Test 1: Module 2 (Inflammation and Healing) Flashcards

1
Q

What is inflammation?

A

a cellular process that is responsible for removing injurious agent, removal of cellular debris and the
initiation of the healing processing. The healing process
occurs to allow restoration of structure and function
whenever possible

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2
Q

What are the cardinal signs of acute inflammation?

A

Heat
Redness
Swelling
Pain
Loss of Function

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3
Q

What is the onset of acute and chronic inflammation?

A

Chronic is delayed onset

Acute is rapid onset

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4
Q

How long do acute and chronic inflammation last?

A

Chronic inflammation lasts a long time (weeks, months, years)

Acute inflammation lasts a short time (days)

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5
Q

Are chronic and acute inflammation specific?

A

Chronic is specific (acquired immunity)

Acute inflammation is non-specific

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6
Q

What is the cause of acute inflammation?

A

Physical or chemical damage

Pathogens

Tissue necrosis

Immune response

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7
Q

What is the cause of chronic inflammation?

A

Persistent damage or infection

Presence of foreign body

Autoimmunity

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8
Q

What is the outcome of acute versus chronic inflammation?

A

Acute inflammation: healing, trigger removal, tissue repair

Chronic inflammation: collateral damage

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9
Q

What are the biomarkers of acute inflammation?

A

IL-6
TNF-alpha
IL-1beta
CRP

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10
Q

How long does inflammation last?

A

Usually 4-6 days

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11
Q

How long does proliferation last?

A

4 - 24 days

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12
Q

How long does remodeling last?

A

21 days - 2 years

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13
Q

Starling Forces

A

govern the passive exchange of water between the capillary
microcirculation and the interstitial fluid.

These forces determine the
directionality & rate of net water
movement between two different
compartments

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14
Q

What happens at the arterial end?

A

Blood pressure (hydrostatic pressure) is higher than osmotic pressure. So fluid exits the capillary

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15
Q

What happens at the venous end?

A

The osmotic pressure is higher than the blood pressure (hydrostatic pressure). So fluid enters the capillary

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16
Q

What causes swelling?

A

Release of inflammatory mediators at the capillary increase the vascular permeability. This causes neutrophils and fluid to leave the capillary which leads to swelling.

17
Q

Hemorrhagic/Sanguineous Exudate

A

Appearance: Bright red or bloody; presence of red blood cells (RBCs)

Significance: Small amounts expected after surgery or trauma. Large amounts may indicate hemorrhage. Sudden large amounts of dark, red blood may indicate a draining hematoma

18
Q

Serosanguineous Exudate

A

Appearance: Blood-tinged yellow or pink; presence of RBCs

Significance: Expected for 48-72 hours after injury or trauma to the microvasculature. A sudden increase may precede wound
dehiscence (rupture or separation).

19
Q

Serous Exudate

A

Appearance: Thin, clear yellow, or straw-colored; contains albumin and immunoglobulins

Significance: Occurs in the early stages of most inflammations; common with blisters, joint effusion with rheumatoid arthritis, viral infections (e.g., skin vesicles caused by herpesvirus);
expected for up to 1 week after trauma or surgery. A sudden
increase may indicate a draining seroma (pocket of serum
within tissue or organ)

20
Q

Purulent Exudate

A

Appearance: Viscous, cloudy, pus; cellular debris from necrotic cells and dying neutrophils (PMNs)

Significance: Usually caused by pus-forming bacteria (streptococci, staphylococci) and indicates infection. May drain suddenly from an abscess (boil).

21
Q

Catarrhal Exudate

A

Appearance: Thin, clear mucus

Significance: Seen with inflammatory process within mucous membranes (e.g., upper respiratory infection).

22
Q

What causes an increased sensation of pain during inflammation?

A
  1. Chemical mediators: Cytokines lower the depolarization threshold for the nociceptors (pain receptors), making them more sensitive to pain.
  2. Direct trauma
  3. Internal pressure from swelling
  4. Swelling of nerve ends
23
Q

What causes swelling?

A

Exudation and leukocytes infiltration into extracellular space

24
Q

What causes heat and redness?

A

Vasodilation and increased blood flow

25
Q

Explain the process of how a leukocyte gets to the spot of trauma (Margination -> Rolling -> Adhesion ->Diapedesis/Transmigration)

A

Margination -> Rolling -> Adhesion -> Diapedesis/Transmigration

Margination is when WBCs accumulate at the endothelial walls (Increased permeability -> Increased cell concentration -> Hemoconcentration -> slows blood flow -> WBC margination)

Rolling: selectin proteins on the endothelial wall act like velcro, so they weakly bind to integrins on the WBC allowing it to roll down the wall

Adhesion: Integrins on the WBC have a higher affinity for the integrin ligand on the endothelial wall at the sight of injury. They stop rolling because of this affinity

Diapedesis: The WBC migrates through the endothelium

26
Q

Chemotaxis and inflammation

A

Inflammatory chemicals call chemokines are released at the sight of injury.

This causes WBCs to go to the sight of injury to begin phagocytosis

27
Q

Mechanisms of Phagocytosis

A
  1. Chemotaxis and adherence of microbe to phagocyte
  2. Ingestion
  3. Formation of phagosome
  4. Lysosome fuses with phagosome to form phagolysosome
  5. Digestion of ingested microbe by enzymes
  6. Discharge of waste
28
Q

What causes fever?

A

Inflammatory mediators and cytokines pass the blood brain barrier, elevating body temperature