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BMS 460 > Inflammation Process > Flashcards

Inflammation Process Flashcards

1
Q

tissue injury causes what?

A

acute inflammation

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2
Q

describe action-counteraction during the inflammation process

A
  • inflammation occurs when cells become injured
  • the response (counteraction) to inflammation is the same regardless of the cause!!
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3
Q

acute inflammation leads to what?

A

release of chemical mediators (histamine, kinins, prostaglandins)

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4
Q

what effects do chemical mediators have?

A
  • vasodilation and increased blood flow (heat, redness)
  • increased capillary permeability (edema, pain)
  • chemotaxis (WBC’s to area)
  • irritation of nerve endings (pain)
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5
Q

what is the goal of increased capillary permeability?

A
  • clot blood (fibrin mesh walls off the area)
  • this works along with vasodilation so more fibrin and other clotting factors can get to the area
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6
Q

what is the goal of chemotaxis?

A
  • white blood cells: phagocytosis (remove cause of inflammation and cell debris)
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7
Q

describe the goal of increased capillary permeability and chemotaxis together

A
  • increased capillary permeability: gets fibrin and other clotting stuff to area
  • chemotaxis: phagocytosis to clean up
  • together: preparation for healing!!
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8
Q

three potential results of healing

A
  • resolution: damaged cells recover, follows reversible damage
  • regeneration: replacement by the same type of cell, follows irreversible damage
  • scar tissue (fibrosis): this is also a response to chronic inflammation. remember that chronic inflammation can cause acute inflammation
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9
Q

chemical: histamine
source and major action?

A

source: mast cell granules
major action: immediate vasodilation and increased capillary permeability

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10
Q

chemical: chemotactic factors
source and major action?

A

source: mast cell granules
major action: attract and activate neutrophils

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11
Q

chemical: platelet-activating factor (PAF)
source and major action?

A

source: cell membranes of platelets
major action: platelet aggregation (stop bleeding)

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12
Q

chemical: cytokines (interleukins, lymphokines)
source and major action?

A

source: T-lymphocytes, macrophages
major action: increase plasma proteins, induce fever, chemotaxis and leukocytosis (occurs with platelet aggregation, causes eosinophilia)

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13
Q

chemical: prostaglandins (PG’s)
source and major action?

A

source: synthesis from arachidonic acid in mast cells
major action: vasodilation, increased capillary permeability, pain, fever, potentiate histamine effect

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14
Q

describe chemical mediators in the inflammatory process

A

this is a complex set of interaction among soluble factors (the mediators?) and cells that can arise in any tissue in response to traumatic, infectious, post-ischemic, toxic or autoimmune injury

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15
Q

define inflammatory cells and give examples

A
  • inflammatory cells: white blood cells (leukocytes) found inside the blood
  • polymorphonuclear neutrophil
  • eosinophil
  • basophil
  • monocyte
  • lymphocyte
  • platelets
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16
Q

define tissue cells and give examples

A
  • tissue cells: found outside blood vessels
  • mast cell (comes from basophil)
  • macrophage (comes from monocyte)
  • plasma cell (comes from lymphocyte)
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17
Q

how are white blood cells (leukocytes) named?

A
  • they are named based on their appearance in blood smears stained with Wright’s (or Giemsa’s) stain
  • criteria used to classify them: cell size, nucleus shape, presence or absence of cytoplasmic granules, and color of granules present
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18
Q

which cells have granules and what color do the granules stain?

A
  • neutrophils: clear?
  • eosinophils: red
  • basophils: purple
  • mast cells: purple (from basophils)
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19
Q

which cells do not have granules?

A
  • monocytes (and macrophages)
  • lymphocytes (and plasma cells)
  • however, these two types of leukocytes may have small, azurophilic granules at a high magnification - these are lysosomes and are called nonspecific granules in blood cells
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20
Q

types of granules in neutrophils

A

specific: phospholipase A2, elastase
azurophilic: phospholipase A2, type IV collagenase (eats bm)

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21
Q

types of granules in eosinophils

A

specific: histaminase, collagenase
azurophilic: collagenase

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22
Q

types of granules in basophils

A

specific: histamine (basophil gives rise to mast cell when it exits the blood vessel)

23
Q

what does tissue injury stimulate?

A

release of chemical mediators (cytokines, chemokines)!

24
Q

what are the two types of chemical mediators?

A

plasma-derived and cell-derived

25
Q

describe plasma-derived chemical mediators

A

circulate in inactive form, must be activated by activators

26
Q

describe cell-derived chemical mediators

A

preformed and stored in granules, or synthesized de novo (on demand)

27
Q

what does it mean when we say that chemical mediators are heterogeneous?

A

they can be:
- biogenic amines (histamine)
- peptides (bradykinin, complement)
- arachidonic acid-derivatives (prostaglandins)

28
Q

what does it mean when we say that chemical mediators are multifunctional?

A
  • vasodilation or constriction
  • activation of inflammatory cells
  • chemotaxis
  • cytotoxicity
  • pain, fever
29
Q

describe the kinetics of immediate and late-phase reactions to allergen

A
  • immediate vascular and smooth muscle reaction develops within minutes after challenge (challenge defined as allergen exposure to a previously sensitized individual)
  • the late phase reaction will develop 2-24 hours later
  • lots of clinical manifestations in immediate reaction
  • fewer clinical manifestations in late-phase reaction
30
Q

describe the morphology of immediate and late-phase reactions to allergen

A

immediate: vasodilation, congestion, edema
late-phase: inflammatory infiltrate rich in eosinophils, neutrophils, and T-lymphocytes

31
Q

what is the importance of arachidonic acid?

A
  • arachidonic acid-derivatives are an important group of inflammatory mediators
  • many first messengers, including neurotransmitters, neuromodulators, and neurohormones, stimulate the release of arachidonic acid in cells
32
Q

what are COX1 and COX2?

A
  • these are cyxlooxygenases that inhibit the formation of prostaglandins from arachidonic acid
  • COX1: constitutive and involved in many physiological functions
  • COX2: inducible at inflammatory sites
33
Q

describe the pathway from membrane phospholipid to prostaglandins (inflammatory mediators)

A
  • cell membrane phospholipids
  • made to arachidonic acid by phospholipases (for example, neutrophils release phospholipase which acts on cell membranes in mast cells)
  • arachidonic acid made into several prostaglandins by cyclooxygenases (like COX1 and COX2)
34
Q

what are the three types of prostaglandins made from arachidonic acid via cyclooxygenases?

A
  • prostacyclin (PGI2): causes vasodilation, inhibits platelet aggregation (associated with bringing platelets to area)
  • thromboxane A2 (TXA2): causes vasoconstriction, promotes platelet aggregation
  • PGD2 and PGE2: vasodilation, increased vascular permeability
35
Q

what is an example of phospholipase action? (see chart on slide 35)

A
  • phospholipase from neutrophils acts on the phospholipids in cell membranes (mast cells), forming the arachidonic acid pool
  • remember neutrophils are part of the primary/nonspecific immune response!
36
Q

what are the consequences of COX inhibition by NSAIDs?

A
  • most NSAIDs inhibit both COX1 and COX2
  • this means they will inhibit the production of prostaglandins such as PGEx, TxA2, and PGI2, all of which have normal physiologic functions in the stomach, intestine, kidney, platelets, and endothelium. these are in response to physiologic stimuli!!
  • inhibition of COX1 can cause gastric ulcers, renal ischemia, and premature closure of the ductus arteriosus
  • because they inhibit both COX isoforms, they are anti-inflammatory, anti-pyretic, analgesic and have anti-platelet effects
37
Q

describe specific COX2 inhibitors

A
  • these capitalize on the anti-inflammatory and analgesic properties of NSAIDs, but bypass the risks associated with COX1 inhibition
  • however, there is risk of MI because they inhibit endothelial function (ask prof question abt this)
38
Q

describe the results of physiologic vs. inflammatory stimuli

A
  • physiologic stimulus –> activates COX1 in stomach, intestines, kidney, platelets, endothelium –> make prostaglandins pGE2, TxA2, PGI2 –> all have physiologic functions
  • inflammatory stimulus –> activates COX2 at inflammatory sites from macrophages and synoviocytes –> makes inflammatory prostaglandins, proteases, and oxygen free radicals –> inflammation!!
39
Q

4 important pathogenic factors of edema

A
  1. increased venous pressure
  2. reduced oncotic pressure of plasma resulting from low albumin concentration
  3. increased permeability of the vessel wall
  4. obstruction of lymphatics
40
Q

4 ways to acquire edema (slide 37)

A
  1. venous thrombosis (blood clotting) and heart failure can lead to increased hydrostatic pressure in capillaries - this means that it would push more fluid out into interstituim?
  2. nephrotic syndrome enteropathy (inability to retain proteins) and liver failure lead to decreased oncotic pressure. this decrease in proteins in the blood, so less fluid stays in blood and more gets pushed into interstitium
  3. inflammation, trauma, and burns result in increased vascular permeability, allowing more water to go into cells (tissue)
  4. parasites, surgery, and tumors can obstruct lymph flow, so this excess fluid stays in the interstitium and does not get picked up by the lymph!!
41
Q

describe some general aspects of neutrophils and macrophages

A
  • have lots of receptors on surface that allow them to bind to microbes/foreign material and internalize
  • product lots of enzymes, some released
  • produce free radicals
42
Q

what does tissue injury stimulate?

A
  • release of chemical mediators to promote vasodilation
  • chemotaxis
  • neutrophils and macrophages bind to capillaries, emigrating into the tissue where they can phagocytose pathogen
43
Q

neutrophilia

A

macrophage-derived IL-1 stimulates the release of neutrophils from bone marrow storage sites - macrophages release this when they are exposed to inflammatory stimuli

44
Q

steps of emigration of neutrophils from blood vessels to tissues

A
  1. adhesion (to capillaries)
  2. insertion of pseudopods (parts of the cell, actin-mediated) between endothelial cells
  3. passage through the basement membrane
  4. ameboid movement towards the source of the chemotactic stimuli (or stimuli (ex: cytokines) that caused macrophages to recruit neutrophils)
  5. phagocytosis of bacteria that were the source of chemotactic stimuli
    (tissue injury, then cytokines, which attract macrophages, which release macrophage-derived IL-1, which recruit neutrophils, then this process)
45
Q

first receptors activated on neutrophil or macrophage during any hose-pathogen interaction

A

members of the toll-like receptor (TLR) family, and the co-receptor which is CD-14. activation of these receptors leads to many of the important cellular functions of neutrophils and macrophages

46
Q

what does the phagolysosome do in neutrophils/macrophages? (slide 38)

A
  • firstly, phagolysosome results when microbe gets phagocytosed (after binding CD14/TLR) and then this phagosome combines with the lysosome
  • nitric oxide synthase (inducible enzyme in the phagolysosome) breaks down pathogen
  • phagocyte oxidase converts O2 to reactive oxygen species (ROS), which also breaks down pathogen
    -phagocyge oxidase also present on cell surface, so releases ROS into ec space, targeting the microbe
  • lysozymes (proteases) are also released at cell surface, causing tissue damage and inflammation
47
Q

the liver is an important target for?

A
  • macrophage-derived cytokines
  • these are IL-1, IL-6, and TNF-alpha
  • they induce the liver to release acute phase proteins
  • this increases the level of fibrinogen
  • fibrinogen coats the surface of red blood cells and reduces their charge so they aggregate more readily
48
Q

describe the ESR test (erythrocyte sedimentation rate)

A
  • greater inflammation means red blood cells settle faster, so higher ESR (because they are coated in fibrinogen so they are trying to aggregate?)
  • this is a nonspecific but clinically useful indicator of inflammation! in other words, doesn’t tell us anything about the cause of the inflammation
49
Q

what is responsible for systemic inflammation?

A
  • the three macrophage-derived cytokines, which we saw target the liver: IL-1, IL-6, and TNF-alpha
  • all of these cytokines act on skeletal muscle to enhance protein catabolism, which increases pool of amino acids for efficient antibody production by plasma cells
  • also result in an increase in body temperature
49
Q

what does the liver release in response to the macrophage-derived cytokines?

A
  • complement (C2-5)
  • clotting factors (fibrinogen, VWB factor)
  • protease inhibitors (AAT): prevent excessive tissue damage
  • serum amyloid A: prevent excessive tissue damage - activity of this protein is also a non-specific indicator of inflammation
  • C-reactive protein (CRP): prevent excessive tissue damage by binding to phospholipids on bacterial cell membranes and acting as an opsonin to facilitate phagocytosis
50
Q

describe how fever occurs

A
  • cytokines (three macrophage-derived ones) act on hypothalamic regulatory center
  • this adjusts the hypothalamic thermostat higher
  • which results in sequelae to raise core temperature by decreasing heat loss (ex: vasoconstriction!)
51
Q

describe the pathway of fever occurence

A

bacterial infection –> macrophages and /or tissue necrosis cause cytokines to be released –> cytokines act on endothelial cells of OVLT in the brain –> norepinephrine stimulates release of arachidonic acid, makes PGE2 –> PGE2 diffuses into hypothalamus and raises set point for thermoregulation

52
Q

wound healing: primary intention

A
  • primary intention is scar!
  • start with incision
  • hours later: scab forms and leukocytes surround deep part in dermis
  • macrophages and fibroblasts create granulation tissue to fill wound, which is perfused, fibrous CT that replaces fibrin clot, can fill wound of any size
  • over time, should turn from fibronectin and fibrin to collagen II and finally collagen I
53
Q

wound healing: secondary intention

A
  • secondary intention is keloid!
  • start with gaping wound, foreign body or bacteria in wound
  • granulation tissue forms, but basically fails, resulting in a scar composed of type II collagen rather than type I

BMS 460 (28 decks)

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