Acute And Chronic Inflammation

Front 1

Acute inflammation: Describe the components of the inflammatory response, particularly the reactions of blood vessels and leukocytes during inflammation

Back 1

Reddish color (erythema): caused by vasodilation of blood vessels, which will also slow down the flow of blood.

Swelling (edema): caused by increased vascular permeability in endothelial walls which will allow for fluids to leak out of the vasculature into the interstitium (protein, white blood cells, plasma, etc)

Pain: often an adverse side effect of other things going on in the inflammatory response

Warmth: due to decreased blood flow and vasodilation

Loss of function

During inflammation, endothelial activation occurs which, along with leukocyte activation, will cause leukocytes to roll on the surface, stop, then undergo extravasion into the interstitium (increased vascular permeability)

Front 2

Acute inflammation: Identify, with illustrative examples, the beneficial and harmful consequences of inflammation

Back 2

Beneficial: inflammation is required to eliminate foreign antigens. It helps attract leukocytes, repairs damaged tissue, activates endothelium to vasodilate, increase vascular permeability, etc.

Harmful: occurs when inflammation is disproportional (hypersensitivity due to allergens), misdirected (autoimmune disorders), or prolonged (chronic inflammation damages tissue resulting in scar tissue/fibrosis)

Front 3

Acute inflammation: Recognize where mediators of inflammation are produced and what the main actions are

Back 3

Cell-derived:

Histamine (mast cells, basophils, platelets): vasodilation, increased vascular permeability, endothelial activation

Prostaglandins (leukocytes, mast cells): pain, vasodilation, increased vascular permeability, fever

Leukotrienes (leukocytes, mast cells): increased vascular permeability, leukocyte attraction and activation, chemotaxis

Cytokines (IL-1 and TNF): fever, endothelial activation, hypotension, weight loss, leukocytosis

Chemokines (leukocytes, activated macrophages): chemotaxis

ROS (leukocytes): killing of microbes, tissue damage

Nitric Oxide (endothelial cells, macrophages): vascular smooth muscle relaxation, killing of microbes

Hint 3

Plasma protein-derived:

Complement (plasma produced in liver): leukocyte chemotaxis and activation, vasodilation, direct target killing)
kinins (plasma produced in liver): increased vascular permeability, smooth muscle contraction, vasodilation, pain

Front 4

Acute inflammation: Define the common morphologic patterns of inflammation

Back 4

vasodilation, edema, vasocongestion, and leukocyte infiltration (mostly neutrophils for acute inflammation)

serous inflammation: outpouring of clear fluid in a confined space; blister/in cavities like the pleural cavity

fibrinous inflammation: rich in fibrin (acellular proteinaceous material): often seen in serosal surfaces (pericardium, peritoneum, pleura)

purulent (supparitive) inflammation: abundant pus (thick, usually yellowish, fluid consisting of dead neutrophils, cellular debris, and microbes); indicates infection

Cellulitis: dense infiltrate of leukocytes through tissue, usually subcutaneous, accompanied by erythema (redness); strongly suggestive of infection.

Ulcer: discontinuity in epithelium with underlying inflammation and repair; acute or chronic

Abscess: focus of inflammation walled off by leukocytes and fibrosis; acute or chronic

Front 5

Acute inflammation: Explain the local and systemic manifestations of inflmmation

Back 5

Local: the 5 cardinal signs of inflammation

Systemic: fever (prostaglandins and cytokines, particularly IL-1 and TNF), septic shock: hypotension, leukocytosis (cytokines), acute phase response: up-regulation of the liver to synthesize plasma proteins which in turn influence the formation of erythrocytes

Front 6

Chronic inflammation: Compare and contract acute vs. chronic inflammation in terms of etiology (causes), time course, pathogenesis, and morphologic changes

Back 6

ACUTE

Etiology: infectious microbe/toxin, tissue necrosis, foreign bodies, physical trauma

Time Course: hours to days

Pathogenesis: vasodilation, increased vascular permeability, leukocyte infiltration (mostly neutrophils), endothelial activation to attract and hold leukocytes

Morphologic changes: leukocyte infiltration (mostly leukocyte), vasodilation, edema, inflammation variations (serous, fibrous, purulent, abscess, cellulitis, and ulcer)

Hint 6

CHRONIC

Etiology: microbes that resist clearance; hypersensitivity, autoimmune disorders

Time Course: days to months

Pathogenesis: lymphocyte and macrophage recruitment and activation.

Morphologic changes: macrophage and lymphocyte infiltration; tissue necrosis; scarring

Front 7

Chronic inflammation: Summarize the components of the mononuclear phagocyte system, including how macrophages are activated and what functions are performed by activated macrophages.

Back 7

Components: monocytes migrating from the blood into tissue and differentiate into macrophages; activated form is much larger, increasingly motile, increasingly metabolically active

Activation: cytokines (INF-g), bacterial endotoxins, microbial products, necrotic by-products, and chemical mediators

Function: phagocytose and destroy foreign invaders; amplify immune responses producing cytokines (positive feedback loop); repair tissue

Front 8

Chronic inflammation: Identify the features of granuloma, and list the major diseases in which granulomatous inflammation is a prominent feature.

Back 8

A granuloma is an accumulation of macrophages (mainly) into dense nodules around an antigen. These antigens are usually large, insoluble substances. This can cause caseation or necrosis of the center which resembles a cheesy, slurry of lipid-rich debris.

Major diseases include: syphilis, tuberculosis

Front 9

Chronic inflammation: Interpret the relationships between immune responses and acute and chronic inflammation

Back 9

Acute inflammation: involves change in vascularization to increase blood flow, structural changes in vessels (increased vascular permeability to allow leukocytes and plasma proteins to leave the circulation), and leukocyte infiltration.

Chronic inflammation is largely a cellular response, with a minor (if any) role of vascular dilation and permeability. (Lymphocytes and macrophages)