Workshop 5 - Inflammation and Healing

Question 1

What is inflammation?

Answer 1

a complex response of the living tissue to an action of various pathogens (physical, biological, chemical)

Question 2

Physical agents (causing inflammation)

Answer 2

trauma, thermal injuries, irradiation

Question 3

Chemical agents (causing inflammation)

Answer 3

heavy metal toxicity, solvents, medications

Question 4

Infectious agents (causing inflammation)

Answer 4

viruses, bacteria, parasites, fungi

Question 5

Immunologic agents (causing inflammation)

Answer 5

autoimmune diseases, immune complex diseases

Question 6

Types of inflammation

Answer 6

acute, chronic

Question 7

What is acute inflammation?

Answer 7

• immediate and early inflammatory response to actions of pathogens
• short
• directed at removing pathogenic agent

Question 8

What is chronic inflammation?

Answer 8

• prolonged inflammatory response to actions of pathogens (lasting weeks/months)
• simultaneous occurrence of active inflammation, tissular damage and repair

Question 9

Characteristics of acute inflammation:

Answer 9

changes in the microcirculation:

• exudation of fluid (edema)
• emigration of leukocytes from circulation to area of injury

Question 10

Vascular changes in acute inflammation

Answer 10

• vasodilation and stasis
• increased permeability
• exudation of fluid

Question 11

Chemical factors in acute inflammation

Answer 11

humoral mediators

• Kinin system (Bradykinin)
• Coagulation cascade
• Complement system (C3a,C5a,C3b)

cellular mediators

• Vasoactive amines (Histamine,Serotonin)
• Arachidonic acid (leads to production of prostaglandins,leukotrienes)
• Proteases and O₂ free radicals (neutrophil factors)

Question 12

Cellular response in acute inflammation

Answer 12

• Margination of neutrophils
• Pavementing of neutrophils
• Diapedesis - Emigration of neutrophils (movement to inflammation site via chemotaxis)
• Phagocytosis

1. Recognition
2. Engulfment
3. Microbial killing

Question 13

Types of cells involved in acute inflammation

Answer 13

• first 24h: polymorphonuclear leukocytes (neutrophils)
• 24-48h: phagocytes (macrophages), lymphocytes and plasma cells

neutrophils remain predominant for several days

Question 14

Inflammatory exudate:

• macroscopic, microscopic

Answer 14

macroscopic:

• yellowish fluid (rich in proteins)

microscopic:

• intense eosinophilic fluid (increased amount of proteins)

Question 15

Inflammatory exudate:

• components

Answer 15

• plasma fluid (rich in albumin, globulin and fibrinogen)
• cells (neutrophils, macrophages)
• tissue debris
• pathogenic agent

Question 16

Inflammatory exudate:

• types

Answer 16

• serous exudate
• fibrinous exudate
• purulent exudate
• catarrhal exudate
• hemorrhagic exudate

Question 17

Serous inflammation

Answer 17

usually viral and high fluid component/protein content

• skin, mucosa (herpes)
• serous cavities (pleural effusion)
• microcavities (seous alveolitis)

Question 18

Serous inflammation:

• macroscopically
• microscopically

Answer 18

macroscopic, e.g. serous pericarditis

• enlarged pericardial cavity filled with exudate

microscopic, e.g. serous alveolitis

• congestion of parieto-alveolar capillaries
• serous exudate within alveolar lumen (eosinophilic fluid with few neutrophils, erythrocytes and bacteria)

Question 19

Fibrinous inflammation

Answer 19

most frequently TB,

rich in fibrin, low in plasma fluid and neutrophils

• mucus membranes (pseudomembranous colitis-dysentery)
• serous cavities, e.g. fibrinous pericarditis (rheumatism, uremia, TB)
• microcavities, e.g. fibrinous alveolitis (stage 2 lobar pneumonia)

Question 20

Fibrinous inflammation

• macroscopically
• microscopically

Answer 20

macroscopically (e.g. fibrinous pericarditis)

• adherent, gray-fibrinous deposit (variable thickness) covering entire pericardium
• thick = cat’s fur / thin = buttered bread

microscopically (e.g. fibrinous pericarditis)

• intense eosinophilic exudate (neutrophils, erythrocytes)
• vascular congestion and neutrophils within pericardium

microscopically (fibrinous alveolitis)

• fibrinous exudate within alveolar lumen (fibrin network, bacteria, few neutrophils)
• alveolar wall thickening (due to alveolar capillary congestion

Question 21

Purulent inflammation

+microscopic (pus smear)

Answer 21

caused by pyogenic bacteria

microscopically (pus smear)

• purulent exudate
• neutrophils, macrophages, erythrocytes, necrotic debris, fibrin, bacteria

Question 22

Purulent inflammation: types

Answer 22

• localized (Abcess)
• diffuse (purulent leptomeningitis

Question 23

Purulent inflammation:

exudate components

Answer 23

• normal and altered neutrophils
• microbial flora (bacteria
• fluid components and fibrin
• tissue/necrotic debris

Question 24

Purulent leptomeningitis:

+macroscopically

+microscopically

Answer 24

Leptomeninge inflammation by meningococcus

macroscopically

• brain covered by thick,white, opaque leptomeninge (containing purulent exudate)
• congestion of cerebral vessel (determination difficult)

microscopically

• meninge is diffusely thickened (diffuse purulent exudate, vascular congestion)
• at level of congested vessels: leukocyte margination, diapedesis

Question 25

Abcess types

Answer 25

* purulent collection with wall and cavity * 2 types: recent & old

Question 26

Abcess: microscopically macroscopically

Answer 26

microscopically: * recent: 1. wall composed by thin fibrin layer 2. abcess cavity containing proteolytic necrotic area and pus (neutrophils, macrophages, necrotic debris) * old: 1. wall is pyogenic membrane 2. abcess cavity containing proteolytic necrotic area and pus macroscopically (hepatic abcess): * within hepatic parenchyma * 3 types: pylephlebitic, cholangitic, pyaemic

Question 27

Abcess: old -wall composition

Answer 27

external layer (abcess capsule) connective vascular tissue (of neoformation) * number of vessels decreases * fibroblast maturation produces collagen and forms thick fibrous wall (capsule) internal layer: * fibrin network containing neutrophils

Question 28

Hepatic (visceral) abcesses: - Types - causes

Answer 28

pylephlebitic: * caused by infectious agents disseminating along portal vein forming a irregular, large, pus-filled cavity (limited by necrotic hepatic parenchyma) cholangitic (limited to hyperemic areas): * caused by infectious agents disseminating along biliary ducts forming irregular, small cavities containing green (biliary pigment) pus renal pyaemic: * caused by hematogenous dissemination of infectious agent leading to congested kidney with multiple, small areas (white-yellow purulent) surrounded by hyperemic areas

Question 29

Catarrhal inflammation:

Answer 29

* acute inflammation of mucosae * produces snotty exudate (rich in mucus) * e.g. catarrhal rhinitis

Question 30

Hemorrhagic inflammation

Answer 30

* caused by infectious agents acting on vessels * causes microhemorrhages with exudate (rich in erythrocytes * e.g. flu

Question 31

Evolution of acute inflammation -possible outcomes

Answer 31

1. **Resolution** (everything back to normal) 2. **Repair** (necrotic tissue is replaced by new tissue or scar formation) 3. **Suppuration** (formation of pus-maybe abcess) 4. **Chronic inflammation** (agent is not neutralized by acute response-immune response follows)