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214 SECtIoN II Pathology ` PATHOLOGY—InfLAMMATIOn Pathology ` PATHOLOGY—InfLAMMATIOn

Erythrocyte RBCs normally remain separated via ⊝ charges. Products of inflammation (eg, fibrinogen) coat
sedimentation rate RBCs Ž  ⊝ charge Ž  RBC aggregation. Denser RBC aggregates fall at a faster rate within a
pipette tube Ž  ESR. Often co-tested with CRP (more specific marker of inflammation).

 ESR  ESR
Most anemias Sickle cell anemia (altered shape)
Infections Polycythemia ( RBCs “dilute” aggregation
Inflammation (eg, giant cell [temporal] arteritis, factors)
polymyalgia rheumatica) HF
Cancer (eg, metastases, multiple myeloma) Microcytosis
Renal disease (end-stage or nephrotic syndrome) Hypofibrinogenemia
Pregnancy

Acute inflammation Transient and early response to injury or infection. Characterized by neutrophils in tissue A ,
A often with associated edema. Rapid onset (seconds to minutes) and short duration (minutes to
days). Represents a reaction of the innate immune system (ie, less specific response than chronic
inflammation).

STIMuLI Infections, trauma, necrosis, foreign bodies.
MeDIATOrS Toll-like receptors, arachidonic acid metabolites, Inflammasome—Cytoplasmic protein complex
neutrophils, eosinophils, antibodies (pre- that recognizes products of dead cells,
existing), mast cells, basophils, complement, microbial products, and crystals (eg, uric acid
Hageman factor (factor XII). crystals) Ž activation of IL-1 and inflammatory
response.
COMPOnenTS ƒ Vascular: vasodilation (Ž  blood flow and To bring cells and proteins to site of injury or
stasis) and  endothelial permeability infection.
ƒ Cellular: extravasation of leukocytes (mainly Leukocyte extravasation has 4 steps: margination
neutrophils) from postcapillary venules and and rolling, adhesion, transmigration, and
accumulation in the focus of injury followed migration (chemoattraction).
by leukocyte activation
OuTCOMeS ƒ Resolution and healing (IL-10, TGF-β) Macrophages predominate in the late stages of
ƒ Persistent acute inflammation (IL-8) acute inflammation (peak 2–3 days after onset)
ƒ Abscess (acute inflammation walled off by and influence outcome by secreting cytokines.
fibrosis)
ƒ Chronic inflammation (antigen presentation
by macrophages and other APCs
+
Ž activation of CD4 Th cells)
ƒ Scarring

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