Examples of Inflamamtory Diseases, Scar Tissue Formation and Poor Wound Healing

Arthritis

Arthritis

All likely auto-antibody related, multi-system with typical patterns of joint involvement, flares/remissions

The synovium of the joints

“Antigen” the body creates antibodies against in rheumatoid arthritis:

Compliment. Directly damages synovium by poking hols (prostaglandins/leukotryenes) AND degranulates mast cells in the area (histamine released)

In rheumatoid arthritis, an auto-antibody reacts to antigen, activates waht?

WBCs digest antigen/auto-antibody complex on the tissue surface, so WBC damages tissue

Compliment damages the synovium by poking holes

Excess fibroblasts, collagen, etc. accumulates as part of repair

How are tissues damaged in RA?

Pannus

scar tissue buildup in rheumatoid arthritis

1. Painful joints

2. Swollen/boggy joints

3. Warm, reddened joints

4. Joint stiffness (pannus)

5. Fatigue, systemic stiffness

S+S/Complications of RA

1. deformity, nodules

2. erosion of the joint

3. atrophy of surrounding muscle from non-use

4. Vasculitis, pleuritis, iritis

Long-term complications of RA: [3]

1. NSAIDs

2. acetaminophen

3. Steroids

4. DMARDs

pharmacological treatment of RA: [4]

1. Joint protection and supportive measures (splints)

2. muscle strengthening

3. ROM exercises

4. Jar grippers

5. heat

Non-pharmological treatment of RA [5]

Osteoarthritis

Wear and tear: cartilage in synovial joints breaks down, Pain is related to loss of cushioning with direct stimulation of nociceptors.

Inflammation is usually secondary, later in the disease

When is inflammation seen in osteoarthritis?

1. acetominophen

2. NSAIDs (late)

3. Glucosamine/chondroitin

Pharmacological treatment for osteoarthritis: [3]

1. Joint protection and supportive measures

2. muscle strengthening

3. ROM exercises

4. jar grippers

5. heat

6. joint replacement

Non-pharmalogical treatment for osteoarthritis:

Asthma

Triggers cause mast cell degranulation in bronchial lining, caused by allergens and irritants

IgE rests on mast cells

allergens bind to IgR, triggers mast cell degeneration

and histamine release

Pathophysiology for allergic asthma: [3]

Irritants directly trigger mast cell degeneration and histamine is released

pathophysiology for asthma (no allergies)

INflammatory reaction from histamine causes damage to respiratory mucosal cells leading to pG synthesis

Secondary response in asthma:

1. vasocdilatoin (red lungs)

2. Increased vasccular permeability (swollen bronchi, wheezing)

3. Chemotaxis (WBC in exudate, sputum)

4. Stimulation of smooth muscle contraction (wheezing)

5. Stimulation of goblet cells (crackles, wheezing)

Histamine and prostaglandin effects of asthma: [5]

• Crackles & wheezing on ausculatation
• Shortness of breath
• Dyspnea, Tachypnea, SOB
• Sometimes stridor
• Increased respiratory rate and effort
• Productive cough
• Tachycardia
• Anxiety
• Other HPA effects

S+S of asthma: [9]

Status asthmaticus

If asthma is not treated, severe air trapping can happen in the lungs. Leads to worsening hypoxemia, hypercapnia, PFTs. Can be life threatening

Thickening of the bronchial tissue due to scarring. The bronchi become hyper-reactice so bronchospasm is easily evoked.

How can asthmatics have long-term low-level inflammation?

1. avoidance of triggers

2. anti-inflammatory drugs (prevents inflammation leading to bronchospasm)

3. Bronchodilators

4. leukotriene receptor antagonist (block inflammatory effects of leukotriene)

How to manage asthma? [4]

1. Brochitis: not episodic, can be resolved.

2. Bronchitis: due to irritation or infection (not allergens and irritants)

3. Bronchitis: more hypersecretion of mucous (not bronchospasm)

Key factors differentiating asthma and bronchitis:

Inflammatory bowel disease

Chronic inflammation of the bowel triggered by anti-colon or anti-digestive system antibodies.

Ulcerative colitis

Generaly, onset 20-40 years of age. Mucousa of the colon, often starts in the rectum as proctitis (inflammatory bowel disease)

Crohn’s disease

Inflammatory bowel disease that is anywhere in the digestive system from the mouth to anus. Typically onset is 10-30 years old

1. compliment is activated so mast cell degranulation. Histamine is released

2. Damage in bowel tissue leads to prostaglandin snthesis which prolongs inflammation

Inflammatory process for both ulcerative colitis and Chron’s

• Mucosa is red (vasodilation)
• Mucosa is mushy, edematous (increased vascular
permeability)
• Erosions in mucosa (WBCs debridement)
– Blood in stool (erosions into capillaries)
• Mucous in stool (stim. of goblet cells)
• Diarrhea (stim. of smooth muscle)
• Severe abdominal pain, cramping (SM contraction
and stim. of nociceptors)
• Weight loss, dehydration and under-nutrition
– May lead to anemia

S+S of inflammatory bowel disease: [9]

1. anti-inflammatory medications

2. steroids

3. nutritional supplementation

4. surgical resection of the bowel

how is inflammatory bowel disease managed?