Pathology of Acute Inflammation Flashcards
(36 cards)
Typical inflammatory reaction develops through a series of 5 sequential steps
1) recognition of injurous agent
2) recruitment of leukocytes (to site of infection. Neutophils. Monocytes -> macrophages)
3) remolval of injurous agent
4) Regulation or control of response:
Switch from inflammatory to antiinflammatory signals
5) Resolution ( repair)
Acute vs Cronic Inflammation
Acute appendicitis
Swollen erythematous appendix
Adhesion with appendix curling and attaches to itself and to the cecum
Perforation of appendix wall secondary to mural necrosis not uncommon if untreated
Common in children. Emergent surgery.
Caused by nonspecific obstruction of the appendiceal lumen:
Fecal material, undigested food, foreign material, and enlarged lymphoid follicle, tumor…
Intraluminal bacterial ovregrowth, bacterial invasion of the wall, inflammation, ischemia, and eventually perforation
Normal appendix
Normal appendiceal epithelium
Lymphoid aggregate
Appendix in acute appendicits
Acute appendicits. Pus. Liquefactive debris.
You can see that there are neutrophils
What process accounts for the appendix being swollen and red?
a) vasodilation, capillary permeability, fluid accumulation
b) release of platelet activating factor by the leukocytes
c) vasoconstriction, capillary obstruction, decreased fluid retention
d) decrease NF-kb in circulation
a) vasodilation, capillary permeability, fluid accumulation
Acute inflammation steps
Local tissue damage
vasodilation
erythema
increased temp
increased capillaty permeability, fluid accumulation (edema, pain)
continued chemotaxis
Acute cholecystitis
Acute cholecystitis
Gallstones are a common cause of morbidity worldwide
90% of acute cholecystitis are associted with gallstones
Gallb is usually enlarged and the wall is thickened by edema, vascular congestion, and hemorrhage, or it may appear necrotic
Precipitating event is occlusion of the neck of the gallb and mural edema
Infection is considered secondary and does not contribute to the onset of acute cholecystitis
Risk factors- DM, obesity, native american
Normal gallbladder
Normal gallbladder with bile pigment
Abnormal gallb
acute cholecystitis
Nucleus less well defined
Abnormal gallb
Acute cholecystitis
We see neutrophils in the tissue
The major inflammatory cells involved in acute cholecystitis causes tissue damage by releasing
a) interleukin 6
b) acute phase proteins
c) reactive oxygen species (ROS)
d) tumor necrosis factor
ROS! We know that the major inflammatory cells here are neutrophils and we know that neutrophils release ROS.
IL-6 is produced by macrophages
Acute phase proteins are produced by liver
TNF is produced by activated macrophages
Neutrophils
Attracted to tissues by factors such as complement, clotting proteins
Active phagocytes in tissue
KILL BY ROS, GRANULE CONTENTS
RELEASE IL-8
Macrophages
Ingest microbes and damaged cells
PRODUCE IL-6, TNF-α, and IL-1
PRODUCE GROWTH FACTORS THAT AID IN REPAIR
Active gastritis
Gastric ulcer is defined by the loss of mucosa (including muscularis mucosae) due to inflammation
Confirmed/ visualized by an endoscope
Biopsy taken at time of the procedure to evaluate for etiology
H pylori seen in 90% of gastric ulcer patients who do not use NSAIDS
The term active is used to indicate ther there is a sustained release of inflammatory mediators and, presumably, a persistant cause for this process
Normal gastric mucosa
notice well defined nuclei
notice the LP is very sparsely cellular
Normal gastric mucosa
Notice thqat the nuclei are well defined and that the LP is sparsely cellular
Abnormal gastric mucosae
look at nuc in the middle of the page
less defined
also LP is very heavily cellular
(note L nuclei look more normal)
ACTIVE GASTRITIS
Active gastritis
We see neutrophils
