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principles of disease > acute and chronic inflammation week 6 > Flashcards

acute and chronic inflammation week 6 Flashcards

1
Q

what is acute inflammation

A

a series of protective changes occurring in living tissue as a response to injury

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2
Q

what are the cardinal signs of inflammation

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

causes of acute inflammation

A
  • micro-organisms (infection)
  • mechanical (trauma) injury to tissue
  • chemical - upset stable environment (change in ph or urine or bile somewhere it shouldn’t be
  • physical - extreme conditions (cold, heat, ionising radiation)
  • dead tissue (cell necrosis irritates nearby cells)
  • hypersensitivity
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4
Q

where does process of acute inflammation take place

A

microcirculation

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5
Q

steps of acute inflammation

A
  • changes in vessel radius - flow
  • change in the permeability of the vessel wall - exudation
  • movement of neutrophils from the vessel to the extravascular space
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6
Q

in acute inflammation, what are the changes in vessel radius

A
  1. transient arteriolar constriction (short time, protective)
  2. local arteriolar dilatation (active hyperaemia)
  3. relaxation of vessel smooth muscle
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7
Q

in acute inflammation, what causes increased permeability

A

locally released chemical mediators (make lining of the vessels leak, fluid and protein leak into the adjacent tissue)

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8
Q

in acute inflammation, what is the effect of increased permeability

A
  • net movement of plasma from capillaries to extravascular space. this process is exudation
  • viscosity of plasma increases because all that is left is big molecules so rate of flow is slower
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9
Q

in acute inflammation, what is leaked in exudate

A

exudate is fluid rich in protein, includes immunoglobulin and fibrinogen

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10
Q

in acute inflammation, what is effect of exudation

A

oedema formed

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11
Q

what is the result of swelling

A

swelling causes pain which reduces function

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12
Q

what is different about flow in vessels in inflammation

A

normally white blood cells would be in centre of vessel and red blood cells would surround them but in inflammation white blood cells migrate to outside perimeter of vessel and red blood cells congregate in middle of vessel

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13
Q

what are the phases of emigration of neutrophils

A
  1. margination - neutrophils move to endothelial aspect of lumen
  2. pavementing - neutrophils adhere to endothelium
  3. emigration - neutrophils squeeze between endothelial cells (active process) to extravascular tissues
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14
Q

what is diapedesis

A

diapedesis is when you sometimes get a red blood cell following a neutrophil through the endothelial cells (passive because no muscle helping RBC)

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15
Q

what is the ideal outcome of acute inflammation

A
  • inciting 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
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16
Q

what are the benefits of acute inflammation

A
  • rapid response to non-specific insult
  • cardinal signs and loss of function (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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17
Q

what are the outcomes of acute inflammation

A

either:

  • resoltion
  • suppuration (pus formation)
  • organisation (about tissue repair)
  • chronic inflammation
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18
Q

in acute inflammation, what do neutrophils do

A
  • mobile phagocytes (recognise foreign antigen, move towards it - chemotaxis, adhere to organism)
  • granules possess antioxidants and enzymes (e.g. proteases)
  • release granule contents
  • phagocytose and destroy foreign antigen
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19
Q

what are the consequences of neutrophil action in acute inflammation

A
  • neutrophils die when granule contents released
  • pus produced (fluid, organisms, endogenous proteins)
  • might extend into other tissues, progressing the inflammation
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20
Q

roles of plasma proteins in inflammation

A

fibrinogen - coagulation factor (clots exudate and therefore localises inflammation)
immunoglobulins in plasma specific for antigen

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21
Q

what are the mediators of acute inflammation

A
  • molecules on endothelial cell surface membrane
  • molecules released from cells
  • molecules in the plasma
  • molecules inside cells
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22
Q

what are the collective effects of mediators in acute inflammation

A
  • vasodilation
  • increased permeability
  • neutrophil adhesion
  • chemotaxis
  • itch and pain
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23
Q

what are some cell surface mediators in acute inflammation

A
  • ICAM - 1 helps neutrophils stick to endothelial cells

- p-selectin interacts with neutrophil surface

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24
Q

in acute inflammation, what are some mediators that are released from cells

A
  • histamine causes vasodilation and increased permeability (results from IgE mediated reaction - allergic reaction)
  • 5-hydroxytryptamine (serotonin) vasoconstriction, released when platelets degranulate in coagulation
  • prostaglandins
  • cytokines and chemokine
  • nitric oxide
  • oxygen free radicals
25
Q

in acute inflammation, what are some intracellular inflammatory pathways

A
  • NF-KB pathway
  • MAPK (regulates inflammatory cells)
  • JAK-SAT (signal transduction)
26
Q

in acute inflammation, in plasma what are the four enzyme cascades

A
  • blood coagulation pathways (clots fibrinogen in exudate)
  • fibrinolysis (breaks down fibrin, products vasoactive, helps maintain blood supply)
  • kinin system (pain)
  • complement cascade (ties inflammation with immune system)
27
Q

what are the systemic effects of acute inflammation

A
  1. pyrexia - raised temperature (endogenous pyrogens from white cells)
  2. feel unwell - malaise, anorexia, nausea (abdominal pain and vomiting in children)
  3. neutrophilic - raised white cell count
28
Q

what are the suppuration outcomes of acute inflammation

A
  1. abcess (pus under pressure under skin)
  2. pus in other places (empyema - in a hollow viscus e.g. gall bladder/pleural cavity, pyaemia - discharge to bloodstream
29
Q

what are the organisation outcomes of acute inflammation

A
  • granulation tissue characteristic
  • healing and repair
  • leads to fibrosis and formation of scar
30
Q

what is granulation tissue

A

formed of

  • new capillaries (angiogenesis)
  • fibroblasts and collagen
  • macrophages
31
Q

what are the dissemination outcomes of acute inflammation

A
  • spread to bloodstream (patient septic)
  • bacteraemia (bacteria in blood)
  • septicaemia (growth of bacteria in blood)
  • toxaemia (toxic products in blood)
32
Q

what is the pathogenesis of septic shock

A
  • bacterial endotoxin released

- activation of coagulation

33
Q

what is chronic inflammation

A
  • inflammation in which the cell population is especially lymphocyte, plasma cells and macrophages
  • features tissue/organ damage, necrosis, loss of function
  • healing and repair
  • tends to be long term
34
Q

what are the clinical presentations of chronic inflammation

A
  • often no specific sore bit
  • malaise and weight loss (e.g. tuberculosis)
  • loss of function (e.g. Crohn’s disease, leprosy)
35
Q

what are the causes of chronic inflammation

A
  • arising from acute inflammation

- arising as primary lesion (no acute phase, only see chronic changes)

36
Q

what is the granulation tissue mechanism

A
  1. capillaries grow into inflammatory mass (angiogenesis)
  2. access of plasma proteins
  3. macrophages from blood and tissue
  4. fibroblasts lay down collagen to repair damaged tissue
  5. collagen replaces inflammatory exudate - patches tissue defects, replaces dead or necrotic tissue, contracts and pulls together
37
Q

what happens in acute and chronic interface

A
  1. acute inflammation
  2. mixture of acute and chronic - exudate, neutrophils but also lymphocytes, plasma cells, fibroblasts, fibrosis
  3. chronic inflammation
38
Q

what are the products of granulation tissue

A
  • fibrous tissue (scar)
  • fibrosis as a problem (e.g. adhesions between loops of bowel following peritonitis
  • chronic inflammation
39
Q

what are the causes of primary chronic inflammation

A
  • autoimmune disease
  • material resistant to digestion (e.g. viruses)
  • exogenous substances (e.g. metal)
  • endogenous substances (e.g. necrotic tissue, hair - cannot easily be phagocytosed)
40
Q

what cells and tissue components are involved in chronic inflammation

A
  1. lymphocytes
  2. plasma cells
  3. macrophages
  4. fibroblasts
  5. granulation tissue
  6. collagen
41
Q

what is a plasma cell

A
  • differentiated B cell

- involved in antibody production

42
Q

what are B cell mechanisms

A
  • differentiate to plasma cells
  • facilitate immune response
  • act with macrophages
  • immune memory
43
Q

what are T cell mechanisms

A
  • produce cytokines which attract and hold and activate macrophages
  • produce interferons which have antiviral effects and attract and stimulate other cells
  • damage and kill other cells and destroy antigen
44
Q

what are natural killer cell’s mechanisms

A
  • Destroy antigens and cells (innate)
45
Q

what are macrophages and what do they do

A
  • macrophages are antigen presenting cells
  • they remove debris
  • monocytes are macrophages in the blood
  • monocytes, histiocytes, activated macrophage, epithelioid cell (in granulomas), giant cell
46
Q

what are the mechanisms of macrophages

A
  • motile phagocyte move from blood
  • take over from neutrophils
  • contain enzymes e.g. lysosome
  • produce interferons and other chemical
  • destroy
47
Q

what are fibroblasts

A
  • motile cells
  • metabolically active
  • make and assemble structural proteins e.g. collagen
48
Q

what is granulomatous inflammation

A
  • characterised by presence of granulomas in tissues and organs
  • stimulated by indigestible antigen
49
Q

what are granulomas

A
  • clusters epithelioid macrophages in tissues
  • may contain giant cells
  • may surround dead material
  • may be surrounded by lymphocytes
  • occasionally contain neutrophils, eosinophils
50
Q

what are giant cells

A
  • fusion of macrophages
  • large cytoplasm
  • multiple nuclei
  • e.g. langhans type classically found in tuberculosis
51
Q

what are some infectious granulomatous diseases

A
  • tuberculosis
  • leprosy
  • syphilis
52
Q

what are some non-infective granulomatous diseases

A
  • rheumatoid disease
  • sarcoidosis (small patches of red and swollen tissue, usually affects lungs and skin)
  • Crohn’s disease
53
Q

describe surgical wound healing

A
  • healing by primary intention
  • minimal gap - blood clot
  • small amount of granulation tissue
  • small linear scar
54
Q

describe healing of larger defects

A
  • healing by secondary intention
  • lots of granulation tissue ingrowth
  • contraction and scarring
55
Q

what are the sequence of events in wound healing

A
  1. injury, blood clot, acute inflammation, fibrin
  2. many growth factors and cytokines involved
  3. granulation tissue growth - angiogenesis
  4. phagocytosis of fibrin
  5. myofibroblasts move in and lay down collagen
  6. contraction of scar
  7. re-epithelialisation
56
Q

what would improve wound healing

A
  • cleanliness
  • apposition of edges (edges close together)(no haematoma)
  • sound nutrition
  • metabolic stability and normality
  • normal inflammatory and coagulation mechanisms
57
Q

what would impair wound healing

A
  • dirty gaping wound, large haematoma
  • poorly nourished
  • abnormal metabolism, diabetes, corticosteroid therapy
  • inhibition of angiogenesis
58
Q

what are the sequence of events in fracture healing

A
  1. trauma, fracture, haematoma (pooling of blood outside blood vessel)
  2. bits of dead bone and soft tissue
  3. acute inflammation, organisation, granulation tissue, macrophages remove debris (bone bits)
  4. granulation tissue contains osteoblasts as well as fibroblasts
    - repair of bone requires formation of callus
59
Q

events of callus formation

A
  • osteoblasts lay down woven bone
  • nodules of cartilage present
  • followed by bone re-modelling

principles of disease (19 decks)

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