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Morphopathology > Workshop 5 - Inflammation and Healing > Flashcards

Workshop 5 - Inflammation and Healing Flashcards

1
Q

What is inflammation?

A

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

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2
Q

Physical agents (causing inflammation)

A

trauma, thermal injuries, irradiation

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3
Q

Chemical agents (causing inflammation)

A

heavy metal toxicity, solvents, medications

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4
Q

Infectious agents (causing inflammation)

A

viruses, bacteria, parasites, fungi

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5
Q

Immunologic agents (causing inflammation)

A

autoimmune diseases, immune complex diseases

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6
Q

Types of inflammation

A

acute, chronic

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7
Q

What is acute inflammation?

A
  • immediate and early inflammatory response to actions of pathogens
  • short
  • directed at removing pathogenic agent
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8
Q

What is chronic inflammation?

A
  • prolonged inflammatory response to actions of pathogens (lasting weeks/months)
  • simultaneous occurrence of active inflammation, tissular damage and repair
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9
Q

Characteristics of acute inflammation:

A

changes in the microcirculation:

  • exudation of fluid (edema)
  • emigration of leukocytes from circulation to area of injury
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10
Q

Vascular changes in acute inflammation

A
  • vasodilation and stasis
  • increased permeability
  • exudation of fluid
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11
Q

Chemical factors in acute inflammation

A

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)
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12
Q

Cellular response in acute inflammation

A
  • Margination of neutrophils
  • Pavementing of neutrophils
  • Diapedesis - Emigration of neutrophils (movement to inflammation site via chemotaxis)
  • Phagocytosis
  1. Recognition
  2. Engulfment
  3. Microbial killing
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13
Q

Types of cells involved in acute inflammation

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

neutrophils remain predominant for several days

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14
Q

Inflammatory exudate:

  • macroscopic, microscopic
A

macroscopic:

  • yellowish fluid (rich in proteins)

microscopic:

  • intense eosinophilic fluid (increased amount of proteins)
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15
Q

Inflammatory exudate:

  • components
A
  • plasma fluid (rich in albumin, globulin and fibrinogen)
  • cells (neutrophils, macrophages)
  • tissue debris
  • pathogenic agent
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16
Q

Inflammatory exudate:

  • types
A
  • serous exudate
  • fibrinous exudate
  • purulent exudate
  • catarrhal exudate
  • hemorrhagic exudate
17
Q

Serous inflammation

A

usually viral and high fluid component/protein content

  • skin, mucosa (herpes)
  • serous cavities (pleural effusion)
  • microcavities (seous alveolitis)
18
Q

Serous inflammation:

  • macroscopically
  • microscopically
A

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)
19
Q

Fibrinous inflammation

A

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)
20
Q

Fibrinous inflammation

  • macroscopically
  • microscopically
A

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
21
Q

Purulent inflammation

+microscopic (pus smear)

A

caused by pyogenic bacteria

microscopically (pus smear)

  • purulent exudate
  • neutrophils, macrophages, erythrocytes, necrotic debris, fibrin, bacteria
22
Q

Purulent inflammation: types

A
  • localized (Abcess)
  • diffuse (purulent leptomeningitis
23
Q

Purulent inflammation:

exudate components

A
  • normal and altered neutrophils
  • microbial flora (bacteria
  • fluid components and fibrin
  • tissue/necrotic debris
24
Q

Purulent leptomeningitis:

+macroscopically

+microscopically

A

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
25
Q

Abcess

types

A
  • purulent collection with wall and cavity
  • 2 types: recent & old
26
Q

Abcess:

microscopically

macroscopically

A

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
27
Q

Abcess: old

-wall composition

A

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
28
Q

Hepatic (visceral) abcesses:

  • Types
  • causes
A

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
29
Q

Catarrhal inflammation:

A
  • acute inflammation of mucosae
  • produces snotty exudate (rich in mucus)
  • e.g. catarrhal rhinitis
30
Q

Hemorrhagic inflammation

A
  • caused by infectious agents acting on vessels
  • causes microhemorrhages with exudate (rich in erythrocytes
  • e.g. flu
31
Q

Evolution of acute inflammation

-possible outcomes

A
  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)
32
Q
A

Morphopathology (7 decks)

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