acute and chronic inflammation Flashcards

1
Q

define inflammation?

A
  • the body’s response to injury or infection using different types of cells
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2
Q

what are the different classifications of inflammation?

A
  • acute / neutrophill mediated
  • chronic / macrophage/lymphocyte mediated
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3
Q

what cells are involved in acute inflammation?

A

neutrophil polymorphs

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4
Q

what is a neutrophil polymorph, where is it made, and whats its lifespan?

A
  • a type of white blood cell
  • made in bone marrow
  • 2 or 3 days
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5
Q

describe the structure of a neutrophil polymorph.

A
  • poly lobed nucleus
  • contains lysosomes
  • contain cytoplasmic granules full of enzymes that kill bacteria
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6
Q

whats the role of neutrophil polymorphs and what happens when they die?

A
  • phagocytose debris and bacteria
  • first cells to arrive at the site of acute inflammation
  • release chemicals that attract other inflammatory cells such as macrophages which then eventually come and engulf them
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7
Q

what cells are involved in chronic inflammation?

A
  • macrophages
  • lymphocytes
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8
Q

whats the role of a macrophage?

A
  • phagocytose debris and bacteria
  • transport material to lymph nodes
  • may transport material to lymphocytes
  • long life span - months to years
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9
Q

whats the role of lymphocytes?

A
  • long-lived cells (years)
  • produces chemicals involved in controlling inflammation and antibodies from B-lymphocytes
  • immunological memory for past infections and antigens
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10
Q

whats the role of a fibroblast?

A
  • produce collagenous connective tissue involved in scarring following some types of inflammation
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11
Q

what is the sequence of acute inflammation?

A
  • injury or infection
  • neutrophils arive and phagocytose and release enzymes
  • macrophages arrive and phagocytose
  • either resolution with clearance of inflammation or progression to chronic inflammation
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12
Q

what are some examples of acute inflammation?

A
  • acute appendicitis
  • frostbite
  • strepococcal sore throat
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13
Q

whats the sequence of chronic inflammation?

A
  • either progression from acute inflammation or starts as chronic inflammation such as infectios monoculceosis
  • no or very few neutrophils
  • macrophages and lymphocytes, then usually fibroblasts
  • can resilve if no tissue damage but often ends up with repair and formation of scar tissue
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14
Q

what are granulomas?

A
  • a particular type of chronic inflammation with collections of macrophages/histocytes
    surrounded by lymphocytes
  • only seen in cases of TB, leprosy, crohn’s, foreign material
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15
Q

when are granulomas seen?

A
  • chrons disease
  • foreign material in tissue
  • tb
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16
Q

what are some similarities and differences of acute vs chronic inflammation?

A

SIMILARITIES:
- both involve types of immune cells
- in both types, vascular changes occur to recruit immune cells to the site of inflammation
DIFFERENCES:
- sudden vs slow onset
- short vs long duration
- acute usually resolves whereas chronic may never resolve

17
Q

what are the first cells on scene to acute inflammation?

A

neutrophil polymorphs

18
Q

how do endothelial cells differ in sites of infection?

A
  • become sticky so inflammatory cells can stick to them
  • grow into areas of damage to form new capillary vessels
19
Q

how does ibuprofen and other NSAIDs treat inflammation in the body?

A

blocks the bodys production of prostoglandins

(NSAIDs (Non-Steroidal Anti-Inflammatory Drugs) do not directly treat infections but help manage symptoms like pain, fever, and inflammation associated with infections. They work by inhibiting cyclooxygenase (COX) enzymes, which reduces the production of prostaglandins—molecules that mediate inflammation, fever, and pain. While effective in symptom relief, NSAIDs do not address the underlying cause of an infection, which typically requires antimicrobial therapy.)

20
Q

name 3 medications which can be used in inflammatory cases?

A
  • corticosteroids
  • antihistamines
  • NSAIDs
21
Q

what are some causes of acute inflammation?

A
  • microbial infections
  • hypersensitivity reactions
  • physical agents eg trauma
  • chemicals eg acids
  • tissue necrosis
22
Q

describe what happens in the early stages of acute inflammation?

A
  • oedema fluid, fibrin, and neutrophil polymorphs accumulate in the extracellular spaces of the damaged tissue
23
Q

what are the 3 stages of EARLY acute inflammatory response?

A
  • changes in vessel calibre and consequently flow
  • increased vascular permeability and formation of the fluid exudate
  • formation of the cellular exudate - emigration of the neutrophil polymorphs into the extravascular space
24
Q

describe the vasuclar component of inflammation?

A
  • increase in diameter (calibre) of blood vessels
  • increase in local blood flow
  • increase in hydrostatic pressure bc of inc flow causes for much more fluid to leave the vessel then to return - also more plasma proteins, increasing the colloid osmotic pressure
  • causing oedema - excess fluid in extravascular space - inflammation
25
Q

describe the process of the accumulation of fluid exudate.

A
  • inc vascular permeability - more large molecules such as proteins can escape
  • includes immunoglobins and fibrin - important in the destruction of microorganisms
  • constantly drained away by the lymph system and replaced by new exudate
26
Q

describe what occurs during the neutrophil polymorph margination and adhesion?

A
  • because of the higher amount of fluid loss from the blood inside the vessels, instead of the cells flowing through the centre of the vessel, they make contact with the endothelial cells lining the inside of the vessel more frequently
  • it is also more sticky so sticks to the wall
  • this is termed pavementing
27
Q

what cells are involved in inflammation`/

A
  • neutrophil polymorphs
  • macrophages
  • lymphocytes
  • endothelial cells
  • fibroblasts
28
Q

whats the role of endothelial cells in inflammation?

A
  • line capillary blood vessels in areas of inflammation
  • become sticky in areas of inflammation so inflammatory cells adhere to them
  • become porous to allow inflammatory cells to pass into tissues
  • grow into areas of damage to form new capillary vessels
29
Q

what are the physiological benefits of inflammation?

A
  • Pathogen Elimination: Targets and destroys harmful microorganisms.
  • Removal of Dead Cells: Clears cellular debris and dead tissue.
  • Containment: Prevents spread of infection or damage.
  • Tissue Repair: Releases growth factors for healing.
  • Increased Blood Flow: Delivers nutrients, oxygen, and removes waste.
  • Enhanced Immune Response: Recruits and activates immune cells.
  • Pain as a Protective Signal: Discourages movement to protect the area.
30
Q

summarise the pathophysiology for inappropriate inflammation?

A
  • Autoimmune Disorders: Immune cells mistakenly target self-tissues.
  • Allergies and Hypersensitivities: Harmless substances cause exaggerated immune reactions.
  • Chronic Inflammatory Diseases: Continuous inflammation damages tissues and leads to fibrosis.
  • Metabolic Inflammation: Fat cells and blood sugar abnormalities drive low-grade inflammation.
  • Persistent Infections: Incomplete clearance of pathogens leads to ongoing immune activation.
  • Environmental and Stress Factors: Toxins and stress dysregulate immune response and increase inflammation.