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Applications Animal Health > C2S Theme 4: Host Defences Against Injury > Flashcards

C2S Theme 4: Host Defences Against Injury Flashcards

1
Q

What are the requirements of the immune system?

A
  1. Self tolerance
  2. Specificity - recognition of self vs non self
  3. Molecular recognition of microbes and self proteins
  4. Destroy microbes or tumors
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2
Q

List some key features of the innate and adaptive immune system

A

innate: non specific, fast acting, present at birth, ‘first line of defence’
adaptive: specific (memory of previous assaults), slow acting, develops over time, more powerful

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3
Q

describe the lineage of leukocytes

A

derived from stem cells
myeloid progenitor cells –> monocytes, macrophages and granulocytes
lymphoid progenitor cells –> lymphoid lineage

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4
Q

how can you classify leukocytes (not through lineage)

A

presence or absence of granules
granulocytes: neutrophils (can’t see the granules)
eosinophils (pink granules) basophils (blue granules)
agranulocytes: lymphocytes, monocytes

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5
Q

What are the 4 mechanisms of the innate immune systems

A
  1. anatomical barrier - villi prevent path from reaching surface, constant flow of mucous carry path away
  2. physiological barrier - complement - incl increase temp, extremes of pH etc destroy enzymes of path
  3. antimicrobial peptides and oxidate radicals - chemical substances that inhibit microbe growth
  4. phagocytosis - uptake of pathogen destroyed by phagolysosome
  5. inflammation - occurs when psychical barrier breached and pathogen recognised by immune cells
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6
Q

what are the cells of the innate immune system

A

granulocytes: neutrophils, eosinophils, basophils, mast cells + monocytes; macrophage and dendritic cells

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7
Q

describe neutrophils and their granules

A

multilobated nucleus
1st line of defence against microbial infection (recruited to tissue first)
granlues: myeloperoxidase, lactoferrin, gelatinise
actively phagocytic
primary aizotrophilic granlues: larger, contain peroxidase, lysozyme and hydrolytic enzymes
secondary specific granules: smaller collagenase, lactoferrin

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8
Q

what is the life span of neutrophils in blood and tissue

A

in blood - 4-10 hr

in tissue 1-2 day

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9
Q

what are the three neutrophil killing mechanisms

A
  1. phagocytosis with phagolysosome
  2. degranulate in close proximity to path
  3. NETS - released extracellular composed of RNA trap bacteria stop from multiplying
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10
Q

what are the major functions of basophils

A

major role in allergic and inflamm reactions
cross linking of surface iGE receptor causes degranulation of histamine, heparin, serotonin and hydrolytic and chemotactic factors
limited phagocytic activity

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11
Q

what are the major functions of mast cells

A

in tissues involved with inflame and release of histamine
= increase vasopermability
precursor in blood is not yet identified
involved in anaphylaxis - cross linking of IgE

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12
Q

what are the major functions of eosinophils

A

major function in control or parasites, in allergic response

major granule: myelin basic protein

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13
Q

what is the life span of the eosinophil in blood and tissue

A

6-12 hrs in blood

2-3 days in tissue

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14
Q

what are the functions of macrophages

A

highly phagocytic
antigen presenting cell
produce colony stimulating factors
produce cytokines - amplify immune response for pro inflammatory reaction
cytokines produced = IL 1, 6, 8, 18, TNF-a, Il-gamma

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15
Q

what are the cells of the adaptive immune system

A

B cell: develop in bone marrow (bursa of fabricius in birds and ileal peyers patches in ruminants) - produce antibodies
T cell: develop in thymus, recog antigen via TCR
x3 types - CD4 = helper T cell
CD8 = cytotoxic T cell
TCR
NK Cell: (technically innate) kill adjacent cell by release of cytotoxic granules and induction of apoptosis

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16
Q

how to innate cells recognise pathogen?

A

pathogen recognition receptors: PRR’s detect microbes by binding to pathogen associated molecular patterns
PRRs expressed by cells of innate immune response
present on APC
recognise unique microbial PAMP shared by groups of related microbes not found associated with mammalian cells
= activation of innate

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17
Q

what are the 4 tissue responses to damage?

A
  1. acute inflame - initial response, unspecific, eliminate dead tissue, allow immune cells access
  2. restitution - damaged area replaced by organised tissue with structure and function = ideal outcome
  3. fibrous repair - scar tissue. tissue architecture destroyed, original cell type cannot regrow. non specialised response to substantial damage
  4. chronic inflammation - damaging agent and tissue destruction persists; ongoing attempts to heal and inflamm
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18
Q

what are the causes of acute inflammation

A

mechanical trauma
thermal, chemical injury,
biological - viral, bacterial, fungal

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19
Q

what are the functions of the acute inflammatory response

A

to bathe the area in inflammatory exudate - carrying proteins, fluid and cells which mediate local defenses, destroy and eliminate biological agents and damaged tissue and debris

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20
Q

what are the 5 cardinal signs of inflammation

A 
redness = rubor 
pain = dolor
swelling = tumor
heat = calsor
loss of function
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21
Q

what are the features of an acute inflammatory response

A

rapid onset
short duration
emigration of leukocytes - typically neutrophils

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22
Q

what are inflammatory autacoids

A
  • low MW molecules, considered as defence mediators due to their formation and release associated with acute inflammation
    they act locally and are rapidly broken down
    modulatory functions incl controlling: smooth muscle tone/length, glandular secretions, permeability , sensory nerves
  • they are an appropriate target for theraputic drugs if the inflamm response becomes outrageous
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23
Q

what are the 5 notable autacoids

A 
histamine
bradykinin
substance p 
ecosanoids
cytokines
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24
Q

where is histamine stored and related from?

A

mast cell - into tissue, mucosal surface
basophil - into blood
enterocrhomaffin like cells - gastric secretions

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25
Q

what stimuli induce histamine release

A 
antigen via IgE
complement fragments c3a and C5a 
cytokines and chemokine
bacterial components
physical trauma
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26
Q

what are the three major functions of histamine

A

reddening - vasodilation
wheal - increase vascular permeability
flare - spread response through sensory fibres
act through GPCR

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27
Q

What are the roles of bradykinin

A

causes vasodilaton, increase vascular permeability and stimulate sensory nerve ending causing pain
vasodilator - main role to stimulate nerve endings
bradykinin is a local peptide mediator in pain and inflame
generated AFTER plasma exudation
broken down by kinase enzyme.

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28
Q

what are the roles of substance P

A 
stored in nerve ending for release
a neuropeptide
released from peripheral terminal of sensory nerve fibres
also from eosinophils
causes pain itch and vasodilation
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29
Q

describe the r/ship between bradykinin, substance P and histamine

A

bradykinin stimulate nerve ending –> release substance P –> stimulate mast cell –> release histamine –> leafiness of blood vessels = redness and inflamm

30
Q

describe the ecosanoids and their roles in inflammation

A

ecosanoids are compounds contains 20 carbons
- prostaglandins
- thromboxane
- leukotrienes
ecosanoids are not stored by cell = produced on demand
actions: act through selective G protein-coupled receptors GPCRs
redness - vasodilation at site of inflammation
swelling - wheal formation due to increase in vascular perm
pain, fever, target for NSAID drugs

31
Q

cytokines as inflam mediators

A

broad category of small proteins - cell signalling
include: chemokine, interleukins, tumor necrosis factor, produced by broad range of cells: mainly immune
moderate balance between humeral and cell response

32
Q

major processes with acute inflammation

A

vasodilation
exudation
emigration

33
Q

sequence of acute inflammation

A
  1. vasodilation - increase blood flow; arteriole dilation, histamine and NO primary
  2. increase microvascular - fluid into tissue
  3. blood flow slows
  4. cellular events - margination, emigration, accumulation of WBC at site of injury
  5. tissue damage/reapir = loss of function
34
Q

Vasodilation

A

induced by mediators: histamine, NO, prostaglandins, bradykinin resulting in the dilation of arterioles, capillaries and post capillary venues
smooth muscle relaxes, increasing blood flow

35
Q

Exudation

A

increases vascular permeability
structural changes in the microvasculature permit plasma proteins and leukocytes to leave circulation
inflammatory exudate:
fluid competent = salts, high protein, dilutes toxin in tissue, allows diffussion of inflammatory mediators, circulation via lymph to local lymph node for antigen presentation
fibrin competent = formed by precursor fibrinogen
polymerises via blood coagulation, long filamentous insoluble fibres form network blocking migration of bacteria

36
Q

what are the first responding WBC in acute inflammation

A

neutrophils

37
Q

describe transudate, exudate and modified transudate

A

transudate: fluid, low protein and cell count - not infectious
exudate: fluid + cells, low protein, many cells - may be infectious
modified transudate - in b/w transudate and exudate. high protein low cell count.

38
Q

leukocyte emigration

A

endothelial cell activation: expression of adhesion molecules

margination: mediator cause neutrophil to adhere to endothelium
emigration: neutrophil move through blood vessel into damage tissue via chemotactic gradient

39
Q

pain

A

cardinal signal of inflamm
caused by
- damage to inflamm mediators on nerve endings
- pressure of nerve endings from tissue swelling
- effect of inflamm mediators on nerve endings
neurogenic inflamm: inflam mediators such as substance P released from nerve endings

40
Q

Itch - pruritus

A

sensation that causes the desire to scratch
unmyelinated nerve fibres for itch and pain both originate in skin
itch may accompany local skin inflam
caused by: effect of inflamm mediators on nerve endings ie/ histamine, serotonin, protaglandings
scratching lead to self trauma –> inflam

41
Q

fever - pyrexia

A

assists the healing process
- increases mobility of leukocytes and phagocytosis
- increases proliferation of T cells
pyrogen is a substance that can induce fever - can be endogenous ie/ cytokes eg/ IL 1, 6 TNF-a
OR exogenous ie/ bacteria
pyrogen causes release of PGE2, PGE2 acts on thermostat in hypothalamus = physiological actions to generate heat

42
Q

what is serous inflamm

A

only water and low MW solutes out of plasma

43
Q

catarrhal inflamm

A

exudate formed on mucosal surface

mucus mixed with serous fluid plus cell debris

44
Q

fibrinous inflamm

A

more severe change in vascular permeability - fibrinogen converted to fibrin, grossly appears as yellow gel, occurs on serosal or mucosal surface

45
Q

suppurative

A 
purulent exudate (pus)
large # cells, tissue damage
46
Q

absces

A

localised collection of pus caused by suppurative
inflame response to pyrogenic bacteria
confined by wall of fibrous inflammation

47
Q

phlegmon

A

spreading digguse suppurative inflammation
within loose CT
margins poorly defined, pus tracking up and down between tendons and mucus

48
Q

empyema

A

accumulation of pus within body cavity

49
Q

resolution of inflammation

A

apoptosis + removal of leukocytes
macrophages switch from pro inflame to phagocytic + anti inflame
stop signals: lipoxins resonins, protections`

50
Q

time frame of acute and chronic inflamm

A

paracute: immediate, min inflammation
acute: <2 days
subacute: 2-7 days
chronic: 7+ chronic

51
Q

when does chronic inflamm occur

A

foreign bodies
autoimmune disease
persistent infection
hypersensitivity/allergic disease

52
Q

features of chronic inflamm

A
  1. changes in cell population
  2. inflamm tissue damage
  3. tissue healing - regen, fibrosis, and scar tissue
53
Q

changes in cell population

A

acute inflamm: predom neutrophil
chronic: lymphocyte - small cell, large nucleus
eosinophil: bilobated, eosinophilic granules
macrophage - foamy cell
plasma cell - -ve image
neutrophil

54
Q

t lymphocyte activation

A

activated in response to specific binding of antigen w/ TCR
proliferation of lymphocytes –> produce cytokines to direct the immune response
APC –> T Cell if its TH1 - macrophage recruitment, IgG prod
if its TH2 - eosinophil recruitment, IgE prod
if its cytotoxic T cell - induce apoptosis

55
Q

subtypes of chronic inflamm

A

lymphocytes - lymphocyte dominated
granulomatous - macrophage
eosinophilic - eosinophil
chronic active - if have neutrophil component

56
Q

lymphatic inflammation

A

also called non-suppurative
mix of lymphocytes: cytotoxic T, helper T, B cells, plasma cell
develops as consequence of persistent antigen - autoimmune, hypersensitiving, idiopathic
features: perivascular distribution:ie/ develop around vessels
sometimes form nodular aggregates - lymphoid follicales

57
Q

granulomatous inflamm

A

macrophage roles - phagocytosis - digest and eliminate foreign aspects
APC
direct inflamm and repair - secrete cytokines, IL2 promote inflame, TGF-b suppress fungal + promote repair
macrophage cause clusters called granulomas
cells may fuse to form giant cells: if they can’t process something

58
Q

subtypes of granlumoatous inflamm

A

pyogranuloma: central accumulation of neutrophils
–> seen with some foreign bodies, bacterial contam, and some infections
caseating granuloma: cheesy centre composed of dead tissue seen particularly with tuberculosis/ and parasites

granulomatous infection: often form discrete or coalescing nodule in tissue. easy to mistake for neoplasia
–> nodules not in every granulomatous disease eg/ johns disease

59
Q

eosioniophilic inflammation

A

primarily parasitic or allergic disease

affected tissues have green appearance

60
Q

tissue destruction

A

tissue damage results from: damage by original insult, release of inflam mediators, cellular phagocytosis or apoptosis, tissue death due to circulatory compromise

61
Q

healing in chronic inflamm

A

attempted regardless of whether insult resolved
usually ineffective without resolution of inflamm mediators
x2 major pathways - regeneration, repair

62
Q

regeneration

A

best case scenario
replacement of damaged tissue with original cell type
deponent on: viability of original cells, type of tissue and preservation of CT scaffold

63
Q

labile cells

A

undergo constant turnover and can regenerate completely from germinal cells eg/ epithelial cells of skin, intestinal epithelium, bone marrow

64
Q

stable cells

A

normally quiescent but have ability to mitotically divide if required eg/ hepatocytes, osteocytes, renal tubular epithelium

65
Q

permanent cell types

A

considered terminally differentiated
do not regenerate
neurons, cardiac muscle
usually highly specialised cells

66
Q

repair

A

replacement of damaged tissue by fibrous CT
restore structure at expense of function
occurs IN COMPETITION with regeneration

67
Q

how does repair work?

A

defect initially filled by formation of granulation tissue

  • -> Fragile, highly vascular, dense cell, oedematous CT
  • -> soft, pink-red, moist, NO NERVES, contain fibroblast and leukocytes
68
Q

granulation tissue development

A
  1. inflammatory phase - clearance of debris and destroyed tissue by macrophages
  2. proliferative phase
    –> angiogenesis: provide O2 and nutrients for healing, hypoxia in damaged tissue stimulate growth factors to trigger blood vessel development
    –> fibroplasia: fibroblast migrate alone fibrin scaffold into revascularised tissue under influence of growth factors and deposit type 3 collagen
  3. maturation phase: reorganisation of collagen and change into collagen type 1
    type 1 collagen stronger, organised parallel with lines of tension
    contraction of CT
    maturation and regression of vasculature –> goes white
69
Q

factors influencing healing

A

infection - gran tissue can’t form in presence of necrotic tissue
nutrition - vitamin C deficient; inhibit collagen maturation
wound movement and pressure - gran tissue is fragile, can’t handle mechanical stress
impaired blood supply - hypoxia inhibit cell viability
concurrent disease: diabetes mellitus predisposed to infection
age: wound repair is slower with age

70
Q

abnormal healing

A

proud flesh - formation of excessive granulation tissue, delays healing
keloid - excessive scar tissue during healing
stricture - scar contracture causing narrowing
adhesion - forms fibrous tissue attachment between adjacent organs restricted movement

Applications Animal Health (9 decks)

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