Acute Inflammation Flashcards

1
Q

What are the 5 cardinal signs of inflammation?

A
  1. Reddening from increased blood flow
  2. Swelling as exudation of fluid from dilated blood vessels into inflamed tissue occurs
  3. Heat as increased blood flow
  4. Pain as chemical mediators are released into damged tissue and by local pressure on nerve endings from the exudate
  5. Loss of function reluctance to sue inflamed portion
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2
Q

What are the causes of inflammation?

A
  • Microorganims and parasites
  • Trauma: mechanical, chemical and thermal insults
  • Abberant immune responses - hypersensitivity and autoimmunity
  • Malignant neoplasms
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3
Q

How do we classify types of inflammation?

A

Acute or Chronic

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4
Q

What does acute mean in terms of inflammation?

A

Sudden onset of inflammtion tha lasts for a few hours or days

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5
Q

What does acute inflammation lead to?

A
  1. Death
  2. Resolve by regeneration and immunity
  3. Fibrotic repair
  4. Become chronic
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6
Q

Grossly how can we tell acute and chronic inflammation apart?

A

Acute - Swollen and dark red in colour
Chronic - Shrunken and light brown/tan

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7
Q

What is Phase 1 of acute inflammation?

A

The Vascular Phase:
1. Within seconds arteriole constricition occurs as smooth muscle responds
2. Hyperaemia (within minutes - days) arteriole and capillary dilation caused by chemical mediators

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8
Q

What is Phase 2 of acute inflammation?

A

Fluid leaves the circulation and begins to accumulate in the tissues this occurs as mast cells release specific mediators into serum
Vascular permeability is increased due to endothelial cell contraction(caused by histamine release) - cell junctions of endothelial cells open and allows protein-rich fluid (exudate) to escape into the surrounding tissue

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9
Q

What are the components that make up exudate?

A
  • Water and electrolytes
  • Plasma proteins (albumin, globulin, fribrinogen)
  • Red blood cells
  • Platlets
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10
Q

What is Phase 3 of acute inflammation?

A

Migration of leukocytes:
a) Margination/Pavementing - Altered blood flow and loss of axial stream (white blood cells move to periphery of vessels and begin to adhere), expression of adhesion molecules
b) Chemotaxis - Neutrophilsd move along a chemotactic gradient macrophages are slightly sloer - chemotaxis attracts leukocytes and activates them
c) Emigration via intracellular junction - motile cells force an opening and the basement membrane is breached

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11
Q

What are neutrophils?

A

White blood cells formed in the bone marrow that contain multilobed nuclei and are indistinctly granulated:
They have a short half-life in the blood (6 hours) and are replaced twice a day
When they enter tissue they do not return to the blood

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12
Q

What are the functions of neutrophils?

A
  1. Phagocytosis of microorganisms or foreign material and fusion of phagosome with lysosomes to kill or degrade material
  2. Secretion and/or release of granuels into exudate to enhance acute inflammatory response
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13
Q

How are neutrophils recruited to the site of inflammation?

A
  • Marginate in small veins (venules) and capillaries
  • Loosely stick to wall of venule/capillary and roll along
  • At junction between endothelial cells, neutrophils migrate out
  • Migration continues to the site of damage
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14
Q

What are eosinophils?

A

White blood cells formed in the bone marrow contain multilobed nuclei and distinct granuels in the cytoplasm:
Similar half life to neutrophils they are prominent within parasitic infection and local allergic reactions

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15
Q

What are mast cells?

A

Heavily granulated mononuclear cells found in tissues they have a long life span (4-12 weeks) depending on their location and degranulate in tissue injury releasing histamine, heparin, and 5-hydroxytryptmine (serotonin) - chemical mediators responsible for vasodilation, chemotaxis and pain

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16
Q

What are basophils?

A

White blood cells formed in the bone marrow with multilobed nuclei with large bluish granuels in the cytoplasm - granuels are similar of that to neutrophils and mast cells - important in IgE mediated injury to tissue and allergic reactions

17
Q

What is a pyrogen?

A

Act on temperature control centres in the hypothalamus of the brain to raise body temperature

18
Q

In what ways are pyrogens produced?

A
  • Neutrophils: prime source of pyrogen when tehy begin to phagocytose, also esoinophils and macrophages
  • Gram-negative organsims: their cell walls contain pyrogens
  • Damaged tissue cells - necrosis release pyrogens
  • Antigen-antobody complexes - may release pyrogens
  • Tumours - may release pyrogens especially metastatic tumours
19
Q

What are tge functions of inflammatory effusion (exudate)?

A
  1. Dilutes toxic agents
  2. Protein components may contain IgG which attack or opsonise the irritant and facilitate phagocytosis by neutrophils and macrophages
  3. May contain fibrin which immobilises the irritant - fibrin is a proteincomponent in the exudate and very sticky and also provides a framework over which the leukocytes crawl to reach the irritant
  4. Chemotactic to neutrophils, bringing more of these cells into the injured area
  5. Will wash away the irritant - if on the surface
  6. Will also bring the irritant via the lymphatic vessles to the local lymph nodes
20
Q

How do we classify inflammation based on fluid type?

A
  1. Serous
  2. Catarrhal
  3. Fibrinous
  4. Diphtheritic
  5. Haemmorrhagic
  6. Purulent
21
Q

Whar is Serous inflammation?

A

Mild vasuclar injury in an organ or vessels underlying a surface:
- a clear/cloudy fluid little protein present
- Vesicles of the skin produce a serous fluid
Sequalae - resolves when the irritant is removed or may progress to a more serious reaction

22
Q

What is Catarrhal inflammation?

A

Mild inflammation on mucous membranes with goblet cells and/or mucous glands :
- varies from watery to gelatinous/ cloudy to pinkish
- Shedding of epithelium, mucus, neutrophils, RBCs and flecks of fibrin
Sequalae - Resolves wen the irritant is removed or can progress

23
Q

What is Fibrinous inflammation?

A

More severe endothelial injury resulting in the escape of fibrinogrn from the blood and conversion to fibrin:
- Yellowish coagulum on the surface of tissue or within its substance
- Common in lungs and on serous surfaces or in hollow organs it may coagulate within the lumen and form a cast
- Pells off from the underlying tissue
Sequalae - Fibrinious exudates may also resolve if fibrin is digested by macrophages

24
Q

What is Diphtheritic inflammation?

A

More severe form of fibrinous exudate in which there is considerable necrosis of underlying tissue:
- Firmly adherent to the underlying tissue attempts at removal cause tearing of the tissue
- Commonly seen with internal surface fungal infections - fungal toxins penetrating the underlying tissue causing coagulative necrosis
- Can be very haemorrhagic
Sequalae - repairs by fibrosis

25
Q

What is Haemorrhagic inflammation?

A

Severe acute to peracute inflammation in which haemorrhahe is the main component:
- Seen in lymph nodes, lungs and intestine in severe inflammation (sometimes occuring in all tissues)
Sequalae - if widespread is most commonly associated with acute deaths however, if strictly localised then it may repair

26
Q

What is Purulent inflammation?

A

Where pus is the predominant feature:
- Proteolytic enzymes released by the dying neutrophils lyse tissue cells producing a fluid
- Colour varies: white, yeloow, gren, brown - depending on the agent
Sequale - the resolution of abcesses depends upon their location

27
Q

What is the sequelae of abscessation?

A
  • If near the surface will rupture onto it
  • Beneficial to the skin where it discharges to the exterior
  • Deterimental if rupture is into the body cavity
28
Q

What are the deleterious effects of inflammation?

A
  • Local tissue swelling
  • Local tissue damage due to inflammatory cells or their products