Acute And Chronic Inflammation Flashcards

1
Q

Inflammation Defintion

A

The local physiological response to tissue injury or infection involving cells such as neutrophils and macrophages

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2
Q

Beneficial effects of inflammation

A
  • Destruction of invading microorganisms
  • The walling off of an abscess cavity, thus preventing spread of infection
  • Reaction to injury to help heal
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3
Q

Problems of Inflammation

A
  • Autoimmunity - e.g. Hashimoto’s thyroiditis
  • An over-reaction to a stimulus
  • An abscess in the brain would act as a space-occupying lesion compressing vital surrounding structures
  • Fibrosis resulting from chronic inflammation may distort the tissues and permanently alter their function
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4
Q

Neutrophil polymorphs role

A

Not very specific
Short lived cells - dead = yellow pus
First on the scene of acute inflammation
Cytoplasmic granules full of enzymes that kill bacteria
Usually die at the scene of inflammation
Release chemicals that attract other inflammatory cells e.g. macrophages
* may see BARR BODIES in female neutrophils = visible silenced X chromosome - LYONISATION)

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5
Q

Macrophages role

A

Long lived cells (weeks to months)
Phagocytic properties
Ingest bacteria and debris
May carry debris away - take into lymphatics
May present antigen to lymphocytes start immune reaction
Named according to location:
- Kupffer cell (liver)
- Melanophage (skin)
- Osteoclast (bone)
- Microglial cell (brain)
- Alveolar/peritoneal macrophages

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6
Q

Lymphocyte role

A

Long lived cells (years)
Produce chemicals which attract in other inflammatory cells
Immunological memory for past infections and antigens
Plasma cells - smaller nucleus with lots of RER to produce antibodies

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7
Q

Endothelial cells role

A

Usually teflon coated - nitric oxide
Line capillary blood vessels in areas of inflammation
Become sticky in areas of inflammation so inflammatory cells adhere to them - lose coating
Become porous to allow inflammatory cells to pass into tissues
Grow into areas of damage to form new capillary vessels

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8
Q

Fibroblasts role

A

Long lived cells
Form collagen in areas of chronic inflammation and repair

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9
Q

5 Cardinal signs of inflammation

A

Rubor (Redness)
Dolor (Pain)
Calor (Heat)
Tumor (Swelling)
Loss of function

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10
Q

Stages of inflammation:

A
  1. INCREASE IN VESSEL CALIBRE + FLOW:
    - Inflammatory cytokines (bradykinin, prostacyclin, NO) mediate VASODILATION
  2. FLUID EXUDATE: Increased vascular permeability and fluid is forced out of the vessel
  3. CELLULAR EXUDATE: emmigration of the neutrophil polymorphs into the extravascular space and become abundant in this fluid.
    Outcome
    = Resolution - goes away
    = Suppuration - pus formation e.g. abscess
    = Organisation - granulation tissue and fibrosis
    = Progression to chronic inflammation
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11
Q

In acute inflammation - Expand on what organisation is?

A

Healing by fibrosis (scar formation) when there is substantial damage to the connective tissue framework and/or the tissue lacks the ability to regenerate specialised cells
When this occurs, dead tissues and acute inflammatory exudate are first removed from the damaged areas by macrophages
The defect then becomes filled by the ingrowth of granulation tissue = this is organisation
The granulation tissue then gradually produces collagen to form a fibrous scar.

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12
Q

Neutrophil action in acute inflammation

A

MARGINATION = Migrate to end of blood vessel
ADHESION = selectins bind to neutrophils, cause “rolling” along blood vessel margin
EMIGRATION + DIAPEDESIS = movement out of the blood vessels though or in between endothelium and other inflammatory cells follow
CHEMOTAXIS = site of inflammation
At the site…
1. PHAGOCYTOSIS
2. PHAGOLYSOSOME + BACTERIAL KILLING
3. MACROPHAGES CLEAR DEBRIS

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13
Q

Causes of acute inflammation

A

Microglial infections e.g. viruses
Hypersensitivity reactions e.g. parasites
Physical agents e.g. trauma/radiation
Chemicals e.g. corrosives/acids
Bacterial toxins
Tissue necrosis e.g. ischaemic infarction

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14
Q

Definition of Chronic Inflammation

A

The subsequent and often pro longed tissue reactions following the initial response
Can be defined as an inflammatory process in which lymphocytes, plasma cells and macrophages predominate
- Autoimmunity, recurrent infections

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15
Q

Chronic inflammation properties

A

Slow onset
Long duration
May never resolve

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16
Q

Causes of chronic inflammation

A

Primary chronic inflammation
Transplant rejection
Progression from acute inflammation
Recurrent episodes of acute inflammation

17
Q

What are granulomas

A

A collection of epithelioid histocytes (macrophages)
Secrete ACE = blood marker and high in a Px with granulomatous disease
Form granulomatous “horseshoe” shape
- central necrosis (“caseasting”) = classically TB
- no central necrosis = sarcoidosis, leprosy, vasculitis, crohns
Granuloma + eosinophil = PARASITE

18
Q

What is granulation tissue?

A

An important component of healing and comprises small blood vessels in a connective tissue matrix with myofibroblasts

19
Q

Role of ibuprofen in inflammation

A

Ibuprofen inhibits prostaglandins synthetase
Prostaglandins = chemical mediators of inflammation