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General - Pathology 🩺 > L5: Acute Inflammation > Flashcards

L5: Acute Inflammation Flashcards

1
Q

What is the definition of inflammation?

A
  • Inflammation is a complex reaction of a tissue and its microcirculation to a pathogenic insult.
  • It is characterized by the generation of inflammatory mediators and movement of fluid & leukocytes from the blood into extravascular tissues.
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2
Q

What is the aim of inflammation?

A
  • Neutralization of irritant
  • Elimination of injurious agent
  • Engulfment/entrapment
  • To get rid of the attacking agent and to prepare tissue for repair
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3
Q

What are the types of inflammation? And what are their characters in brief?

A

1) Acute inflammation:
- Elimination of injurious agent
- Lasting for a few minutes up to a few days (7 max)
- Fluid and plasma protein exudation.
- Neutrophils (then monocytes)are the main inflammatory cells.

(2) Chronic inflammation: (tissue damage and repair happen simuantansouely)
- Lasting for a longer duration (days to years). (Up to 25 years).
- Vascular proliferation and scarring.
- Lymphocytes and macrophages are the predominant cells

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4
Q

What are the cardinal signs of acute inflammation?

A
  • Redness (rubor) - Swelling ( tumor) - Heat ( calor)

- Pain (dolor) - Loss of function ( functio laesa), the fifth cardinal sign added by Virchow

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5
Q

What are the major components (changes - mechanism - pathogenesis )of acute inflammation?

A

1- Vascular changes: - Vasodilation and increased blood flow - Increased vascular permeability

2- Cellular events: - Leucocyte transmigration - Phagocytosis

3- Chemical mediators (acute & chronic).

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6
Q

What are the vasoactive changes that occur in acute inflammation?

A
  • Change in diameter

- Increased capillary permeability

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7
Q

Change in diameter process in acute inflammation

A

Transient VC then permanent VD of arterioles, capillaries, and postcapillary venules. This results in a marked increase in the blood flow to the area which is manifested clinically by local redness and hotness of the affected area.

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8
Q

Increased capillary permeability in acute inflammation.

A

It is due to endothelial changes in the form of either:

  • Endothelial swelling with the widening of Intra endothelial gaps of postcapillary venules. OR Major endothelial damage involving arterioles, capillaries, and venule
    This results in leakage of proteinaceous fluid (Exudate) which causes inflammatory edema.
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9
Q

Compare between transudate and exudate

A 
Transudate:
▪ Due to increased hydrostatic pressure.
▪ Low protein content. (clear)
▪ Does not coagulate on standing.
▪ Low specific gravity ( less than 1012)
▪ Can occur early in inflammation
Exudate:
▪ Due to increased vascular permeability.
▪ Rich in protein esp. fibrin (turbid)
▪ Coagulates on standing.
▪ High specific gravity ( more than 1018
▪ Contains inflammatory cells Exudate.
▪ Occurs late in inflammation
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10
Q

What are the cellular events that happen in acute inflammation?

A

1- Leucocyte movement and functions.
2- Chemotaxis
3- Phagocytosis

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11
Q

Leucocyte movement and functions in acute inflammation

A

Inside the area of inflammation, leukocytes move out of the blood vessels (Emigration)…….Includes margination, pave mentation, rolling, adhesion and transmigration.

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12
Q

What is emigration?

A

It is the passage of inflammatory leukocytes between the endothelial cells into the adjacent interstitial tissue.

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13
Q

Margination in acute inflammation

A

Occurs as leukocytes localize to the outer margin of blood flow adjacent to the vascular endothelium.

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14
Q

pavementation in acute inflammation

A

leukocytes line the endothelial surface.

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15
Q

Describe rolling in acute inflammation and what it is mediated by.

A

Is mediated by the action of E selectins which bind endothelial cells loosely to leukocytes ( Through sialyl Lewis X modified glycoprotein) producing a characteristic rolling movement of leukocytes along the endothelial surface.

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16
Q

Adhesion in acute inflammation

A

Leukocytes adhere to the endothelial surface through the interaction of integrins (leukocytes) and the immunoglobulin family adhesion proteins (endothelium)

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17
Q

Transmigration In acute inflammation

A

It is the movement of leukocytes across the endothelium.

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18
Q

What is chemotaxis?

A

It is the directional movement of leucocytes towards the irritant within the area of inflammation

19
Q

What is phagocytosis?

A

It is the ingestion and destruction of particulate material (tissue debris, living or dead bacteria, and other foreign cells) by phagocytic cells mainly neutrophils and monocytes macrophages.

20
Q

What are the steps of phagocytosis?

A
  1. Recognition and attachment
  2. Engulfment
  3. Degradation (killing)
21
Q

What are the types of Chemical mediators?

A
  • Exogenous of microbial origin (E.coli chemotactic).

* Endogenous mediators from cells or plasma.

22
Q

What are the chemical mediators responsible for vascular dilatation?

A

histamine

23
Q

What are the chemical mediators responsible for vascular permeability?

A

histamine and kinins

24
Q

What are the chemical mediators responsible for chemotaxis?

A

Leukotrienes, lysosomal components and C5a.

25
Q

What are the chemical mediators responsible for pain?

A

Bradykinin (from plasma), prostaglandins (fro necrotic cells)

26
Q

What are the systemic effects of acute inflammation? And what are they caused by?

A
  1. Fever: caused by pyrogens (i.e. fever producing substances):
    ▪ • Exogenous: released from bacteria and fungi.
    ▪ • Endogenous: cytokines as interleukin 1 (IL-1) and
    tumor necrosis factor (TNF).
  2. Leucocytosis: caused by IL-1 and TNF that stimulate the release of leukocytes from bone marrow.
27
Q

What are the types of acute inflammation?

A

According to the presence or absence of pus, acute inflammation is either suppurative or non-suppurative

28
Q

What is suppurative (purulent) inflammation? And what is it caused by?

A
  • Severe acute inflammation with pus formation

- It is caused by pyogenic bacteria e.g. staph aureus, strept. Pyogenes, E.coli …..

29
Q

What is pus?

A

Pus is semi-fluid, viscous material formed of dead and dying neutrophils, microorganisms, plasma proteins, fluid exudate, and necrotic liquefied tissue.

30
Q

What are the types of suppurative inflammation?

A

A. Localized (Abcess or furuncle or carbuncle)

B. Diffuse

31
Q

What is abscess?

A

It is a localized suppurative inflammation characterized by the formation of an irregular cavity containing pus

32
Q

What is found in the irregular cavity of the abscess?

A
  • It is formed of 3 zones.
    a. Central zone of necrotic tissue and dead neutrophils.
    b. Midzone of pus
    c. Peripheral zone of inflamed tissue (pyogenic membrane).
33
Q

What is the fate of abscess?

A

▪ If not evacuated:

a. Change to a chronic abscess.
b. Blood or lymphatic spread.

▪ If evacuated:

a. Healing by granulation tissue.
b. Sinus formation. (Sinus = blind-ended tract opening to the surface)
c. Fistula formation. (Fistula = tract joining two Surfaces)
d. Ulcer formation (Ulcer = defect in the surface lining of the skin or mucous Membrane) e.g peptic ulcer

34
Q

What is a boil?

A

Small abscess related to hair follicles, sweat, or sebaceous glands.

35
Q

What is carbuncle?

A

Multiple communicating suppurative foci in the subcutaneous tissue opening to the surface by multiple sinuses. It is common in diabetic patients

36
Q

What is the cause of cellulitis and what are its sites?

A

▪ Due to streptococcal infection which produce enzymes that facilitate the spread of infection e.g
(Fibrinolysin - Hyalourinidase - Leucocidin)

▪ Sites:
Loose connective e.g orbit, wall of the appendix

37
Q

What are the types of non-suppurative inflammation?

A

1- Serous and serofibrinous inflammation…

2- Catarrhal inflammation…e.g common cold

3- Pseudomembranous inflammation…e.g diphtheria & bacillary dysentery.

4- Hemorrhagic inflammation ….Vascular damage and hemorrhage

5- Necrotizing inflammation …. Excess tissue necrosis

6- Allergic inflammation… From Antigen/Antibody reaction

38
Q

What is serous inflammation? And where does it occur?

A

Excess watery fluid Exudate - Occurs in burns and some viral infections where (blisters) are formed.

39
Q

What is serofibrionous inflammation and what are its sites?

A
  • Exudation of serous fluid rich in fibrin.

- Occurs in serous sacs and lung alveoli in lobar pneumonia.

40
Q

What are the types of sirofibrionous inflammation?

A

▪ Wet type = excess serous than fibrin.

▪ Dry-type = excess fibrin Than serous fluid.

41
Q

What is catarrhal inflammation and its sites and what is an example for it?

A

▪ Mild acute inflammation of the mucous membranes with excess watery mucous secretion.
▪ Sites
- Mucous membranes of respiratory and GIT.
Ex:- common cold

42
Q

What is Pseudomembranous inflammation?

A

▪ A severe form of non-suppurative inflammation caused by toxin-producing strains as:-

a. Diphtheria
b. Shigella (bacillary dysentery) and Clostridium difficile.

43
Q

What is the fate of acute inflammation?

A

▪ Resolution
(the hoped-for result)

▪ Abscess
(via liquefactive necrosis)

▪ Scar (sometimes occurs even if the pathogen is eliminated)

▪ Persistent inflammation
(chronic inflammation) due to a failure to completely eliminate the pathological insult (injury)

General - Pathology 🩺 (9 decks)

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