Unit 2 Flashcards

1
Q

What is inflammation?

A
  • Part of the bodies normal defense mechanism
  • Purpose: to isolate and eliminate noxious agents that cause tissue injury
  • Response is non-specific: no memory associated with inflammation
  • May be present in chronic or acute forms

*any word with itist at the end means inflammation

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2
Q

What is the etiology of inflammation? (7 things)

A
  • Direct damage: cuts/sprains
  • Chemical injury
  • Ischemia (short term lack of oxygen, usually no damage)/infarction (long term lack of oxygen, damage usually present)
  • Allergy
  • Physical agents: burns
  • Foreign bodies: splinter
  • Infection
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3
Q

Signs and symptoms of inflammation

A
  • Redness (sign): hyperemia
  • Edema (sign): increase vascular permeability
  • Heat (symptom): hyperemia
  • Pain (symptom): Edema (pressure of fluid on nerves and pro-inflammatory mediators on nerves
  • Loss of function (symptom): Iscehmia (loss of cellular function) and Edema (loss of mechanical function)
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4
Q

Systemic effects of inflammation

A
  • General sense of feeling unwell
  • Loss of appetite
  • Fatigue
  • Headache
  • Low grade fever
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5
Q

Define Chronic inflammation

A
  • May develop from acute inflammation (ex: TB (chronic infection))
  • May have its own etiology (ex: intercellular infections (viral or bacterial)
  • May result from chronic irritation to tissue (ex: cigarette smoke)
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6
Q

Chronic inflammation vs acute

A

Chronic inflammation is associated with

  • Less swelling and exudate formation
  • More lymphocytes, macrophages and fibroblasts in the site
  • Often more tissue destruction
  • Often more scarring (more collagen laid down)
  • Formation of granuloma (mass of cells protecting an area from infection/inflammation)
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7
Q

Describe Inflammation treatment (RICE)

A
  • Rest
  • Ice: promotes vasodilation
  • Compress: helps prevent fluid accumulation
  • Elevation: helps fluid drain from edematious sites
  • Heat application depends on circumstances: may promote vasodilation and mobility which may increase local circulation
  • Pharmacological inflammation treatment: aspirin, non-steriodal anti-inflammatory agents (NSAID) (ex: ibuprofen) and steriodal anti-inflammatory agents (ex: gluccoroticoids which may be prednisone)
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8
Q

Describe the factors affecting healingFactors

A
  • Age: cells divide more slowly in older patients
  • Nutritional Status: need building blocks for tissue repair
  • Haemoglobin Level: need adequate O2 levels for tissue metabolism
  • Patent Circulation: blood carries nutrients and O2 to damage tissues
  • Wound Cleanliness: presence of bacteria or foreign matter promote inflammation and prevent tissues from knitting together
  • Complications: ex radiation or chemotherapy drugs prevent cell division
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9
Q

Describe scar tissue complications (loss of function)

A

Results from loss of functional cells (ex: hair follicles, secretory gland cells, sensory receptors or results from loss of specialized tissue architecture required for function (ex: lobule structure of liver, nephron structure of kidney)

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10
Q

Describe scar tissue complications (structural)

A
  • Contractures: shrinkage of non elastic collagen (ex: joint insolubility)
  • Obstruction: scar tissue narrows tubular tissues (stenosis)
  • Adhesions: Scar tissue may cause 2 adjacent tissues to stick to one another in abnormal manner, may distort tissue or may prevent tissue from gliding smoothly past one another
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11
Q

Describe scar tissue complications (ulceration)

A

-Impaired blood flow in regions adjacent to scar tissue, may result in local tissue necrosis

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12
Q

Describe scar tissue complications (keloid scars)

A

Hypertrophic scar tissue:

  • Much more scar needed to tissue repair
  • Dense mass of scar tissue that extends into surround dermal tissue
  • Most common in skin with higher melanin deposition
  • Commonly observed in shoulder region, chest and earlobes
  • Harmless, but may have aesthetic implications
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