Inflammation 1 2 Flashcards Preview

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Flashcards in Inflammation 1 2 Deck (21):
1

Celsus definition of inflammation

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

2

Modern definition

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

3

Inflammatory exudation

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

4

How do blood vessels enlarge?

Histamine and Nitric oxide cause vasodilation. Blood flows slower

5

What makes blood vessels leaky?

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

6

Name some permeability factors in inflammation

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

7

Complement overview

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

8

Interacting plasma enzyme cascades (4)

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

9

Most important protein and polypeptide mediators are…

Bradykinin, C3a and C5a, thrombin

10

Pus

purulent

11

Abscess vs empyema

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

12

What makes cells move into the tissues?

Neutrophils move in response to chemotaxis

13

Neutrophils in acute inflammatory response

Almost the defining feature of inflammation. Arrive right away.

14

How do neutrophils kill?

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

15

Define chronic inflammation

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

16

3 ways that chronic inflammation is different from acute

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.

17

How are cells different in chronic inflammation?

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

18

What is a granuloma?

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

19

Compare the immune response in acute and chronic inflammation

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

20

Repair in chronic inflammation

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

21

What molecular markers mediate tissue repair in chronic inflammation?

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