Pathology more inflammation

Question 1

3 outcomes of acute inflammation

Answer 1

1. Complete resolution
2. Healing by connective tissue replacement (fibrosis)
3. Progression to chronic inflammation

Question 2

complete resolution of acute inflammation

Answer 2

Restoration of the site of inflammation to normal
Outcome if injury short-lived or little tissue destruction occurs

1. return to normal vascular permeability;
2. drainage of edema fluid and proteins into lymphatics or
3. by pinocytosis into macrophages;
4. phagocytosis of apoptotic neutrophils and
5. phagocytosis of necrotic debris; and
6. disposal of macrophages. Macrophages also produce growth factors that initiate the subsequent process of repair.

Note the central role of macrophages in resolution

Question 3

healing by connective tissue replacement (fibrosis)

Answer 3

Substantial tissue destruction
Tissues can’t regenerate
Abundant fibrin exudation that can’t be cleared

Question 4

fibrin vs fibrous

Answer 4

fibrin: acute inflammation, protein, loosely adherent
fibrous: collagen, chronic inflammation, tough, firmly adherent

Question 5

progression to chronic inflammation

Answer 5

If there is persistence of the injurious agent or interference with normal healing

Question 6

morphologic patterns of acute inflammation

Answer 6

Serous Inflammation
Fibrinous Inflammation
Suppurative inflammation
Ulcers

Question 7

serous inflammation

Answer 7

acute inflammatory
Thin, watery fluid derived from plasma or mesothelial cells
* Mesothelial cells line the peritoneum, pleura, and pericardium
* Fluid in these 3 cavities is called EFFUSION

Question 8

fibrinous inflammation

Answer 8

acute inflammatory
Characterized by accumulation of fibrin
* Fibrinogen (soluble plasma protein) leaves blood vessel and is converted to fibrin

Large vascular leaks or procoagulant stimulus
Characteristic of inflammation in body cavity linings
If fibrin not removed, can stimulate proliferation of fibroblasts and vessels and lead to scarring (fibrosis)

Question 9

suppurative/purulent inflammation

Answer 9

acute inflammation
Characterized by production of pus/purulent exudate
* Neutrophils, liquefactive necrosis, edema

Pyogenic bacteria (ex. Staphylococcus) produce pus
Abscess: localized collection of purulent inflammation

Question 10

ulcers

Answer 10

local defect or excavation of the surface of organ or tissue
* Mucosa of GI tract, genitourinary tract
* Skin/subcutis

Question 11

ulcer vs erosion

Answer 11

ulcer: excavation that goes below basement membrane
erosion: excavation NOT below basement membrane

Question 12

chronic inflammation

Answer 12

inflammation of prolonged duration (weeks to years) in which active inflammation, tissue destruction, and attempts at repair proceed simultaneously.
* May follow acute inflammation
* May skip acute inflammation

Question 13

causes of chronic inflammation

Answer 13

Persistent infections
* by certain microorganisms (eg. Mycobacterial infections)

Prolonged exposure to toxic agents
* Examples: Hairy vetch

Foreign bodies
* Plant fibers, silica

Autoimmunity
* Autoantigens evoke a self-perpetuating immune reaction (eg. Lupus erythematosus)

Question 14

morphologic features of chronic inflammation

Answer 14

Infiltration with mononuclear cells
* macrophages, lymphocytes, & plasma cells

Tissue destruction by persistent, offending agents or inflammatory cells

Healing by connective tissue replacement = fibrosis (collagen)
* angiogenesis + immature fibrous tissue = granulation tissue

Question 15

acute vs chronic inflammation

Answer 15

ACUTE INFLAMMATION
* Vascular changes
* Edema
* Neutrophils

CHRONIC INFLAMMATION
* Macrophages
* Lymphocytes
* Plasma cells
* Tissue destruction by inflammatory cells
* Fibrosis

Question 16

What can macrophages be activated by?

Answer 16

Microbial products: LPS (endotoxin)
Cytokines: IFN-γ

Question 17

What does activation of macrophages cause:

Answer 17

increased:
* Cell size
* Lysosomal enzymes
* Metabolism
* Ability to phagocytose and kill ingested microbes

Question 18

M1 activated macrophage

Answer 18

classically activated by IFNg (Tcell) and microbes
pro inflammatory

Question 19

M2 activated macrophage

Answer 19

activated by IL-4 and other cytokines
aid in repair, not pro inflam

Question 20

lymphocytes in chronic inflammation

Answer 20

Involved in antibody and cell-mediated immune reactions

Lymphocytes migrate to sites of inflammation using adhesion molecules and chemokines

Bidirectional interaction between lymphocytes and macrophages

Question 21

plasma cells

Answer 21

Develop from activated B cells
Produce antibody at the site of persistent antigens

Question 22

eosinophils

Answer 22

Respond to parasitic infections or allergies (IgE)
Granules contain major basic protein (MBP) -> toxic to parasites and causes tissue destruction

Question 23

neutrophils in chronic inflammation

Answer 23

May be an important component in foci of chronic inflammation (eg. chronic bacterial infections)

Question 24

Granulomatous inflammation

Answer 24

Distinctive pattern of **chronic inflammation **characterized by the presence of epithelioid macrophages +/- giant cells (fused epithelioid cells)
caused by:
* Infectious agents (Mycobacterium infections: Tuberculosis, Leprosy, Johne’s disease)
* Fungal infections: (Aspergillus, Blastomyces, Coccidiodes, etc)
* Brucellosis
* Foreign substances: (Talc, suture material, barium, hair)

Question 25

Granuloma

Answer 25

focal area of granulomatous inflammation
Central epithelioid macrophages surrounded by a collar of lymphocytes and plasma cells
CASEOUS necrosis is seen with granuloma formation in some cases

Question 26

systemic effects of inflammation

Answer 26

“Acute phase reactions”
Fever
* Due to synthesis of prostaglandins -> tells the brain to increase temperature set point

Synthesis of acute phase proteins
* C-reactive protein, serum amyloid A, fibrinogen

Leukocytosis: increased numbers of circulating leukocytes
* Accelerated release of leukocytes from bone marrow