found betwen the RPE and bruchs membrane
transiet strutures
4 types: hard, soft, basal and calcific

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20
Q

hard drusen

A

Well-demarcated
PAS-positive
Made of hyaline

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21
Q

soft drusen

A

Poorly defined
Represent removal of RPE from the Bruch membrane

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22
Q

basal drusen

A

Diffuse small drusen found in the macula

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23
Q

calcific drusen

A

Refractile drusen found near areas of RPE atrophy.

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24
Q

reticular pseudodrusen

A

Found between inner segment and outer segment (IS/OS) junction and RPE
Associated with the transition to advanced forms of AMD i.e. geographic AMD.
Made of extracellular material

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25
pseudodrusen on FAF
Reduced signal from blocking and increased the signal from RPE distress.
26
mechanisms of cell death
1. necorsis = death of a group of cells, always pathological 2. apoptosis = programmed cell death
27
reversible injury
1. hydropic swelling - cell becomes swollen, usually 2nd to trauma 2. atrophy - decrease in cell size and number
28
acute inflammation
 Reaction to injury be it physical, chemical, infective, immunological  Vascular phase followed by cellular phase
29
classic signs of acute inflammation
Classic signs: redness, heat, swelling, pain, loss of function  Hyperaemia: initial vasoconstriction then dilation  Vasodilation slows blood flow causing cells to move to the sides (margination)  Exudation: protein-rich fluid moves into interstitial fluid (dilutes toxins)  Leucocyte migration for phagocytosis: extravasation and chemotaxis  Non-adaptive, no memory, non-specific
30
duration of acute inflammation and outcome
lasts 1-2 days resolve (if no tissue destruction and exudate is removed), suppurate, repair with organisation/scarring (if the exudate persists), progress to chronic inflammation. If tissue is destroyed, regeneration can occur if the lost cells are labile or stable. If permanent cells are lost, a vascularised connective tissue scar forms
31
chemical mediators in vascular pahse
 Histamine: from degranulated mast cells. Increases vascular permeability (C3a and C5a) and vasodilation of venules. Short-term effect (5-15 minutes)  Kinins: more prolonged venule and capillary vasodilation response  Prostaglandin: dilates arterioles. More persistent response (4-24 hours)
32
cell type on bacterial infection
bacterial
33
cell type on parasitic infection
eosinophil
34
cell type in viral infection
monocytes
35
neutrophil rolling
Bonds are established (by selectins on endothelium and integrins on neutrophils) between endothelium and white cells following margination (normally, both neutrophils and endothelium have negative charge and so do not contact)
36
platelet activaition
Platelet activating factor activates neutrophils and induces beta-integrins expression on their cell membranes which further promote adhesion with the endothelium
37
trigger for migration of neutrophils
ransmigration of the neutrophils between endothelial cells then occurs, stimulated by IL-8
38
chemotaxis
following transmigration, the movement of cells is mediated by chemotaxis, along the concentration gradient of chemotactic agents. It is the directional and purposive movement of phagocytic cells towards areas of injury/invasion
39
steps in chemotaxis
o Reception of signals o Response to signals (transduction)
40
examples of chemotaxis
o Cytokines from other leucocytes o Complement components (C5 and C5a) o Arachidonic acid derivatives (eicosanoids eg. leukotrienes and prostaglandin E) o Pathogens o Lymphokines (produced by T helper lymphocytes)
41
role of leucocytes
Once within the injured tissue, leucocytes can undertake phagocytosis  Recognition, aided by opsonisation o Opsonins: IgG and C3b  Bacterium/foreign object engulfed by a phagosome
42
phagosome
Phagosome fuses with lysosome: associated with the “respiratory burst” of metabolic activity producing hydrogen peroxide
43
macrophages
Within tissues, monocytes undergo enlargement, increased lysosome numbers, Golgi and ER development
44
macrophage activation
 Increased phagocytic capacity  Production of hydrolytic enzymes, pyrogen and interferon (blocks translation of viral mRNA)  Stimulates fibroblast proliferation and further polymorph production  Lymphocytes activating factor (IL-1) stimulates T helper cells
45
role of macropahges
 Stimulated by C3b  Capable of cell division  Contribute to antigen presentation  Can fuse to form multinucleated giant cells (increased phagocytic activity)  Epithelioid cells within granulomas are derived from a single macrophage (increased secretory capacity)
46
granulomatous KPs
“mutton-fat” KPs) are composed on macrophages compared to non-granulomatous KPs which are mainly lymphocytes and PMLs
47
complement systemt
 Involved in acute inflammation, phagocytosis, clotting, immune and hypersensitivity reactions (C3a and C5a are anaphylatoxins)
48
what stimulates complement
 Classical and alternative pathways are both stimulated by plasmin
49
components of the complement systtem
 C3a and C5a increases vascular permeability as above. C5a is 1000 times more active  C5b joins with C6, C7, C8 and C9 to form the membrane attack complex which is capable of cell lysis
50
plasma cascade system
Factor XII (Hageman factor) of the clotting cascade has a central role in activating 3 systems operating within plasma
51
systems operative within the plasma cascade system
 Kinin system (via activating prekallikrein) to produce potent vasodilators  Clotting cascade (via stimulating factor XI)  Complement system (via activating plasminogen to plasmin) All three have positive feedback loops to activate more Hageman factor
52
chronic inflammation
 Response to persistent pathogen/irritant (need not be infectious)  NB: acute phase does not need to be prolonged (eg. in TB it is very brief)  Cellular response predominates: mixed proliferation and destruction
53
granuloma
 failure of acute inflammatory neutrophils to clear the inciting agent, meaning macrophages take over  Derived from macrophages and their lineage  Caseation is a feature of tuberculous granuloma
54
structure of granuloma
 Inner core of macrophages and epithelioid cells with increased secretory capacity  Core surrounded by layer of activated macrophages (containing ingested microoganisms) and T lymphocytes  Outer layer containing fibroblasts and multinucleated giant cells
55
delayed hypersenitivy response and granuloma
 Response to breakdown of endogenous materials (eg. chalazion: reaction to rupture of a blocked meibomian gland duct releasing irritant keratin)  Response to exogenous non-biological materials ie. foreign body  Mainly mycobacteria eg. TB or leprosy and fungi  Unknown eg sarcoidosis (non-caseating)
56
non-granulomatous inflammation
characterised by lymphocytes and plasma cells  Behcet’s disease  Multiple sclerosis
57
corneal angiogenesis
 Response to inflammation promoted by fibrin and its degradation products
58
endothelial activation
Endothelial activation (within 24 hours)  Endothelium retracts and nucleoli enlarge  Endothelial basal lamina broken down by plasminogen activator  Produced by fibroblasts, macrophages and others
59
vascular sprotuing
 Sprouts from post-capillary venules and capillaries  Lumen formation and anastomosis of blind channels
60
vascular maturation
deposition of ECM and laminin and basal lamina formation
61
latent period
 Vasodilation  Vascular permeability of neighbouring vessels  Stromal oedema
62
tissue damage from ionising radiation
Direct killing of cells ( free radicals release, ionic forms of hydrogen and hydroxyl result in a break in DNA structure) Cellular DNA changes Damage to blood vessels leading to secondary ischaemic necrosis
63
occular manifestataions of damaged from ionising radation
Necrosis of sclera ( can occur with mitomycin C) Dry eye syndrome ( usually occur with doses of 60-70gy) Punctate epithelial erosion Cataracts
64
radiation induced cataract
( may take up to 20 years after exposure before developing cataract) Young patients more susceptible as more active lens cells growing . The lens is the most radiosensitive structure with an average latent period of 2-3 years.
65
raidation retinopathy
Slowly progressive Microangiopathic changes can mimic diabetic retinopathy. 4) The delay is usually 2-3 years for radiation optic neuropathy
66
commotio retinae
Caused by shockwaves from trauma Induces outer retinal sheen-like whitening OCT findings Photoreceptor and retinal pigment epithelium (RPE) disruption Vision can go down to 6/60
67
chorodial rupture
Disruption to Bruch's membrane/RPE Associated with subretinal bleeding Usually around optic disc or periphery (occasionally in the macula) Choroidal neovascularization (CNV) can grow at rupture site.
68
post-traumatic macular hole
Traumatic vitreomacular traction Submacular haemorrhage from choroidal rupture Severe commotio retinae
69
retinal sclopetaria
Caused by high-velocity projectile injury to the orbit Causes choroidal and retinal damage Can present with subretinal, retinal and vitreous haemorrhage Over time retinal scars will form