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Pathology > Tissue damage and Inflammation > Flashcards

Tissue damage and Inflammation Flashcards

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
Q

pseudodrusen on FAF

A

Reduced signal from blocking and increased the signal from RPE distress.

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26
Q

mechanisms of cell death

A
  1. necorsis = death of a group of cells, always pathological
  2. apoptosis = programmed cell death
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27
Q

reversible injury

A
  1. hydropic swelling - cell becomes swollen, usually 2nd to trauma
  2. atrophy - decrease in cell size and number
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28
Q

acute inflammation

A

 Reaction to injury be it physical, chemical, infective, immunological
 Vascular phase followed by cellular phase

29
Q

classic signs of acute inflammation

A

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
Q

duration of acute inflammation and outcome

A

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
Q

chemical mediators in vascular pahse

A

 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
Q

cell type on bacterial infection

A

bacterial

33
Q

cell type on parasitic infection

A

eosinophil

34
Q

cell type in viral infection

A

monocytes

35
Q

neutrophil rolling

A

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
Q

platelet activaition

A

Platelet activating factor activates neutrophils and induces beta-integrins
expression on their cell membranes which further promote adhesion with the endothelium

37
Q

trigger for migration of neutrophils

A

ransmigration of the neutrophils between endothelial cells then occurs,
stimulated by IL-8

38
Q

chemotaxis

A

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
Q

steps in chemotaxis

A

o Reception of signals
o Response to signals (transduction)

40
Q

examples of chemotaxis

A

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
Q

role of leucocytes

A

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
Q

phagosome

A

Phagosome fuses with lysosome: associated with the “respiratory burst” of
metabolic activity producing hydrogen peroxide

43
Q

macrophages

A

Within tissues, monocytes undergo enlargement, increased lysosome numbers,
Golgi and ER development

44
Q

macrophage activation

A

 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
Q

role of macropahges

A

 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
Q

granulomatous KPs

A

“mutton-fat” KPs) are composed on
macrophages compared to non-granulomatous KPs which are mainly lymphocytes and PMLs

47
Q

complement systemt

A

 Involved in acute inflammation, phagocytosis, clotting, immune and
hypersensitivity reactions (C3a and C5a are anaphylatoxins)

48
Q

what stimulates complement

A

 Classical and alternative pathways are both stimulated by plasmin

49
Q

components of the complement systtem

A

 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
Q

plasma cascade system

A

Factor XII (Hageman factor) of the clotting cascade has a central role in activating
3 systems operating within plasma

51
Q

systems operative within the plasma cascade system

A

 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
Q

chronic inflammation

A

 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
Q

granuloma

A

 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
Q

structure of granuloma

A

 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
Q

delayed hypersenitivy response and granuloma

A

 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
Q

non-granulomatous inflammation

A

characterised by lymphocytes and plasma cells
 Behcet’s disease
 Multiple sclerosis

57
Q

corneal angiogenesis

A

 Response to inflammation promoted by fibrin and its degradation products

58
Q

endothelial activation

A

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
Q

vascular sprotuing

A

 Sprouts from post-capillary venules and capillaries
 Lumen formation and anastomosis of blind channels

60
Q

vascular maturation

A

deposition of ECM and laminin and basal lamina formation

61
Q

latent period

A

 Vasodilation
 Vascular permeability of neighbouring vessels
 Stromal oedema

62
Q

tissue damage from ionising radiation

A

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
Q

occular manifestataions of damaged from ionising radation

A

Necrosis of sclera ( can occur with mitomycin C)
Dry eye syndrome ( usually occur with doses of 60-70gy)
Punctate epithelial erosion
Cataracts

64
Q

radiation induced cataract

A

( 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
Q

raidation retinopathy

A

Slowly progressive
Microangiopathic changes can mimic diabetic retinopathy.

4) The delay is usually 2-3 years for radiation optic neuropathy

66
Q

commotio retinae

A

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
Q

chorodial rupture

A

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
Q

post-traumatic macular hole

A

Traumatic vitreomacular traction
Submacular haemorrhage from choroidal rupture
Severe commotio retinae

69
Q

retinal sclopetaria

A

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

Pathology (6 decks)

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