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Inflammation Chapter 2 Ms. Harris Pathophysiology Fall 2009

Inflammation Chapter 2 Ms. Harris Pathophysiology Fall 2009

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Page 1: Inflammation Chapter 2 Ms. Harris Pathophysiology Fall 2009

Inflammation Chapter 2

Ms. Harris

Pathophysiology

Fall 2009

Page 2: Inflammation Chapter 2 Ms. Harris Pathophysiology Fall 2009

Body’s Defenses

1) What is the body’s FIRST line of defense?– Mechanical barriers like the skin and mucous

membranes! (non-specific)

2) 2nd line of defense?– Phagocytosis and inflammation (non-specific)

• Phagocytosis uses neutrophils (leukocytes) and macrophages to “gobble up” foreign matter.

Page 3: Inflammation Chapter 2 Ms. Harris Pathophysiology Fall 2009

Body’s Defenses

3. 3rd line of defense?– The immune system! (specific)

• Produces antibodies following exposure.

Page 4: Inflammation Chapter 2 Ms. Harris Pathophysiology Fall 2009

Inflammation

• Serves as a warning of a problem, which may be hidden in the body.

• What’s the difference between infection and inflammation?

Page 5: Inflammation Chapter 2 Ms. Harris Pathophysiology Fall 2009

Inflammation Definition

• the body’s non-specific response to tissue injury– Localize it and remove it!

Page 6: Inflammation Chapter 2 Ms. Harris Pathophysiology Fall 2009

What does inflammation look like?

• Redness

• Swelling

• Warmth

• Pain

• Loss of function

Page 7: Inflammation Chapter 2 Ms. Harris Pathophysiology Fall 2009

What causes inflammation?

• Cuts

• Sprains

• Ischemia

• Allergic reactions

• Burns

• Foreign bodies (like a splinter)

• infection

Page 8: Inflammation Chapter 2 Ms. Harris Pathophysiology Fall 2009

-itis = inflammation of

• Appendicitis = ???

• Gastroenteritis = ???

• Senioritis = ???

Page 9: Inflammation Chapter 2 Ms. Harris Pathophysiology Fall 2009

Acute Inflammation- Inflammatory Response

1. Injury Occurs2. Damaged cells release chemical messengers

in to the blood and interstitial fluid– Histamines, leukotrienes, prostaglandins, etc. (see

Table 2-1 and know these 3!!!!)

3. These chemicals affect blood vessels and nerves in the affected area.

4. Body naturally inactivates these chemicals when inflammatory response is no longer necessary.

Page 10: Inflammation Chapter 2 Ms. Harris Pathophysiology Fall 2009

Histamines• Released immediately to cause vasodilation and

increase capillary permeability.

Leukotrienes• Prolong inflammation; cause vasodilation,

increase capillary permeability, chemotaxis

Prostaglandins• Prolong inflammation; cause vasodilation,

increase capillary permeability, pain, and fever

Page 12: Inflammation Chapter 2 Ms. Harris Pathophysiology Fall 2009

Chemotaxis

• Leukocytes are attracted to the area to destroy and remove foreign material– Bacteria, dead cells, etc.

• These leukocytes then die and lysosomal enzymes break them and nearby cells down, prolonging inflammation. (edema)

Page 13: Inflammation Chapter 2 Ms. Harris Pathophysiology Fall 2009

Local Effects – why?

• Redness and warmth

• Swelling or edema

• Pain

• Loss of function

Page 14: Inflammation Chapter 2 Ms. Harris Pathophysiology Fall 2009

Interstitial Fluid = Exudate

• Serous- watery; allergic rxns. and burns

• Fibrinous- thick and sticky

• Purulent- (a.k.a. pus) thick, yellow/ greenish color; contains more leukocytes, microorganisms, debris. Indicates bacterial infection

• Abcess- localized pocket of purulent exudate

• Hemorrhagic- bloody exudate (blood vessels have been damaged

Page 15: Inflammation Chapter 2 Ms. Harris Pathophysiology Fall 2009

???

Page 16: Inflammation Chapter 2 Ms. Harris Pathophysiology Fall 2009

Systemic Effects

• Fever (a.k.a. pyrexia)

• Malaise

• Fatigue

• Headache

• anorexia

Page 17: Inflammation Chapter 2 Ms. Harris Pathophysiology Fall 2009

Fever… good or bad???

• Also called pyrexia.

• Can be low grade or high, depending on the pathogenic organism.

• Caused by the release of pyrogens which also cause shivering, cutaneous vasoconstriction (feeling “clammy”)

Page 18: Inflammation Chapter 2 Ms. Harris Pathophysiology Fall 2009

Diagnosis

• Almost always a blood test– Increased leukocytes– Increased # enzymes– Differential counts (# for each of the types of

WBCs)– Eo counts (if allergies are suspected)

Page 19: Inflammation Chapter 2 Ms. Harris Pathophysiology Fall 2009

Course of Inflammation

• If caused by brief exposure (like a burn), inflammation will reside within 48 hours.

• Otherwise, inflammation will persist until the harmful agent is removed.– If too long, extensive necrosis may occur

• Ulcers, perforations

Page 20: Inflammation Chapter 2 Ms. Harris Pathophysiology Fall 2009

Chronic Inflammation

• Ex: Arthritis

• Less swelling and exudate, but more lymphocytes and macrophages

• More necrosis

Page 23: Inflammation Chapter 2 Ms. Harris Pathophysiology Fall 2009

• NSAIDs: (Advil, Motrin, Celebrex) non-steroidal anti-inflammatory drugs

– Decreases prostaglandins– Pros: Anti-Inflammatory, analgesic,

antipyretic• Typically used to treat inflammation of the

muscular and skeletal systems

– Cons: same as aspirin but less severe

Page 24: Inflammation Chapter 2 Ms. Harris Pathophysiology Fall 2009

• Prednisone (a steroid)– Extremely valuable in short-term relief of

inflammation• Blocks immune response• Decreases capillary permeability

– REALLY bad long term affects:• Causes atrophy• Increases blood pressure• Kidney and liver damage