Lecture 2 - Inflammation

Question 1

Cardinal Signs of Inflammation

macroscopic lvl

Answer 1

Latin Words:

• Calor - heat
• Rubor - redness
• Tumor - swelling
• Dolar - pain
• Functio laesa - loss of function

Ex: Bug bite - we see these signs

Question 2

Acute Inflammation

Answer 2

rapid onset with short duration (minutes to days)
Would see:
- vascular changes (vasoconstriction and dilation)
-cellular events like leukocyte recruitment, its adhesion and transmigration, Leukocyte-induce tissue injury, defects of leukocyte function
-RESOLUTION (Note: this does not occur in chronic inflammation)

Question 3

Chronic Inflammation

Answer 3

slow onset that may last months to years. Involves more lymphocyte function and more likely to include fibrosis (scarring).
Simultaneous occurrence of: active inflammation, tissue injury, and healing.

Question 4

Stimuli of Acute Inflammation

Answer 4

• infections
• trauma (phyical/chemical agents
• tissue necrosis (ischemia and traumatic events
• foreign bodies (ex. sliver)
• immune reactions

Question 5

Transudate

Answer 5

The escape of protein poor fluid from blood vessel and into extracellular spaces.

Further explanation:
Due to enlargement of tissue (vasodilation), cells separate slightly, fluid seeps out into extracellular spaces (Protein poor fluid).

Question 6

Exudate

Answer 6

Protein rich fluid due to the addition of chemical mediators to site.

Question 7

Diapedesis

Answer 7

The passage of WBC’s through cell junctions of the venules. They do this along a chemical gradient.

Question 8

Chemotaxis

Answer 8

Movement along a chemical gradient (movement in response to a chemical stimulus) .

Endogenous substances - produced inside the body itself
Exogenous substances - produced by bacteria or other harmful thing.

Question 9

Morphological Patterns of Acute Inflammation

Answer 9

• Serous inflammation
• Fibrinous inflammation
• Purulent (supprative) inflammation

Question 10

Serous inflammation

Answer 10

weakest exudate: watery and relatively has protein poor fluid. Seen in effusions/vesicles (blisters)

Question 11

Fibrinous inflammation

Answer 11

More severe inflammation. Sticky, clear, thicker exudate due to protein like fibrinogen. Can scar.

Question 12

Purulent (supprative) inflammation

Answer 12

strongest exudation, pus form. Involves bacteria. Ex. Pimple -> abscess. Protein rich, white exudate.

Question 13

Characteristics of Chronic Inflammation

Answer 13

• infiltration with mononuclear cells (polynuclear cells in acute inflammation)
• tissue destruction (lymphocytes are powerful)
• repair

Question 14

Cells of Chronic inflammation

Answer 14

• macrophage = derived from monocytes, seen in all stages of chronic inflammation. Phagocytize things.
• lymphocytes = T cells and B cells; react w. macrophages and other WBC’s to make cells persist
• plasma cells - derived from B cells. Produce antibodies to ultimately destroy tissue.
• eosinophils - associated with parasite infections and IgE allergies
• Mast cells - least numerous of WBC’s; release histamines (allergy response).

Question 15

Granulomatous Inflammation

Answer 15

Type of chronic inflammation and casseous necrosis. Characterized by epitheliod pattern of macrophages. Seen in TB, fungal infection, Treponema pallidum, and foreign body reactions.

Question 16

Pyrogens

Answer 16

Causes fever, an acute phase response (systemic inflammatory response). Can be endogenous or exogenous.
Pyrogens stimulate prostaglandins which leads to fever. Neurotransmitters stimulated to block prostaglandin production and “reset” temperature point.

Fever can speed up chemical reaction in the body.

Question 17

Leukocytosis

Answer 17

increase in number of circulating WBC’s. Caused initially by increase output of WBC by bone marrow. “Left shift” = increased output of less mature WBC.