Pathology of Acute Inflammation

Question 1

Typical inflammatory reaction develops through a series of 5 sequential steps

Answer 1

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)

Question 2

Acute vs Cronic Inflammation

Answer 2

Question 3

Acute appendicitis

Answer 3

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

Question 4

Answer 4

Normal appendix

Question 5

Answer 5

Normal appendiceal epithelium

Question 6

Answer 6

Lymphoid aggregate

Question 7

Answer 7

Appendix in acute appendicits

Question 8

Answer 8

Acute appendicits. Pus. Liquefactive debris.

You can see that there are neutrophils

Question 9

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

Answer 9

a) vasodilation, capillary permeability, fluid accumulation

Question 10

Acute inflammation steps

Answer 10

Local tissue damage

vasodilation

erythema

increased temp

increased capillaty permeability, fluid accumulation (edema, pain)

continued chemotaxis

Question 11

Answer 11

Acute cholecystitis

Question 12

Acute cholecystitis

Answer 12

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

Question 13

Answer 13

Normal gallbladder

Question 14

Answer 14

Normal gallbladder with bile pigment

Question 15

Answer 15

Abnormal gallb

acute cholecystitis

Nucleus less well defined

Question 16

Answer 16

Abnormal gallb

Acute cholecystitis

We see neutrophils in the tissue

Question 17

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

Answer 17

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

Question 18

Neutrophils

Answer 18

Attracted to tissues by factors such as complement, clotting proteins

Active phagocytes in tissue

KILL BY ROS, GRANULE CONTENTS

RELEASE IL-8

Question 19

Macrophages

Answer 19

Ingest microbes and damaged cells

PRODUCE IL-6, TNF-α, and IL-1

PRODUCE GROWTH FACTORS THAT AID IN REPAIR

Question 20

Active gastritis

Answer 20

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

Question 21

Answer 21

Normal gastric mucosa

notice well defined nuclei

notice the LP is very sparsely cellular

Question 22

Answer 22

Normal gastric mucosa

Notice thqat the nuclei are well defined and that the LP is sparsely cellular

Question 23

Answer 23

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

Question 24

Answer 24

Active gastritis

We see neutrophils

Question 25

Answer 25

Active gastritis

Notice stain for H pylori

Question 26

The chemical signals that cause the neutrophils to be recruited at the site of infection are collectively called

a) migration
b) chemotaxis
c) phagocytosis
d) permeability

Answer 26

CHEMOTAXIS

Question 27

Chemotaxis

Answer 27

Chemical signals that cause immune cells to migrate to a site of injury or infection

Done through chemotactic gradient

Cells go through endothelial cells into tissue space

Question 28

Toxic Shock Syndrome

Answer 28

Assocated with S aureus

1980 menses related TSS rose bc of absorbent tampons

Toxin production is an important pathogenic mechanism, as evidince by clinical manifestations of shock, erythoderma, and multiorgan system involvement

Question 29

Answer 29

Normal fallopian tube

Question 30

Answer 30

Normal fallopian tube

tubal epithelium

Sparce cells below basement memb

Question 31

Answer 31

Abnormal fallopian tube

Dialated vasculature (blood)

A lot of purple = nuclei of inflammatory cells

Question 32

Answer 32

Acute salpingitis

on the l we can see necrotic tissue

on the R of the white space we can wee neutrophils

Question 33

The patient with TSS within 48 hours of admission secondary to multiorgan failure. The process can be summarized as

a) shock from systematic inflammation
b) shock from localized inflammation
c) shock from massive vasoconstriction
d) shock from increase cardiac output

Answer 33

a) shock from systematic inflammation

Question 34

Vasculature reactions of acute inflammation consist of change in blood flow and permebility of vessels

Answer 34

Question 35

Acute inflammatory response treminates with removal of offending agents and dead tissue

Answer 35

Question 36

Outcomes of acute inflammtion

Answer 36

resolution

healing by fibrosis

or

chronic inflammation