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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
what stimuli induce histamine release
``` antigen via IgE complement fragments c3a and C5a cytokines and chemokine bacterial components physical trauma ```
26
what are the three major functions of histamine
reddening - vasodilation wheal - increase vascular permeability flare - spread response through sensory fibres act through GPCR
27
What are the roles of bradykinin
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.
28
what are the roles of substance P
``` stored in nerve ending for release a neuropeptide released from peripheral terminal of sensory nerve fibres also from eosinophils causes pain itch and vasodilation ```
29
describe the r/ship between bradykinin, substance P and histamine
bradykinin stimulate nerve ending --> release substance P --> stimulate mast cell --> release histamine --> leafiness of blood vessels = redness and inflamm
30
describe the ecosanoids and their roles in inflammation
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
cytokines as inflam mediators
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
major processes with acute inflammation
vasodilation exudation emigration
33
sequence of acute inflammation
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
Vasodilation
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
Exudation
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
what are the first responding WBC in acute inflammation
neutrophils
37
describe transudate, exudate and modified transudate
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
leukocyte emigration
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
pain
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
Itch - pruritus
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
fever - pyrexia
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
what is serous inflamm
only water and low MW solutes out of plasma
43
catarrhal inflamm
exudate formed on mucosal surface | mucus mixed with serous fluid plus cell debris
44
fibrinous inflamm
more severe change in vascular permeability - fibrinogen converted to fibrin, grossly appears as yellow gel, occurs on serosal or mucosal surface
45
suppurative
``` purulent exudate (pus) large # cells, tissue damage ```
46
absces
localised collection of pus caused by suppurative inflame response to pyrogenic bacteria confined by wall of fibrous inflammation
47
phlegmon
spreading digguse suppurative inflammation within loose CT margins poorly defined, pus tracking up and down between tendons and mucus
48
empyema
accumulation of pus within body cavity
49
resolution of inflammation
apoptosis + removal of leukocytes macrophages switch from pro inflame to phagocytic + anti inflame stop signals: lipoxins resonins, protections`
50
time frame of acute and chronic inflamm
paracute: immediate, min inflammation acute: <2 days subacute: 2-7 days chronic: 7+ chronic
51
when does chronic inflamm occur
foreign bodies autoimmune disease persistent infection hypersensitivity/allergic disease
52
features of chronic inflamm
1. changes in cell population 2. inflamm tissue damage 3. tissue healing - regen, fibrosis, and scar tissue
53
changes in cell population
acute inflamm: predom neutrophil chronic: lymphocyte - small cell, large nucleus eosinophil: bilobated, eosinophilic granules macrophage - foamy cell plasma cell - -ve image neutrophil
54
t lymphocyte activation
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
subtypes of chronic inflamm
lymphocytes - lymphocyte dominated granulomatous - macrophage eosinophilic - eosinophil chronic active - if have neutrophil component
56
lymphatic inflammation
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
granulomatous inflamm
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
subtypes of granlumoatous inflamm
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
eosioniophilic inflammation
primarily parasitic or allergic disease | affected tissues have green appearance
60
tissue destruction
tissue damage results from: damage by original insult, release of inflam mediators, cellular phagocytosis or apoptosis, tissue death due to circulatory compromise
61
healing in chronic inflamm
attempted regardless of whether insult resolved usually ineffective without resolution of inflamm mediators x2 major pathways - regeneration, repair
62
regeneration
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
labile cells
undergo constant turnover and can regenerate completely from germinal cells eg/ epithelial cells of skin, intestinal epithelium, bone marrow
64
stable cells
normally quiescent but have ability to mitotically divide if required eg/ hepatocytes, osteocytes, renal tubular epithelium
65
permanent cell types
considered terminally differentiated do not regenerate neurons, cardiac muscle usually highly specialised cells
66
repair
replacement of damaged tissue by fibrous CT restore structure at expense of function occurs IN COMPETITION with regeneration
67
how does repair work?
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
granulation tissue development
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
factors influencing healing
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
abnormal healing
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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