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Pathology > Inflammation & Tissue Repair > Flashcards

Inflammation & Tissue Repair Flashcards

1
Q

What is inflammation?

A

Inflammation is the vascularised tissue response to injury.

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2
Q

What is a vascular and avascular tissue? give examples

A

Vascular tissue have blood supply to it, avascular do not.

Examples of vascular tissues:
- Muscle tissue, tissues of liver and lungs

Examples of avascular
- Cornea and lens of the eye, cartilage etc

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3
Q

Avascular tissues have no direct blood supply, how do they receive nutrients?

A

Through diffusion

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4
Q

In what type of tissues is inflammation usually not manifested?

A

Avascular

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5
Q

What is the function of inflammation?

A

It is a protective response
Serves to bring defense & healing mechanisms to the site of injury.

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6
Q

What are the cardinal signs and cause of acute inflammation?

A

Rubor (redness) - due to dilatation of small blood vessels
Tumor (swelling) - due to accumulation of fluid
Calor (heat) - due to increased blood flow
Dolor (pain) - due to stretching and distortion of skin due to bradykinin.

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7
Q

What are the benefits of Inflammation?

A

If inflammation occurs in a small period of time it is beneficial.

   1. Dilutes, destroys or neutralizes the offending agents  Brings antibodies, complement factors, and immune cells to fight against the infection.
  1. Inflammation is followed by repair
    During this process dead cells are removed so that healing can take place.
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8
Q

What are the harmful effects of inflammation?

A

If inflammation prolongs (AKA chronic inflammation) both the initially inflammatory reaction & the subsequent healing process can case harm in delicate tissues.

Chronic inflammation is associated with healing process - leads to fibrous tissue deposition, which interferes with the normal functioning of that organ.

Inflammation causes insulin resistance = increase in risk of heart disease

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9
Q

What are the causative agents of inflammation?

A
  1. Infection
  2. Trauma
  3. Necrosis
  4. Immune-mediated
  5. Toxin
  6. Chemical
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10
Q

Describe the process of inflammation.

A
  1. Vasodilation and permeability of blood vessels increase
  2. Phagocyte migration and phagocytosis
  3. Tissue repair and healing
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11
Q

What are the types of inflammation?

A

Acute (short duration - days to few weeks)
Chronic (longer duration - weeks to years)

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12
Q

What is the inflammatory response?

A

The body’s second line of defense against invasion of pathogens.

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13
Q

Describe the steps of the inflammatory response

A
  1. DAMAGE TO TISSUE
    bacteria enters cell - when they die liberate FPRs - attracts neutrophils towards site of inflammation
  2. MAST CELLS RELEASR HISTAMINES
    present under the skin - when they are damaged liberate histamines
    causes vasodilation - pores between endothelium widens causing fluid (contains antibodies and other elements to help kill pathogens) to leak out into tissue.
  3. PHAGOCYTE MIGRATION TO ENGULF + KILL BACTERIA
    Phagocytes try engulf bacteria and kill it
  4. Platelets aggregate to seal the capillaries in the wounded area.
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14
Q

Vascular reactions of inflammation

A
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15
Q

Cellular reactions of inflammation

A

Neutrophils (1st) and monocytes (2nd) move to inner surface of capillaries (uni directional) and then migrate through capillary wall to site of injury

Chemotaxis - attracts neutrophil to site of inflammation

immune cells to move toward the periphery of the vessel, roll along the vascular wall and adhere to endothelial cells

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16
Q

What is chemotaxis?

A

Movement of cells towards the site of inflammation in
response to chemotactic substances

17
Q

What are the mediators of inflammation?

A

Two types:
1. Plasma derived
2. Cell derived

18
Q

Mediators of Inflammation - Plasma-derived

A
  1. Hageman factor ( AKA clotting factor 12)
    a) Important in order to start the cascade of clotting
    b) leads to formation of thrombin which breaks down fibrinogen into fibrin
    c) fibrin causes vasodilation

Factor 12 also causes the activation of the inactive protein kallikrein - when activated - becomes an active enzyme - like kinins
Then through a series of reactions leads to the production of bradykinin (causes vasodilation and pain)

  1. Bacteria activates complement system - C3a and C5a act on mast cells to produce histamines = vasodilation
19
Q

Mediators of Inflammation - Cell-derived

A

All produce chemicals responsible for vasodilation:

  1. Mast cells/basophil degranulation - histamines
  2. Platelets - serotonin
  3. Inflammatory cells - platelet activation factor, prostaglandins
  4. Endothelium - produces nitric oxide, platelet activation factor and prostaglandins
20
Q

Cell derived lipid mediators of inflammation

A
21
Q

Is the inflammatory fluid an exudate or transudate and why?

A

Exudate
Reason: due to increased vascular permeability

rich in protein
many WBC
appearance: turbid

22
Q

What are examples of acute inflammation?

A

Pneumonia and acute appendicitis are the examples of acute inflammation of lung and appendix respectively.

In pneumonia, the alveolar sacs get filled with protein rich fluid (exudate) and inflammatory cells initially with neutrophils and later with macrophages.

23
Q

What are the outcomes of acute inflammation?

A
  1. Resolution - restoration to normal with minimal scar formation
  2. Scaring - fibrosis replaces part of the normal tissue and may cause deformity
  3. Septicemia - may lead to disseminated intravascular coagulation, shock or death
  4. Chronic inflammation - persistent inflammation or spread
24
Q

Chronic inflammation

A

An inflammatory response of prolonged duration (weeks – months, years)

Provoked by the persistence of the causative stimulus

Simultaneous presence of inflammation, tissue destruction and repair

May or may not be associated with granuloma

Infiltration by macrophages, lymphocytes and plasma cells

25
Q

What is the cause of chronic inflammation?

A

Infectious organism that resist clearance and form a persistent infection in tissue or undrained abscess cavities

Auto immune diseases

Exposure to irritant non-living foreign material that has not been removed

26
Q

Process of chronic inflammation

A
  1. Infiltration of macrophages /lymphocytes
  2. Tissue destruction and repair by granulation tissue
  3. Production of collagen tissue
27
Q

Possible sequence of events in chronic viral infection of liver

A
  1. Normal liver + Hepatitis C viral infection
  2. Chronic hepatitis
  3. Cirrhosis
  4. Hepatocellular carcinoma (HCC)
28
Q

Tuberculosis

A
  • A chronic infection disease mainly affecting the lungs
  • Caused by pathogen Mycobacterium tuberculosis.
  • characterized by granuloma formation and many granuloma join together to form tubercle
  • Tubercles join together to form the lesions

Inflammation + Healing simultaneously > fibrosis of lung > chronic cough, low grade fever and breathing problems

Casseous necrosis can also be detected in the centre of a Mtb granuloma

29
Q

What are the 3 laboratory findings to diagnose Inflammation?

A

ESR (erythrocyte sedimentation rate)

C-reactive protein

Leukocytosis

30
Q

Laboratory findings of Inflammation - ESR

A

Raised in chronic inflammatory diseases
Normal ESR reading is <7mm/hour

31
Q

Laboratory findings of Inflammation - C-reactive protein

A

Produced by the liver

Marker of inflammation & effectiveness of treatment - high concentration

32
Q

Laboratory findings of Inflammation - Leukocytosis

A

Numbers of neutrophils increase in the blood during acute inflammation (normal: 75%)

Lymphocyte increase in the blood is typical of chronic inflammation (normal: 20%)

33
Q

What is the process of Healing & Repair (3Rs)?

A

1) Removal of dead and foreign material

2) Regeneration of injured tissue from cells of the same type

3) Replacement of damaged tissue by new connective tissue

34
Q

Wound Healing - Skin

A

Immediate — Early Response
Events (0 ≥ 4 days)
- Clot formation (1-5 minutes)
- Increased blood flow (20-30 minutes)
- Increased neutrophils
- Increased macrophages

Proliferation/Granulation Response
Events (4 ≥ 21 days)
- Endothelial proliferation (angiogenesis)
- Fibroblast proliferation (granulation)
- Epithelial proliferation (closure)
- Matrix production
- Wound contraction

Remodelling response
Events (3 ≥ 90 weeks)
- Collagen synthesis
- Vascular regression
- Remodelling of tissue

35
Q

Treatment of Inflammation

A

Antihistamines
Aspirin
NSAIDS
Glucocorticoids
Others
- gold compounds
- antimalarial agents
- Immunodulating agents

Pathology (11 decks)

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