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PATH > Unit 3: Inflammation > Flashcards

Unit 3: Inflammation Flashcards

1
Q

what is inflammation

A

complex, predetermined response to injury - consists of a microcirculatory response and mobilization of phagocytic cells

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2
Q

what is acute inflammation

A

first line of defence against a physical injury, chemical injury, or infectious agent

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3
Q

4 signs of acute inflammation

A

redness, heat, swelling and pain

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4
Q

what initiates inflammation

A

anything that causes tissue injury

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5
Q

2 components for the process of acute inflammation

A
  1. Vascular change: vessels dilate to increase blood flow to area, allow plasma proteins to get to injured site
  2. Cellular response: leukocytes (WBCs) move from microcirculation to site of injury
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6
Q

what triggers the vascular change and cellular response components of acute inflammation

A

Macrophages recognize damaged cells and liberate mediators which trigger the reactions

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7
Q

what happens in vascular injury

A
  • changes in the capillaries, venules and arterioles
  • vessels vasodilate to bring more blood to area: cause of redness
  • Vessels become leaky so fluid moves to tissue spaces: cause of swelling
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8
Q

what 3 things happen following vessel injury

A
  1. Transient vasoconstriction
  2. Dilation of blood vessels caused by chemical mediators
  3. Histamine released my mast cells causes capillary dilation
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9
Q

role of mast cells in acute inflammation

A

Injury to surface of mast cell leads to “degranulation” which releases histamine, causing capillary dilation

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10
Q

what is hyperaemia

A

increased blood flow in tissues, due to vasodilation

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11
Q

what is the bodies response to inflammation

A
  • hyperaemia due to arteriolar dilation
  • increased permeability of vessels causes leakiness
  • exudation, causes swelling and accumulation of inflammatory exudate
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12
Q

true or false, acute inflammation is a cause of localized edema

A

true

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13
Q

what is exudation

A

increased amounts of fluid and larger protein molecules pass out the vessels and into extracellular space

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14
Q

what are causes of increased vascular permeability (7)

A
  1. endothelial cell contraction via histamine
  2. Prolonged “retraction” of endothelial cell via TNF and IL-1
  3. Direct injury to the endothelium causes endothelial cell necrosis
  4. Leukocyte-mediated endothelial injury as proteolytic enzymes and toxic O2 species
    are released
  5. increased transcytosis via vesicles
  6. Newly forming immature blood vessels are “leaky”
  7. blood becomes thicker (stasis) since fluid moves into interstitial space
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15
Q

what is inflammatory exudation

A

increased movement of fluid where larger proteins and cells move out of the vasculature due to increased vascular permeability

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16
Q

what is exudate

A

fluid that forms in tissues or at tissue surfaces
- composition is plasma like

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17
Q

what is transudate

A

fluid which leaves the vessels due to increased hydrostatic pressure - OR which fails to return to the vasculature to to osmotic pressure
- the “ultrafiltrate of plasma”
- doesn’t include. immunoglobins, fibrinogen, etc.

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18
Q

how do exudates differ from transudates

A
  1. exudates composition is “plasma-like”, transudates are like and ultra filtrate of plasma
  2. exudates form with increased vascular permeability, transudates form with normal VP
  3. protein content is high in exudates, low in transudates
  4. cells (degenerate neutrophils) are numerous in exudate, cells are low but healthy in transudate
  5. exudate is turbine and yellow/white is appearance, transudate is clear/colourless
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19
Q

how do transudates form

A

when fluid leaks out of vessels because of increased HP or decreased OP (net pressure >0)

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20
Q

how do exudates form

A

formed in inflammation because vascular permeability increases due to retraction of endothelial cells, creating spaced for fluid and proteins to pass through

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21
Q

what is fibrin

A

a large protein molecule that aids in localizing the inflammatory process
- founds in exudates but not transudates

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22
Q

how is fibrin produced in inflammation

A
  • tissue thromboplastin is released by tissue injury - many injuries which initiate inflammation also initiate fibrin formation
  • monomeric fibrin is acted on by coagulation factor XIII to produce fibrillary polymer
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23
Q

leukocyte recruitment and activation in inflammation (brief)

A
  • in acute inflammation inflammatory cells emigrate from the blood into the area of injury
  • inflammatory cells are first attracted to the injured area
  • then attach themselves to the capillary wall
  • then squeeze through or between endothelial cells
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24
Q

what are the inflammatory cells

A

white blood cells (leukocytes)
- derived from myeloid cells in bone marrow, move to bloodstream when mature
- either become mononuclear cells or granulocyte’s

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25
Q

what are granulocytes

A
  • leukocytes with a multilobulated nucleus and contains cytoplasmic granules
  • include neutrophils, basophils and mast cells
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26
Q

what are mononuclear cells

A
  • smooth round cells which have a great role in chronic inflammation
  • include lymphocytes, plasma cells, monocytes and macrophages
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27
Q

characteristics of neutrophils

A
  • type of granulocyte
  • GREATEST ROLE in acute inflammation, most seen WCB in early stages
  • actively motile, have enzymes that degrade material
    main function = phagocytosis of microorganisms
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28
Q

which leukocyte has the greatest role in acute inflammation

A

neutrophils

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29
Q

what is neutropenia

A

low neutrophil numbers
- can be a side effect of cancer therapy
- causes increased risk of incfection

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30
Q

what are eosinophils

A
  • important WBCs in certain disease processes
  • granulocytes - contain different enzymes than neutrophils
  • recruited to fight parasitic disease
  • directly involved in hypersensitivity response
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31
Q

what are lymphocytes

A
  • mononuclear cells that can be attracted to inflammatory site by other lymphocytes
  • some may develop into plasma cells (antibody producing cells)
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32
Q

what are monocytes

A
  • mononuclear cells that are present in the blood and migrate to other tissues
  • once fixed into tissues they are termed MACROPHAGES
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33
Q

what are macrophages

A
  • mononuclear cells in acute inflammation
  • main role = phagocytosis and clean up of cellular debris
  • additional roles include secreting endogenous pyrogen and complement compounds
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34
Q

What are the 5 steps of leukocyte recruitment from the circulation to the injured area

A
  1. Margination, rolling and adhesion of lymphocytes
  2. transmigration of leukocytes
  3. chemotaxis
  4. leukocyte activation
  5. Phagocytosis and pathogen degradation
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35
Q

what are selectins and integrins

A
  • molecules involved in getting leukocytes out of vessels
    selectins: select the leukocyte they want to migrate within the vessel with
    integrins: integrate the leukocyte into tissues
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36
Q

what is diapedesis

A

how leukocytes leave vessels by squeezing through junctions
- facilitated by PECAM-1

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37
Q

step 1 of leukocyte recruitment: Margination, rolling and adhesion of lymphocytes

A
  • normal laminar flow of blood becomes disordered sue to vessel dilation and WBCs move to vessel wall
  • leukocytes increase contact with endothelium (marginate)
  • they then roll along the endothelial surface, causing it to become sticky
  • leukocytes adhere to vessel wal
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38
Q

step 2 of leukocyte recruitment: transmigration of leukocytes

A
  • leukocytes that have adheres to the vessel wall leave by diapedesis
  • leukocytes move past the basement membrane by degrading them with collagenases
  • then move into the interstitial space
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39
Q

step 3 of leukocyte recruitment: chemotaxis

A
  • chemical mediators act as chemotactic signals for leukocytes
  • chemotactic molecules bind specific receptors on leukocyte surface
  • increases intracellular calcium and assembles intracellular contractile elements
  • contractile elements allow leukocytes tp move by extending pseudopods
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40
Q

step 4 of leukocyte recruitment: leukocyte activation

A
  • receptors on leukocytes recognize PAMPs on bacteria and pathogens
  • receptors on PAMPs recognize pathogenic components which directly activate leukocytes
  • opsonins can also bind foreign substances to indirectly activate leukocytes
  • a pathogen entering the tissue can also activate them
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41
Q

step 5 of leukocyte recruitment: Phagocytosis and pathogen degradation

A
  • neutrophils and macrophages ingest and destroy particles
  • phagocyte/particle complex of coated with IgG or C3b (opsonization) to enhance phagocytosis
  • after binding of opsonized particles, the particle is engulfed by the phagocytic cell - forms a phagosome
  • stimulates increase of ROS production
  • ROS mediate killing of most pathogens
  • pathogens further degraded by fusion of the phagosome with lysosomes which release acid hydrolyzes
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42
Q

what are the mediators of acute inflammation

A

chemicals derived from either plasma or cells
from plasma: exist in inactive form
from cells: either pre-formed and stored in granules or formed when needed

43
Q

what are major groups of inflammatory mediators

A
  1. vasoactive amines
  2. plasma proteases
  3. lysosomal constituents
  4. arachidonic acid metabolism
  5. platelet-activating factor
  6. cytokines
44
Q

vasoactive amines as inflammatory mediators

A
  • mainly histamine and serotonin
  • histamine is released from mast cells, and some from basophils and platelets
  • serotonin is released during platelet aggregation
  • both cause vasodilation and increased permeability
  • cause IMMEDIATE PHASE, greatest role of all mediators
45
Q

plasma proteases as inflammatory mediators

A
  • initial activation by factor XII
  • endothelial injury exposes XIIa which cleaved protein substrates in the Kinin system, coagulation cascade and complement system
  • in Kinin system: XIIa cleaves prekallikrein - Kallikrein becomes Bradykinin which increases vascular permeability
  • in coagulation cascade: XIIa initiates the cascade which activated thrombin to produce fibrin - breakdown of fibrin increases vascular permeability
  • in complement: C5a and C3a stimulate histamine release from mast cells. C5a activates phagocytes in arachnoid acid metabolism. C3a acts as an opsonin
46
Q

lysosomal constituants as inflammatory mediators

A
  • neutrophils generate toxic O2 free radicals and proteases
  • endothelial damage is caused, increases vascular permeability
47
Q

arachidonic acid metabolism as an inflammatory mediator

A
  • unsaturated FAs are found in membranes of inflammatory cells
  • phospholipase causes release of arachnoid acid - leads to production of prostaglandins, leukotrienes and lipoxins
  • this cascade is the target of anti-inflammatory drugs
48
Q

platelet-activating factor as an inflammatory mediator

A
  • generated from cell membranes by phospholipase A
  • causes platelet aggregation and activation
  • increased vascular permeability at low levels, vasoconstriction at high levels
49
Q

cytokines as inflammatory mediators

A
  • cytokines are products of activated lymphocytes and macrophages
  • produced during inflammatory and immune responses by macrophages and dendritic cells
  • most important = interleukin 1 (IL-1) and tumour necrosis factor (TNF)
  • induce endothelial activation (and expression of selectins and integrins)
  • IL-1 activates tissue fibroblasts, TNF activates neutrophils
50
Q

what are anti-inflammatory drugs

A
  • drugs which suppress the response to injurious agents
  • do not treat the cause itself
51
Q

what are NSAIDs

A

non-steroidal anti-inflammatory drugs
- include aspirin and ibuprofen
- act by inhibiting the conversion of arachadoic acid to prostaglandins
- have both anti-inflammatory and analgesic activity
- first choice of treatment for chronic inflammation

52
Q

how can corticosteroids modify the inflammatory response

A
  • block the conversion of phospholipids to arachadoic acid
  • diminish vasodilation and decrease permeability (reduce exudation)
  • stabilize lysosomal membranes (reduce release of amines)
  • suppress the immune response
    examples of corticosteroids are prednisone, dexamethasone and betamethasone
53
Q

localized pain as a sign of acute inflammation

A
  • initial response to injury, “defence system”
  • can be caused by stimulation of nerve endings
  • bradykinin, histamine and serotonin have role in signalling pain
  • bradykinin moderated pain sensation through nerve endings
  • increase in tissue tension due to swelling leads to pain
54
Q

sign vs symptom

A

sign: any objective evidence of disease
- apparent on physical examination
symptom: any subjective evidence of disease
- perceived by the patient

55
Q

what is a fever

A

elevation in core body temperature
- pyrogens are agents that induce fever
- endogenous pyrogens are generated from neutrophils in acute inflammation - e.g. IL-1 and TNF
- act on the hypothalamus via prostaglandin synthesis
- fever causes increase in metabolic rate
- can be beneficial to inhibit growth of organisms
- can be bad by helping infection and stimulating

56
Q

what is hypothermia

A

decrease in core body temperature
- opposite of fever
- can be medically induced to slow bodies metabolism

57
Q

changes in peripheral WBC count as a systemic sign of inflammation

A

leukocytosis = increased WBC numbers
- may see immature neutrophils in the blood, indicated need for neutrophils
- IL-1 and TNF need to mediate neutrophil release from bone marrow
leukopenia = decreased WBC count
- often seen when neutrophils are decreased and lymphocytes are increased

58
Q

clinical changes in plasma proteins

A

“active phase reactants” are when plasma proteins increase in acute inflammation
- increased levels are a non-specific indication of inflammation

59
Q

what are the 3 outcomes of acute inflammation

A
  1. resolution
  2. healing by fibrosis
  3. chronic inflammation
60
Q

what is resolution of inflammation

A

returning back to normal state after a disruption
- cellular debris and swelling are removed by macrophage activity and lymphatic flow

61
Q

what is suppurative inflammation

A

the formation of pus resulting from liquefactive necrosis

62
Q

what is pus

A

the resulting liquified mass of liquefactive necrosis
- made up of necrotic tissue, dead organisms and neutrophils

63
Q

what is an abscess

A
  • a build-up of pus that forms when it becomes walled off by fibrous tissue
  • often red and swollen, may feel pain upon touch
64
Q

how are abscesses resolved

A
  • may rupture and drain pus to heal on their own
  • small abscesses may be removed by macrophages
  • if abscess rupture doesn’t fully drain it may reform or remain as chronic inflammation
65
Q

what is the worst case scenario of an abscess

A

bacteria escapes the site causing local spread of infection (cellulitis) and sepsis

66
Q

what is sepsis

A

the spread of bacteria and/or their toxins via the blood stream
- if bacteria are virulent, can cause widespread cytokine release and antibiotics are not effective
- can then lead to DIC, then septic shock, then death

67
Q

what is bacteremia

A

when bacteria travels in the bloodstream without causing illness, but leads to abscess development in other organs
- valves of the heart are predisposed to this

68
Q

what is chronic inflammation

A

the result of continued inflammatory response in combination with an immune response against the agent

69
Q

where is bacteremia seen in growing kids and animals

A

in growth plates (epiphyses)

70
Q

chronic inflammation is characterized by…

A
  • some degree of an immune response
  • infiltration and accumulation of macrophages
  • healing of tissue through the development of granulation tissue
  • ongoing tissue injury
71
Q

why might chronic inflammation occur?

A
  • may follow acute inflammation If response failed to eliminate the causative agent
  • can occur without an acute phase
  • may arise in association to an antigen, pressmen injury or autoimmune disease
72
Q

chronic inflammation example: tuberculosis

A
  • diseases that causes chronic inflammation of the lungs or other tissues
  • there are some drug resistant strains
  • systemic signs include fever, weight loss and fatigue
  • local signs include coughing and hemoptysis (coughing blood)
73
Q

presence of what cells indicate chronic inflammation

A
  • effector T cells
  • plasma cells
  • macrophages
74
Q

what determines if the chronic inflammation is successful or not

A
  1. the extent of the immunologic response
  2. the degree of activation and killing by T cells
  3. antibody formation by plasma cells and its interaction with the agent
  4. activation of macrophages by lymphokines (produced by T cells)
75
Q

what is granulomatous inflammation

A

specific type of chronic inflammation induced by epithelioid macrophages
- a T cell mediated response may occur first
- effector T cells produce lymphokines that cause macrophages to remain in the area and form granulomas

76
Q

what are epithelioid cells

A
  • macrophages with a foamy pale cytoplasm, due to extensive secretory rough ER
  • can secrete lysosomes and other enzymes, but not as efficient as phagocytosis
77
Q

most common type of granulomatous inflammation

A

tuberculosis
- macrophages accumulate and form granulomas bound mycobacteria TB

78
Q

what are differential diagnoses for granulomatous inflammation

A
  1. atypical bacteria
  2. fungal pathogens within tissues
  3. parasites within tissues
  4. inert foreign bodies
  5. some immune-mediated diseases
79
Q

why might granulomatous inflammation arise from impaired phagocytosis

A
  • the casual agent is phagocytosed but survives in the macrophage
  • phagocytosis of the casual agent is impaired
80
Q

what is Leprosy

A

a disease that causes skin thickening and extensive tissue destruction to fingers and face
- patients have weak T cell responsiveness against the leprosy bacteria

81
Q

what are foreign body granulomas

A
  • develop in response to foreign materials that are too large to be phagocytosed
  • macrophages gather around the foreign material and attempt to remove it by non immune phagocytosis
82
Q

how can foreign body granulomas be used as a sign for drug abuse

A

Talc particles and cotton fibres from filtering of drugs can be found in the liver

83
Q

what is a sponge count

A
  • small gauze pads used in surgery are packed with a specific number of sponges
  • packs are counted at the end of surgery before the body is closed to ensure none were left in the body
  • if one was left, could lead to adhesions between abdominal organs - chronic inflammatory response
84
Q

what is furunculosis

A

an ingrown hair - type of granulomatous inflammation
- immune system doesn’t recognize the hair as “self” due to the keratin

85
Q

what is non-granulomatous chronic inflammation

A
  • inflammation WITHOUT epithelial cells
  • presence of sensitized lymphocytes, plasma cells, and macrophages scattered through affected tissue, along with areas of necrosis and fibrosis
86
Q

what are the causes of non-granulomatous chronic inflammation

A
  1. chronic viral infection: evoke B and T cell response
  2. other chronic infection: macrophage survives following phagocytosis, “foamy” macrophages can accumulate without forming granulomas
  3. chronic autoimmune disease: reaction against “self” antigen
  4. allergic conditions and parasitic infections: cells accumulate in tissues of hypersensitivity runs
  5. Chronic toxic disease: cells may become antigenic, dominated by necrosis and fibrosis
87
Q

what is chronic suppurative inflammation

A
  • body cannot clear a pus-producing stimulus
  • shows as area with necrosis, pus formation, fibrosis and mononuclear cells
88
Q

mixed chronic and acute inflammation: pus formation

A
  • initial injection of bacteria in subcutaneous tissue causes cellulitis - form pus pockets
  • body attempts to spread infection by walling damaged tissue off with granulation tissue
  • result is thick wall and central cavity filled with pus
89
Q

what is osteomyelitis

A

the result of infection of bone with pyrogenic bacteria
- includes rapid and sever tissue necrosis
2 types: hematogenous and secondary

90
Q

hematogenous osteomyelitis

A
  • bacteria is carried to bone by the blood stream
  • bacterial seeding site in children is epiphyseal cartilage
91
Q

secondary osteomyelitis

A

bacteria develops secondary to extension from a wound or adjacent site of infection
- can occur at open fracture site or surgery incision

92
Q

what is sequeststrum

A

a fragment of deviated bone that persists
- can lead to osteomyelitis
- difficult to resolve when chronic because lost blood supply is needed to deliver leukocytes and antibodies

93
Q

how can anemia as a sign of chronic inflammation

A
  • caused by inflammatory mediators such as cytokines
  • result is reduced transport of stored iron into the plasma, despite normal iron stores
94
Q

what is amyloidosis

A

a group of diseases characterized by the deposit of amyloid in the interstitial of tissues
- can occur due to inflammatory processed, immune conditions or genetic conditions

95
Q

what is an amyloid

A

an abnormally folded insoluble protein
- consists of beta-pleated fibrillar protein

96
Q

3 most common forms of amyloid

A
  1. Serum amyloid-association non-immunoglobin protein: amyloid associated with chronic inflammation
  2. Immunoglobin light chain amyloid: produced by plasma cells or B cell tumours
  3. Amyloid beta: characterizes cerebral plaque lesions of Alzheimer’s
97
Q

3 typed of amyloidosis

A
  1. systemic amyloidosis
  2. localized amyloidosis
  3. familial amyloidosis
98
Q

what is systemic amyloidosis

A
  • involves several organ systems
  • primary systemic is most common (AL amyloid). abnormal plasma cells secrete only light chain unit of immunoglobin
  • secondary is amyloid depositions occur widely in the body
99
Q

what is localized amyloidosis

A
  • deposits within a single cell or organ
  • ## amyloid plaques in the brain are seen in Alzheimers
100
Q

what is familial amyloidosis

A
  • amyloid deposited locally in organs such as heart, kidney or nervous tissue (rare)
101
Q

functional problems associated with amyloidosis

A
  • tissue is less flexible than normal
  • nutrients can’t diffuse as easily
  • amyloid in renal glomerulus alters normal filtration or kidney
  • amyloid of heart leads to heart failure
  • AB amyloid deposits and Tau deposits in brain are related to cognitive decline
102
Q

what happens if there is amyloid deposition in renal glomerulus

A

there will be protein loss in urine

103
Q
A

PATH (11 decks)

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