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Pathology I > Acute Inflammation 1 > Flashcards

Acute Inflammation 1 Flashcards

1
Q

Describe inflammation.

A

-reaction of vascularized living tissues to injury
-goal:
>inactivation, dilute, destroy pathogens, toxins, foreign material
>bring phagocytes & immune cells to site of injury
>begin repair
-acute VS chronic
-prolonged or excessive inflam = detrimental

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2
Q

Describe infection VS inflammation.

A
  1. Infection
    -invasion & multiplication of pathogen in body
  2. Inflammation
    -body protective response against infection
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3
Q

Describe innate VS adaptive response to inflammation.

A
  1. Innate (initial response)
    -non specific
    -no memory
    -incl epi barrier, inflam, NK cells
  2. Adaptive
    -antigen specific recognition molecules
    -T & B lymphocytes
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4
Q

Describe the types of tissue injury.

A
  1. Physical trauma = cut, abrasion, friction, crush, pressure
  2. Chemical = acid/alkali, pancreatitis
  3. Thermal = burn, frost
  4. Infection = virus, bacteria, fungi, Protozoa, parasites
  5. Radiation = UV light
  6. Immunological = autoimmunity, hypersensitivity
  7. Ischemia = inflam when blood flow re established
  8. Necrosis = inflam at margins
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5
Q

Describe history of inflammation.

A
  1. Celsus = redness, heat, swelling, pain
  2. Virchow = loss of function
  3. John hunter = response, not disease
  4. Metchnikoff = demonstrate phagocytosis via drawings
  5. Nuttal = antibacterial properties of blood
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6
Q

Describe the 5 cardinal signs of acute inflammation.

A
  1. Redness = rubor
    -inc blood flow (hyperaemia)
  2. Swelling = tumor
    -accumulation of fluid (edema, hyperemia) & cells
  3. Heat = calor
    -inc blood flow from core
  4. Pain = dolor
    -release of chemicals that stim nerve endings
  5. Loss of function = functio laesa
    -multiple causes
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7
Q

Describe the role of chemical mediators in inflammation.

A

-initiate & orchestrate vascular & cellular response
-goal: accumulation of fluid, protein, & leukocytes in extravascular space -> elim injurious agent & begin tissue repair

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8
Q

Describe the vascular response.

A
  1. vasodilation (hyperaemia, congestion)
    -inc blood flow & widen endothelial gaps
    >inc vascular permeability -> vascular stasis
    -exduation of fluid (plasma), plasma protein, & leukocytes into extravascular space
    -plasma dilutes effects of inciting stimulus
    -fibrin formation in extravascular area *
    >confine stimulus to an isolated area
    >provide leukocyte w target
    >framework for fibroblast & endothelial cell migration in wound healing
    -extravascular fluid = ‘exudate’
    >forms in inflam bc inc inter endothelial space
    >exudates have high protein & nucleated cell counts (NCC)
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9
Q

Describe the formation of transudates & exudates.

Effusion
A
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10
Q

Describe exudates VS transudates.

A
  1. Exudate
    -inflam
    -high protein (TP)
    -high NCC
    -active process (inc vascular permeability)
  2. Transudates
    -non inflam
    -low protein
    -low NCC
    -passive process (imbalance in osmotic or hydrostatic pressure)
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11
Q

Describe the different morphological types of acute inflammation.

A
  1. Suppurative/purulent
    -fluid w many neutrophils, inc protein
  2. Fibrinous
    -fluid w few cells, high protein
  3. Serous
    -fluid w few cells, low protein
  4. Catarrhal/mucoid
    -thick fluid w mucus (GIT, respiratory tract)
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12
Q

Describe step 1 of acute inflammation.

A

Vasodilation
-follow transient period of vasospasm (facilitate hemostasis)
-histamine, NO, PGs = from damaged cells, mast cells
-serotonin = from platelets
-leads to hyperemia *

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13
Q

Describe step 2 of acute inflammation.

A

Inc vascular permeability
-loosening of junctions between endothelial cells
-vasoactive amines, complement, LTs
-leak plasma (dilutes)
>complement
>antibodies
>clotting factors: fibrinogen -> fibrin *

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14
Q

Describe step 3 of acute inflammation.

A

Emigration of leukocytes cell response
Leukocyte adhesion cascade: KNOW STEPS
1. Margination/pavementing of neutrophils
-move toward periphery of lumen
2. Rolling
-weak binding of selectin
3. Adhesion
-B2 integrins (leukocyte) bind ICAM (endothelial cells)
4. Emigration
-transendothelial migration
5. Chemotaxis
-migration within exudate

Margination
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15
Q

Describe adhesion molecules.

A

-surface receptors on leukocytes & endothelium
>sites of interaction
-facilitate movement of leukocytes
-diff types:
>selectins - tethering, weak (E,P,L) mostly on endothelium
>integrins - firmer (B1 & B2 integrins on leukocytes)
>immunoglobulin fam - ICAM, VCAM, PECAM (on endothelium)

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16
Q

Describe extravasation, chemotaxis, activation.

A

-chemotaxis & activation -> phagocytosis & degranulation
-function of cell response:
>destruction of microbes & foreign material
>neutralization of toxins
>mediation of immune response
>clearing of necrotic tissue
>regen of tissue

17
Q

Describe leukocyte extravasation.

A

‘Diapedesis’
-occurs in post capillary venules
-chemokines act on leukocytes = stim cells to migrate thru inter endothelial spaces
-leukocytes pierce BM = enter extravascular space & follow chemotatic gradient
-leukocytes adhere via adhesion mol (integrins) to glycoproteins in extracellular matrix

18
Q

Describe chemotaxis.

A

-migration of leukocytes to site of injury along chem gradient
-exogenous attracting agent = bacterial products
-endogenous chemoattractants = component of complement system (C5a), arachidonic acid metabolites (leukotriene B4) & chemokines
>neutrophils 1st to arrive in acute inflam *
>eosinophils migrate to area if allergy or parasite *

19
Q

Describe leukocyte activation for phagocytosis.

A

*once neutrophils & monocytes are at the injury site they express receptors:
1. TLR = recog microbial prod & stim prod of cytokines & microbicides by leukocytes
2. GPCR = recog bacterial peptides, chemokines, complement & induce migration of cells from blood & prod of microbicidal substances
3. Receptors for opsonins = bind to particles covered by protein/opsonins (antibodies, complement) -> cell activation & enhanced phagocytosis & intracellular killing
4. Receptors for cytokines = cytokine, gamma interferon is made by NK cells reacting to antigens -> macrophage activation

20
Q

Describe the result of activation of surface receptors on leukocytes.

A
  1. Prod of arachidonic acid metabolites from phospholipid (membranes) -> due to activation of phospholipase (secondary to inc intracellular Ca)
  2. Degranulation & secretion of lysosomal enzymes & oxidative burst
  3. Cytokine secretion amplify & regulate inflam response via activated macrophages
  4. Modulation of leukocyte adhesion mol -> expression of adhesion mol on endothelial cells & -> leukocyte avidity
21
Q

Describe step 4 of acute inflammation.

A

Phagocytosis cell response
-neutrophils first leukocyte to arrive
-engulf & destroy injurious agents
>internalize bacteria, foreign body, dead cell, debris
>fuse w lysosomes & digest content
>oxidative burst produce ROS - free radicals
-secrete substances into exudate like collagenase to degrade dead & damaged tissue components but can also damage vital tissue

22
Q

Describe the summary of acute cell response (steps 3 & 4).

A
  1. Leukocyte adhesion
    -express adhesion mol on surface of leukocytes & endothelial cells in blood vessels (selectins & integrins)
    -induced by secretion of chemical mediators (cytokines & chemokines)
  2. Leukocyte extravasation
    -migration out of blood vessel into extravascular tissue
  3. Leukocyte chemotaxis
    -movement to site of inflam via exogenous & endogenous chemoattractants
  4. Leukocyte activation
    -TLR, GPCR
  5. Leukocyte phagocytosis
    -cell engulf & neutralize injurious agents

Pathology I (17 decks)

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