2.4 Path: Inflammation Flashcards
What is inflammation?
A Vascularized Living Tissue Response to Injury
= MUST BE ALIVE to have an inflammatory response
Compare and contrast acute/chronic inflammation generally
Acute: onset minutes to days, prominent cell is the NEUTROPHIL
Stereotypic response- follows a set sequence of events
Chronic- Days, weeks, months
Variable pattern
Cells- Macrophage and lymphocytes
In acute ex: swelling, warm, pain; In chronic ex- RA, resulted in joint fibrosis
What are the events in acute inflammation?
Inflammatory response at micro-circulatory level : arterioles, capillaries, venuoles
Trigger incites inflammatory response —> Quick vasoconstriction (1 sec) then vasodilation
When body senses inflammation, all vessels nearby dilate = loss of normal vessel tone —> stasis of blood flow (much slower blood flow than normal)
Hyperemia= accumulation of blood from stasis of blood flow
If near the surface, can see hyperemia. = RUBOR of inflammation
Increases the temperature of the area, caused by hyperemia
Ina cute inflammation, how does fluid get into the interstitial space?
Due to dilation, vessels get leaky, and contents of vessels leak out. Several mechanisms do this.
Mediators (cytokines) cause an inflammatory response and cause contraction of endothelial cells, so leakage between cells into interstitial space
gaps between endothelial cells, hydrostatic pressure
Ina cute inflammation, how to neutrophils respond?
When cells dilate, the endothelial cells (line vasculature) are important response cell. Sense inflammatory signal thru complicated pathway. Endothelial cells recruit neutrophils out of laminar flow.
Margination= attraction of neutrophils from laminar flow to endothelium. THEN
Rolling- Neutrophil rolls along endothelium until they find a gap and then inter to the interstitial space
Adhesion= stick to wall
Migration= neutrophil to site of inflammation
What is hyperemia?
dilated engorged blood vessels filled with RBC’s
What is neutrophil infiltrate?
pale, purulent exudate aka “pus”, neutrophils in extracellular, extravascular space
What is fibrin’s role in acute inflammation?
Fibrin- (NOT fibrosis) A protein that is produced by circulating factors, called coagulation cascade. When triggered can create a thrombus. In inflammation created fibrin.
What is an abscess?
Localized collection of neutrophils with “pseudocapsule
Liquefactive (tissue turns to liquid) necrosis
What are the harmful effects of inflammation?
Extracellular leakage of lysosomal enzymes during phagocytosis
Free radicals
Tissue Damage
How is “shock lung”/ARDS an example of the harmful effects of inflammation?
Lung tissue is damaged by an inflammatory response
Some injury happens eg trauma, sepsis and the lung sense damage, neutrophils enter lung, granules released, then pt undergoes a sicker response
What cell mediates acute inflammation? Chronic?
Acute- neutrophil
Chronic- macrophage
What are the sx of chronic inflammation?
Low Grade Fever, “Night Sweats” Weight Loss Chronic Fatigue, Cough Recurrent Pain Progressive Loss of Function
What are the vascular and tissue events in chronic inflammation?
Initial: Proliferation of capillary sized vessels,i.e. Angiogenesis
Activation and proliferation of fibroblasts
Production of matrix and new collagen
Later (days to weeks):
Vessels mature
Fibroblasts become quiescent
Collagen is permanent deposited
Collagen remodeling results in tissue destruction, i.e. Fibrosis
What is granulation tissue?
Activated “Juicy” Fibroblasts
New Glycosaminoglycans
Angiogenesis
Mixed Inflammatory Cells
Body makes new blood vessels, inflammatory cells present. New matrix, collagen.
This tissue eventually goes away, and we have fibrosis
