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Principles of Disease > PoD - Acute Inflammation > Flashcards

PoD - Acute Inflammation Flashcards

1
Q

what is inflammation?

A
  • series of dynamic, protective changes occurring in living tissue in response to injury
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2
Q

what are the cardinal signs of inflammation?

A
  • rubor (redness)
  • calor (heat)
  • tumor (swelling)
  • dolor (pain)
    loss of function
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3
Q

what are the causes of AI?

A
  • micro-organisms
  • trauma to the tissue
  • chemical (upset stable environment)
  • physical (extreme environmental environment)
  • dead tissue (necrosis irritates adjacent tissue)
  • hypersensitivity
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4
Q

where does AI happen?

A
  • series of microscopic events
  • localised to affected tissue
  • takes place in the microcirculation (extracellular space)
  • results in clinical symptoms
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5
Q

what are the main steps in AI?

A
  • changes in vessel radius = flow
  • changes in the permeability of the vessel wall
  • emigration of neutrophils
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6
Q

what happens to change the vessel radius?

A
  • transient arteriolar constriction
  • local arteriolar dilation
  • relaxation of vessel smooth muscle
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7
Q

how does increasing radius of vessel impact flow?

A
  • a small change in radius makes a vast change in amount of flow
  • increased arteriolar radius causes increased local tissue blood flow
  • causes redness and heat
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8
Q

what happens as a result of changes in cell wall permeability?

A
  • net movement of plasma from capillaries to extravascular space
  • called exudation
  • oedema is accumulation of the exudation - swelling of tissue in acute inflammation
  • swelling causes pain (stretching of nerves) - aims to reduce function (protective)
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9
Q

how does increased permeability change blood flow?

A
  • loss of fluid = increased viscosity (thicker)
  • reduced rate of flow (stasis)
  • causes RBCs to aggregate in centre and neutrophils to move towards edge
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10
Q

what is the most important cell in AI?

A
  • neutrophil polymorphonuclear leukocyte
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11
Q

what are the phases of neutrophil emigration?

A
  • margination (neutrophils move to endothelial aspect of lumen)
  • pavementing (neutrophil adhere to endothelium)
  • emigration (neutrophils squeeze between endothelial cells to extravascular tissues)
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12
Q

what is the ideal outcome of AI?

A
  • offensive agent isolated and destroyed
  • macrophages move in from blood and phagocytose debris, then leave
  • epithelial surfaces regenerate
  • inflammatory exudate filters away
  • vascular changes return to normal
  • inflammation resolves
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13
Q

what are the benefits of AI?

A
  • rapid response to non-specific insult
  • transient protection of inflamed area
  • neutrophils destroy organisms and denature antigen for macrophages
  • plasma proteins localise process
  • resolution and return to normal
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14
Q

what are neutrophils?

A
  • mobile phagocytes
  • recognise foreign antigen
  • move towards it
  • adhere to organism
  • release granular contents (oxidants/enzymes)
  • phagocytose & destroy foreign antigen
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15
Q

what are the consequences of neutrophil action?

A
  • neutrophils die when granule contents released
  • produce pus
  • may extend into other tissues, progressing the inflammation
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16
Q

what plasma proteins are present in inflammation?

A
  • fibrinogen - coagulation factor, forms fibrin which is involved with clotting - localises the inflammatory process
  • immunoglobulins - specific for antigens
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17
Q

what are the effects of mediators?

A
  • vasodilation
  • increased permeability
  • neutrophil adhesion
  • chemotaxis
  • itch and pain
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18
Q

what do releasing histamine do?

A
  • histamine is stored as preformed granules in mast cells
  • released as a result of local injury (IgE mediated reactions)
  • causes vasodilation, increased permeability
  • acts via H1 receptors on endothelial cells
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19
Q

what is serotonin’s role in inflammation?

A
  • preformed in platelets
  • released when platelets degranulate in coagulation
  • involved in vasoconstriction
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20
Q

what are prostaglandins?

A
  • produced in many cells (endothelium cells, leukocytes)
  • mostly promote histamine action and inhibit inflammatory cells
  • has be known to promote platelet aggregation and vasoconstriction
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21
Q

what are cytokines/chemokines?

A
  • molecules produces by macrophages, lymphocytes, endothelium in response to inflammatory stimuli
  • different molecules have different effects (pro-/anti-inflammatory)
  • stimulate intracellular pathways
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22
Q

what is PAMP?

A
  • pattern associated molecular patterns

- pattern on microbial antigen that immune cells are hard wired to recognise

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23
Q

what is DAMP?

A
  • danger associated molecular patterns
  • substances released in response to stimulus
  • stimulate pattern recognition receptors on cell membrane
  • activate inflammatory response
24
Q

what is MAPK?

A
  • mitogen-activated protein kinase
  • stimulated in inflammation via surface receptors (TLRs)
  • regulate pro-inflammatory cytokine production and inflammatory cell recruitment
25
Q

what is JAK-STAT?

A
  • janus kinase signal transducer and activator to transcription
  • direct translation of extracellular signal to molecular expression
26
Q

how is plasma involved in coagulation?

A
  • coagulating factors present in plasma

- fibrinogen concerted to fibrin to form clots

27
Q

what happens in fibrinolysis?

A
  • process of breaking down fibrin, helps to maintain blood supply
28
Q

what does kinin system do?

A
  • produces bradykinin which is associated with pain
29
Q

what are the immediate effects of inflammation ?

A
  • pyrexia (raised temperature)
  • feel unwell (malaise, anorexia, nausea)
  • neutrophilia (raised WBC count)
30
Q

what are the longer term effects of inflammation?

A
  • lymphadenopathy (lymph node enlargement)
  • weight loss
  • anaemia
31
Q

what is suppuration?

A
  • pus formation
32
Q

what is pus?

A
  • collection of dead tissue, organisms, exudate, neutrophils, fibrin, RBCs, debris
  • (pyogenic) membrane surrounds pus to localise it
33
Q

what is an abscess?

A
  • collection of pus under pressure
  • can be single or multi-loculated
  • tends to point and produce discharge
  • can collapse which indicates healing and repair
34
Q

what is the outcome of organisation?

A
  • granulation tissue present
  • tends to have a patch-job look
  • formed of new capillaries (angiogenesis), fibroblasts & collagen (lay down new tissue) and macrophages (clear debris)
  • leads to fibrosis and formation of scar
35
Q

what are the effects of systemic infection?

A
  • shock (inability to perfuse tissues)

- septic shock - vasodilation/tachycardia/hypotension/pyrexia

36
Q

how does septic shock occur?

A
  • systemic release of chemical mediators from cells into plasma leads to vasodilation (loss of systemic vascular resistance - causes heart rate to increase to match cardiac output)
  • bacterial endotoxin released (pyrexia)
  • activation of coagulation (haemorrhagic skin rash)
  • HR insufficient to maintain CO = low BP
  • reduced perfusion of tissues (tissue hypoxia –> loss of cell tissue/organ function)
37
Q

what is the outcome of septic shock?

A
  • rapidly fatal
  • tissue hypoxia
  • haemorrhage
  • requires urgent intervention and support
38
Q

what are the microscopic characteristics of CHRONIC inflammation?

A
  • inflammation in which the cell population is especially:
    lymphocytes
    plasma cells
    macrophages
  • features of tissue/organ damage - healed with patch
  • signs of healing and repair (granulation tissue/scarring/fibrosis)
39
Q

what are the clinical presentations of CI?

A
  • non-specific ‘sore’ bit
  • malaise and weight-loss
  • loss of function
40
Q

when do we get CI?

A
  • typically follows on from acute inflammation (large volume of damage, inability to remove debris, failure to resolve)
  • can arise as a primary lesion
41
Q

what is angiogenesis?

A
  • the formation of new blood vessels
  • vascular endothelial growth factor (VEGF) is released by hypoxic cells which stimulates proliferation
  • enzyme secretion aids process
  • enables blood supply to enter damaged tissue
42
Q

what is the link between angiogenesis and tumour growth?

A
  • angiogenesis occurs as the tumour grows

- more angiogenesis = increased growth

43
Q

what is primary chronic inflammation?

A
  • where there is no initial phase of acute inflammation
  • autoimmune diseases are an example of 1st CI where auto-antibodies are directed against own cell and tissue components. Destroy or damage organs, tissues, cells (lupus)
44
Q

what is the role of a lymphocyte in CI?

A
  • T cells (helper/killer) and B cells
  • B cells = differentiate into plasma cells (antibodies) which facilitate immune response, act with macrophages and make up immune memory
  • T cells = produce cytokines (attract/hold/activate immune cells), produce interferons (anti-viral effects, attract other cells), damage & kill antigen (chemical granule proteins)
  • NK cell = destroy antigens and cells
45
Q

what is the role of a macrophage in CI?

A
  • remove debris
  • presents antigens
  • mobile phagocyte is able to move from blood, contain enzyme (lysozome) and other chemicals which destroy cells and influence inflammation
46
Q

what is the role of fibroblasts in CI?

A
  • motile cells
  • metabolically active
  • make and assemble structural proteins (collagens)
47
Q

what is granulomatous inflammation?

A
  • granulomas (granulomata) in tissues and organs

- stimulated by indigestible antigen - body can’t get rid of it

48
Q

what is a granuloma composed of?

A
  • macrophages
  • giant cells
  • neutrophils
  • eosinophils
  • dead material
    Often surrounded by lymphocytes
49
Q

what are giant cells?

A
  • fusion of macrophages to form larger cells
  • large cytoplasm w/ multiple nuclei
  • Langerhans type and foreign body type (associated with pyogenic granulation tissue, acutely inflamed, pus)
50
Q

what are examples of infectious granulomatous diseases?

A
  • tuberculosis (mycobacterium tuberculosis)
  • leprosy (mycobacterium leprae)
  • syphilis (treponema pallidum)
51
Q

what are examples of non-infectious granulomas?

A
  • rheumatoid disease (tissue specific auto-immunity)
  • sarcoidosis
  • Crohn’s disease
52
Q

how does surgical wound and larger wound healing, differ?

A 
Surgery 
- healing by primary intention 
- minimal gap - blood clot 
- small amount of granulation tissue 
- small linear scar
Larger Wounds 
- healing by secondary intention 
- lots of granulation tissue ingrowth 
- puckering/contraction of skin and scarring (messy)
53
Q

what is the sequence of events in wound healing?

A
  • injury, blood clot, acute inflammation, fibrin
  • many growth factors & cytokines involved
  • granulation tissue growth - angiogenesis
  • phagocytosis of fibrin
  • myofibroblasts move in and lay down collagen
  • contraction of scar
  • re-epithelialisation
54
Q

what helps wound healing?

A
  • cleanliness
  • clean edges
  • sound nutrition
  • metabolic stability and normality
  • normal inflammatory & coag mechanisms
  • local mediators
55
Q

what is a callus after bone fracture?

A
  • after a bone fracture, osteoblasts lay down new bone
  • nodules of cartilage present
  • bone remodelling (osteoclasts remove dead bone, progressive replacement of woven bone by lamellar bone, reformation of cortical/trabecular bone)

Principles of Disease (15 decks)

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