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General Pathology > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

What are the main differences between Acute and Chronic Inflammation?

A

Acute Inflammation:

  • Rapid Onset
  • Short Duration (hours-few days)
  • Neutrophils and macrophages
  • Exudation of fluid/plasma proteins

Chronic Inflammation:

  • May follow Acute Inflammation
  • Longer Duration
  • Lymphocytes, plasma cells, macrophages
  • Fibrosis, Tissue destruction and reparative processes
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2
Q

What are the Cardinal Signals of Acute Inflammation

A
  • Rubor (Redness)
  • Tumor (Swelling)
  • Calor (Warmth)
  • Dolor (Pain)
  • Functio Laesa (Loss of function)
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3
Q

Causes of Acute Inflammation

A
  • Infections
  • Physical Agents (Mechanical, Heat, Cold, Ionising Radiation)
  • Chemical Agents
  • Ischaemia
  • Immunological Reaction
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4
Q

Tissue changes in Acute Inflammation

A
  1. Hyperaemia
  2. Exudation of fluid and plasma protein
  3. Emigration of leukocytes
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5
Q

What happens during hyperaemia

A
  1. Lewis Triple Response
    a. Initial Vasodilation (white line)
    b. Arteriole Dilation (red line/Flush)
    c. Capillary Dilation and Vascular Congestion (surrounding redness/Flare)
    d. Oedema (weal)
  2. Dilation of Arterioles and Capillaries - reflex action + chemical mediators eg. histamine
  3. Increased permeability of blood vessel wall - contraction/direct damage of endothelial cells, transport of fluids and proteins through endothelial cells (transcytosis)
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6
Q

What happens during exudation of fluid and plasma proteins

A
  1. Vascular Dilation and increased permeability + osmotic pressure + Protein exudation (Fibrinogen forming fibrin network and immunoglobulins)
  2. Oedema (swelling of inflammed tissue)
  3. Increased lymphatic outflow (Lymphangitis/Lymph node reaction)
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7
Q

what leukocytes are emigrated during emigration of leukocytes (WBCs)

A
  • Mononuclear cells - Lymphocytes, Monocytes, Macrophages, Histocytes
  • Polymorphonuclear leukocytes/Granulocytes - Eosinophils, Neutrophils, Basophils
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8
Q

What happens during emigration of leukocytes (WBCs)

A
  1. Margination, rolling and adhesions of leukocytes (Decrease in speed of bloodflow + Expression of adhesion molecules of leukocytes and endothelial cells eg. selectins, intergrins)
  2. Transmigration across endothelium
  3. Movement towards chemotactic molecules (Fibrin meshwork, complement component, C5a)
  4. Phagocytosis (remove offending agents)
  5. Secretion of chemical mediators (cytokines)
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9
Q

Leukocytic actions

A
  1. Phagocytosis
  2. Killing and degradation of ingested material (with ROS and degradative enzymes such as elastase) - Extracellular ROS may damage normal tissue :(
  3. Production of growth factor (for tissue repair)
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10
Q

Chemical mediators of inflammation

A

Plasma derived:

  1. Complement (chemotactic, opsonisation, direct damage)
  2. Kinins (Increase vascular permeability, vasodilation, pain)
  3. Clotting factors (inflammation and blood clotting promote each other)

Cell-derived:

  1. Macrophages, Leukocytes, Endothelium, Mast Cells
  2. Histamin, Serotonin, Nitric Oxide
  3. Arachidonic Acid Metabolites (Prostaglandins and Leukotrienes)
  4. Cytokines/ Chemokines eg. Tissue necrosis factor, Interleukin-1
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11
Q

Termination of acute inflammatory response

A
  1. Rapid degradation of chemical mediators
  2. Short half-lives of neutrophils
  3. Activation of anti-inflammatory mechanisms (eg. IL-10)
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12
Q

Possible Sequelae (consequences) of Acute Inflammation

A
  1. Complete resolution :) - little/no necrosis
  2. Healing by scarring (tissues that do not regenerate) - substantial necrosis, abundant fibrin exudation
  3. Suppuration/Abscess formation - Profuse neutrophils infiltration. necrotic tissue undergoes softening and liquefaction by proteolytic enzymes (eg. Meningitis)
  4. Chronic Inflammation
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13
Q

What is the Sequelae of Acute Inflammation dependent on

A
  1. Amount of Tissue Damaged

2. Whether the causative agent remains

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14
Q

What is an abscess

A

Collection of pus lined by pyogenic membrane

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15
Q

Patterns of acute inflammation

A
  1. Fibrinopurulent exudate (thick yellowish)
  2. Purulent exudate/pus (liquid yellowish) - a lot of neutrophils and dead tissue
  3. Serous exudate (watery) - burns
  4. Haemorrhagic exudate (bloody) - blood vessels
  5. Ulcer (local defect of tissue)
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16
Q

Does chronic inflammation mean there is no healing?

A

No. It just means that attempts at healing occur at the same time as destruction and inflammation.

17
Q

What are the benefits of inflammation?

A
  1. Increase blood flow increases oxygen and nutrient supply
  2. Diluting harmful toxins and delivering plasma proteins like antibodies
  3. Necessary for would repair/healing
  4. Leukocytes - phagocytosis of bacteria and debris (acute); acquired immune response (chronic)
18
Q

Is excessive inflammation bad? Why?

A

Yes.
It causes allergic reactions to common environmental objects. It also causes autoimmune disorders (eg. Hashimoto’s thyroiditis)
It also has a subtle role in other diseases such as ischaemic heart diseases.

General Pathology (10 decks)

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