Inflammation 1 2

Question 1

Celsus definition of inflammation

Answer 1

Calor (warmth), Dolor (pain), Rubor (redness), Tumor (swelling)

Question 2

Modern definition

Answer 2

reaction to microcirculation characterized by movement of fluid and leukocytes from blood to extravascular tissues

Question 3

Inflammatory exudation

Answer 3

fluid that leaks out, sometimes onto surface. Exudate (the liquid) is thick, sticky, probably clot.

Question 4

How do blood vessels enlarge?

Answer 4

Histamine and Nitric oxide cause vasodilation. Blood flows slower

Question 5

What makes blood vessels leaky?

Answer 5

2 possibiilities - endothelial cell contraction (make gaps in response to permeability factors) or endothelial cell damage

Question 6

Name some permeability factors in inflammation

Answer 6

Histamine, serotonin (from platelets), arachidonic acid derivatives (eicosanoids: prostaglandins (most in cyclogenase pathway) and leukotrienes), plasma enzyme cascades, complement, bradykinin, etc.

Question 7

Complement overview

Answer 7

3 paths (classical, alternate, lectin). Main functions: anaphylotoxin (vessels) (C3a, C5a), chemotaxis (C5a), opsonization (C3b), target cell lysis (C9)

Question 8

Interacting plasma enzyme cascades (4)

Answer 8

Complement, kinin system, coagulation, fibrinolytic (plasmin) system

Question 9

Most important protein and polypeptide mediators are…

Answer 9

Bradykinin, C3a and C5a, thrombin

Question 10

Pus

Answer 10

purulent

Question 11

Abscess vs empyema

Answer 11

Abscess = collection of pus in space formed by destruction of normal tissues; empyema: collection of pus in space that naturally occurs

Question 12

What makes cells move into the tissues?

Answer 12

Neutrophils move in response to chemotaxis

Question 13

Neutrophils in acute inflammatory response

Answer 13

Almost the defining feature of inflammation. Arrive right away.

Question 14

How do neutrophils kill?

Answer 14

Phagocytosis, oxidative killing, hydrolytic enzymes. Destructive, indiscriminate, “dumb”.

Question 15

Define chronic inflammation

Answer 15

Imprecisely. Duration (weeks to months), steady state of inflammation, damage, and repair. It can be acute inflammation that doesn’t resolve; persistent infections/injuries/toxins; autoimmune and other immune diseases

Question 16

3 ways that chronic inflammation is different from acute

Answer 16

The cells are different (neutrophils vs mononuclear phagocytes). Chronicity often (not always) is associated with immunologic specificity, whereas acute is nonspecific. Chronicity is usually associated with tissue repair and is slow, acute is fast.

Question 17

How are cells different in chronic inflammation?

Answer 17

Lymphocytes and plasma cells (nothing special, just lots of them) and Mononuclear phagocytes: aka blood monocytes or macrophages; like Neutrophils (eat and kill) BUT also make cytokines and activate lymphocytes, which kickstarts the specific immune response. Can form granulomas

Question 18

What is a granuloma?

Answer 18

Collection of mononuclear phagocytes in tissue. Seen in some specific diseases like TB and fungal infections.

Question 19

Compare the immune response in acute and chronic inflammation

Answer 19

Acute: response is immediate and nonspecific. Chronic: delayed and specific.

Question 20

Repair in chronic inflammation

Answer 20

Regeneration, repair, remodel. Excess fibrous tissue - scarring/fibrosis. Progresses from granulation tissues (capillaries) then fibrosis, leads to permanent structural change.

Question 21

What molecular markers mediate tissue repair in chronic inflammation?

Answer 21

Fibrogenic cytokines: FGF, TGF, MDGF, PDGF, and others.