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Foundations III > inflammation > Flashcards

inflammation Flashcards

1
Q

inflammation definition

A

response to infection or tissue necrosis that allows inflammatory cells, plasma proteins, and fluid to enter the interstitial space with the goal of eliminating the pathogen/clearing debris

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2
Q

features of inflammation

A

rubor, calor, dolor, tumor, decreased function

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3
Q

steps of inflammation

A
  1. recognition of injurious agent
  2. recruitment of WBCs
  3. removal of agent
  4. regulation of response
  5. repair
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4
Q

characteristics of acute inflammation

A
  • innate immunity
  • immediate response
  • pyogenic
  • neutrophils, antibodies, complement
  • associated with extracellular organisms
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5
Q

characteristics of chronic inflammation

A
  • adaptive immunity
  • delayed response
  • more specific
  • lymphocytes, plasma cells, monocytes/macrophages
  • associated with intracellular organisms
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6
Q

pro-inflammatory cytokines

A

IL1 and IL6 => fever
IL8 => attracts neutrophils
TNFa => increased cyclooxygenase

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7
Q

pro-inflammatory mediators (endothelial cell contraction)

A

prostaglandins, leukotrienes, bradykinins, histamines

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8
Q

prostaglandins

A

arachidonic acid products that mediate vasodilation and increased vascular permeability, pain, and fever

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9
Q

leukotrienes

A

arachidonic acid products that attract neutrophils, mediate bronchospasm, and increased vascular permeability

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10
Q

bradykinins (from kallikrein)

A

mediate vasodilation via NO, increased vascular permeability, and pain

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11
Q

histamines

A

mediate vasodilation, endothelial cell contraction, and increased vascular permeability

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12
Q

what is the function of the vascular component of inflammation?

A

vasodilation (for increased blood flow) and increased vascular permeability (via endothelial cell contraction and damage)

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13
Q

what are the cellular components of acute inflammation?

A

neutrophils:

  • drawn towards inflammatory mediators from mast cells and macrophages
  • phagocytose and destroy organisms
  • release cytokines to draw more neutrophils

monocytes:
- release more cytokines

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14
Q

what are the cellular components of chronic inflammation?

A

if neutrophils can’t remove the organisms, they produce cytokines to draw:

  • lymphocytes
  • plasma cells
  • monocytes and macrophages
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15
Q

steps of neutrophil recruitment in the blood vessel

A
  1. margination
  2. rolling
  3. adhesion
  4. transmigration and chemotaxis
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16
Q

neutrophil margination

A

vasodilation and increased vascular permeability => slow blood flow => white cells move to periphery of vessel

17
Q

neutrophil rolling

A
  1. histamine, IL1, and TNFa => P-selectin and E-selectin expression on endothelial cells
  2. sialyl lewis X on neutrophils binds to P-selectin and E-selectin
  3. selectin-neutrophil binding causes slow rolling of neutrophil on vessel wall
18
Q

neutrophil adhesion

A
  1. C5a and leukotrienes => integrin expression on neutrophils
  2. TNFa and IK1 => ICAM and VCAM (cellular adhesion molecules) on the endothelium
  3. integrin - ICAM/VCAM interaction causes adhesion of neutrophil to endothelium
19
Q

neutrophil transmigration

A

neutrophils migrate through the endothelium via diapedesis and move towards chemokines (IL8 and C5a) via chemotaxis

20
Q

what is the cause and presentation of leukocyte adhesion deficiency (LAD)?

A

caused by: defect in integrins (CD18 subunit)

causes: delayed separation of umbilical cord, recurrent bacterial infections, high neutrophil counts in blood (they can’t escape to tissues)

21
Q

what are the stages of phagocytosis?

A
  1. recognition and attachment
  2. engulfment
  3. destruction
22
Q

what receptors are involved in recognition?

A
  • PRRs for PAMPs: TLRs, NOD, RIG-I, MBL

- receptors for opsonins: complement C3b, IgM, IgG

23
Q

how does a neutrophil engulf a bacterium?

A
  1. C3b (opsonin) binds to bacterial capsule
  2. Binds to C3b receptors on a neutrophil
  3. Neutrophil invaginates membrane to form phagosome
24
Q

how do neutrophils destroy phagocytosed bacteria?

A

phagosome fuses with lysosome (which contains killing enzymes), forming a phagolysosome

25
Q

what enzymes are involved in oxygen dependent killing of organisms?

A

Respiratory burst:

  1. NADPH oxidase forms superoxidase radical
  2. superoxide dismutase forms hydrogen peroxide
  3. myeloperoxidase catalyzes production of hypochlorite (in neutrophils only–most effective killer)
26
Q

how to catalase + organisms evade immunity?

A

bacterial catalase breaks down hydrogen peroxide, decreasing the formation of hypochlorite by myeloperoxidase

27
Q

what are the cause and presentation of chronic granulomatous disease?

A

cause: defect in NADPH oxidase => can’t product hydrogen peroxide to kill bugs
causes: recurrent infections from catalase + organisms and failure to kill organisms => granulomas

28
Q

what are the cause and presentation of chediak-higashi?

A

cause: genetic defect in vesicle formation and trafficking => can’t form phagolysosome
causes: neutropenia with giant granules (lysosomes with built up myeloperoxidase) in neutrophils and monocytes, oculocutaneous albinism, susceptibility to pyogenic infections

29
Q

how do inflammation/neutrophils damage tissues?

A
  • neutrophils non-specifically release enzymes and free oxygen radicals into the extracellular space
  • if a pathogen is not cleared, neutrophils continue to be activated => lots of free oxygen radicals => DNA damage and potential dysplastic/neoplastic change
30
Q

how is inflammation resolved?

A

some tissues can regenerate (such as the top layer of the epithelim)

  1. macrophages release anti-inflammatory molecules (TGFB)
  2. macrophages recruit fibroblasts and release vascularization factors (forming granulation tissue)
  3. if tissue architecture was lost: fibroblasts deposit collagen and ECM to form scars
31
Q

what are the components of granulation tissue?

A

fluid/empty space, blood vessels, collagen/fibroblasts

32
Q

what are the two pathways of wound healing and when is each used?

A

First intention/primary union:

  • wound only involves epithelium
  • wound edges are approximated

Secondary intention/secondary union

  • tissue loss is extensive
  • would edges cannot be brought together
33
Q

what are the steps of healing by first intention?

A
  1. hemorrhage and blood clot
  2. acute inflammation and scab formation
  3. proliferation: formation of epithelial cell layer under scab and granulation tissue below
  4. organization: fibroblasts make collagen and inflammation decreases
  5. scar formation: epidermis is intact but there is a loss of sweat glands and hair follicles and there is fibrous tissue beneath
34
Q

how is healing by secondary intention different?

A
  • larger clot
  • more inflammation
  • more granulation tissue
  • wound contraction mediated by fibroblasts
35
Q

what is fibrosis?

A

parenchymal organ damage caused by excessive collagen/ECM deposition in response to injury => organ disfunction

mediated by TGFB and occurs when tissue cannot regenerate

Foundations III (26 decks)

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