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General Pathology - Part 2. Pathology > 10.09 Acute Inflammation > Flashcards

10.09 Acute Inflammation Flashcards

1
Q

components of acute inflammation

  • from blood
  • from connective tissue
A
  • from blood: polymophonuclear leukocytes (neutrophils), lymphocytes, platelets, monocyte, clotting factors, eosinophil and basophil
  • from connective tissue: mast cell, fibroblast, macrophage
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2
Q

five cardinal signs of acute inflammation

A

swelling, redness, temperature, pain and loss of function

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3
Q

granulocytes

A
  • neutrophils (PMNs)
  • eosinohpils (more for hypersensitivty)
  • basophils
  • macrophages (mostly for chronic inflammation but also in the late stages of acute inflammation).
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4
Q

vascular event

A
  • vasoconstriction
  • vasodilation
  • exudation
  • stasis
  • adhesion and rolling
  • margination (pavementing)
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5
Q

vascular event: vasoconstriction

A

temporary and neurological response.

when body senses pressure or injury, it initially constricts blood vessels to minimize bleeding. it’s followed by vessel dilation

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6
Q

vascular event: vasodilation

A

starts from artery to capillaries to vein.

increased hydrostatic pressure pushes fluid out of vessels into the injured site.

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7
Q

vascular event: exudation

A

fluid leakage

  • endothelial cells contract to produce interendothelial gaps
  • increased vascular permeability
  • immediate transient (hrs), immediate prolonged (physical damage to vessels; days), and delayed prolonged (e.g., sunburn)
  • mild (watery, serous; bullous disease-bollous dermititis)
  • moderate (fibrinous: some proteins; “bread and butter” pericarditis)
  • supprative (purulent, puss, pyogenic; acute appendititis)
  • severe (hemorrhage)
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8
Q

vascular event: stasis

A
  • blood thickens and slows down (due to decrease in fluid from exudation)
  • RBCs stick together in the middle of the vessel and WBCs are pushed out
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9
Q

vascular event: adhesion and rolling

A
  • in normal state, WBCs and endothelium have same elec. charges. During inflamm., endoth change elec. charges.
  • activated macrophages in the site releases cytokines that leak thru endoth to attrack WBCs to endoth.
  • leukocytes temporarily bind to endoth at P- and E-selectin >> integrin on leukocyte bind to integrin ligand (ICAM-1) for more stable adhesion >> PECAM-1 (CD31) on both leukocyte and endoth bind to allow leukocyte to squeeze through endothelium into the tissue
  • chemotaxis: chemicals released from the injured site create chemotactic factor gradient which attrack neutrophils
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10
Q

vascular event: margination (pavementing)

A

lining of the blood vessels with WBCs

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11
Q

cellular events

A
  • emigration (diapedesis)
  • chemotaxis
  • opsonization
  • phatocytosis
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12
Q

cellular events: emigration (diapedesis)

A
  • pavementing and migration
  • squeezing through the endothelium into the tissue
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13
Q

cellular event: chemotaxis

A
  • drawing of cells through chemotactic gradient secreted by activated macrophages
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14
Q

cellular event: opsonization

A
  • opsonins: molecular taggs attached to offending agents for neutrophil recognition
  • complement 3 breakdown product
  • non-immune immunoglobulin G (IgG)
  • plasma carbohydrate-binding lectins (collectins)
  • receptors: C3b, Fc and C1q
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15
Q

cellular event: phagocytosis

A
  • attachment of neutrophil to opsonized agnet >> engulfment >> discharge of lysosomal granule contents into phagosome >> killing and digestion of agent (using ROS and RNS)
  • lysosomes don’t wait until phagosome is completely formed: lysosomal substances can leak out and destroy nearby anything >> can lead to significant damage
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16
Q

plasma-derived mediators for acute inflammation

A
  • clotting-fibrinolytic: factor XIII, plasmin
  • kinins: e.g., bradykinin
  • complement: e.g., C3a,b, C5a,b proteins
    • C3b attaches to microbe for recognition
    • C3a and C5a recruits and activates leukocytes
  • factor XII starts the cascade
    • kinin cascade will inhibit the whole process
    • clotting cascade will continue the process leading to acute inflamm.
17
Q

cell-derived mediators for acute inflammation

A
  • arachidonic acid derivatives (leads to production of prostaglandins, etc)
    • PG, TX: cyclooxygenases
    • LT, LX: lipoxygenases
  • vasoactive amines from mast cell: histamine and serotonin
  • cytokines: IL-1/TNF
  • nitric oxide from macrophages: stimulates vascular smooth muscle relaxation and vasodilation (also results in leukocytes and platelet adhesion).
18
Q

arachidonic acid

A
  • when worked by 5-lipoxygenase: leads to vasoconstriction and increased permeability
  • when worked by 12-lipoxygenase: leads to vasodilation, inhibition of neutrophil chemotaxis and stimulates monocyte adhesion
  • when worked by cyclooxygenase then prostacyclin PGI2 (from WBC), vasodilation, inhibits platelet aggregation
  • when worked by COX then thromboxane A2 (from platlet), vasoconstriction and platelet aggregation.
  • if just COX, leads to vasodilation and edema.
19
Q

TNF/IL-1

local and systemic effects

A
  • locally: leukocyte adhesion, activation and fibroblast prolifeation and collagen synthesis
  • systemically: fever, leukocytosis, decrese appetite and more sleep
20
Q

subtypes of acute inflammation: within skin

A
  1. abscesses: focal area of suppuration (puss)
  2. phlegmons (cellulitis): spreading of abscesses (e.g., streptococcal: tissues dissolved by neutrophils)
21
Q

subtypes of acute inflammation: on surfaces: (skin, mucous membrane)

A
  • ulcers: focal necrosis and inflammation (“crater-like”)
  • pseudomembranes: diffused ulceration.
  • e.g., pseudomembranous colitis: most common hospital-induced lethal disease
22
Q

systemic effects of acute inflammation

A
  • fever: endogenous pyrogens: IL-1, IL-6, TNF-alpha, PGE, NO
  • leukocytosis: IL1, TNF, CSF, GSF
  • acute phase reactants (produced in liver): CRP, complement, serum amyloid A (SAA)
23
Q

acute inflammation outcomes

A
  1. resolution
  2. abscesses: mass tissue destruction that needs phagocytosis
  3. chronic inflammation: if acute wasn’t enough

General Pathology - Part 2. Pathology (10 decks)

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