Class 6 - Inflammation Flashcards

1
Q

What is inflammation?

A

A protective process that is initiated to minimize or remove the pathologic agent or stimulus triggering the inflammation and to promote healing

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2
Q

Inflammation and infection relationship

A

Inflammation is always present with inflammation, but inflammation can occur in the absence of infection

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3
Q

Causes of inflammation

A

Infection and immunity

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4
Q

Inflammation can be:

A

Acute or Chronic or Repair/Restorative

Local or Systemic

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5
Q

Inflammation is triggered by:

A
  • Mechanical trauma
  • Thermal, electrical or chemical injury
  • Radiation damage
  • Biological assault (infection)
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6
Q

The goal of a normal inflammatory response

A
  • Restore normal cell function
  • Fibrous repair when cells can’t be restored
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7
Q

Physiological process of a normal inflammatory response

A

White blood cells and chemicals that serve to protect the body from invaders or cellular/tissue damage are involved

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8
Q

Types of WBCs

A

Granulocytes (mature, around 8-15 days = segmented [segs], immature = bands)
Agranulocytes

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9
Q

Granulocytes

A

Neutrophils (helps in phagocytosis)
Eosinophils (fights against parasitic infections)
Basophils (produces inflammatory and allergic reactions)
Tissue mast cells (signal for more neutrophils)

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10
Q

Agranulocytes

A

Lymphocytes (produce specific immune responses - B lymphocytes, T lymphocytes, Natural Killer Cells)
Monocytes (fights off bacteria, viruses, and fungi)

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11
Q

Chemotaxis

A

Proinflammatory response - WBCs head towards inflammation when chemotaxis occurs

Stimulated by:
- Bacterial or viral extoxins
- Degenerative by-products of inflammation
- Products of complement system activation
- Reactive products of plasma clotting

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12
Q

Proinflammatory hormones

A

Prostaglandins
Histamines
Cytokines

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13
Q

Functions of proinflammatory hormones

A
  • Increase blood flow to the area of injury
  • Attract leukocytes to area of injury
  • Increase vascular permeability
  • Activate components of an immune response
  • Promote angiogenesis
  • Stimulate connective tissue growth
  • Cause fever
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14
Q

Stage 1 of vascular response

A
  • Injured tissues, local granulocytes, and tissue masts secrete proinflammatory hormones
  • Macrophages secrete proinflammatory hormones
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15
Q

What do injured tissues, local granulocytes, and tissue masts secreting proinflamamtory hormones do?

A

Small veins constrict and aerterioles dilate (blood flow increases delivering nutirents like O2 and glucose to injured tissues)
- Hyperemia/redness, warmth, edema

Capillary leak/permeability (swelling/edema and pain)

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16
Q

What do macrophages that secrete proinflammatory hormones do?

A

Mature WBCs quicker and promote neutrophil invasion

17
Q

Stage 2 of vascular response

Cellular response

A
  • Granulocytes and tissue mast cells become activated
  • Exudate forms
  • Macrophages increase and stimulate monocyte production
  • Arachidonic acid cascade
18
Q

Granulocytes and tissue mast cells become activated

A
  • Neutrophilia occurs 12 hrs after injury & Phagocytosis
  • Eosinophils, basophils, and mast cells promote continuous inflammatory response
19
Q

Exudate forms

A

Dead WBCs, necrotic tissue, leaked cell fluid

20
Q

Arachidonic acid cascade

A

Increases inflammation
- Fatty acids in membrance of injured cells turn into arachidonic acid which is then converted (by COX enzyme) into substances (histamine, leukotrienes, prostaglandins, serotonin, kinins) that promote more inflammation

21
Q

Stage 3 of vascular response

Tissue repair and replacement

A
  • All WBCs involved start the replacement of lost/damaged tissues by stimulating healthy cells to divide
  • WBCs trigger blood vessel growth and scar tissue formation for those cells that cannot divide
    • Function of these cells are lost

The stages can overlap - they are not discrete

22
Q

Local responses

A

Swelling
Pain
Heat
Redness
Exudate/impaired function - serous/fibrinous/purulent/hemorrhagic

23
Q

Chronic inflammation

A
  • Macropages are the star
    • Release tissue thromboplastin - facilitates hemostasis, promotes fibroblasts
    • Removes necrotic tissue and pathogens (debridement) continuous release of proinflammatory cells
  • Thickening and scarring of connective tissue
  • May be subclinical
24
Q

What is subclinical?

A
  • No overt symptoms (more systemic manifestations)
  • Investigate through blood tests: CRP and ESR
  • May need a WBC scan to identify areas of inflammation
25
Systemic responses
Neutrophilia Fever Malaise Loss of appetite Muscle catabolism
26
What is ESR?
Fibrinogen levels go up in the serum which causes RBCs to clump. **CHRONIC INFLAMMATION MARKER ** | Erythrocyte sedimentation rate
27
What is hs-CRP?
Dead and dying cells release chemical factors, which cause the liver to produce CRP. **PROTEIN LIVER MAKES HS-CRP DURING ACUTE INFLAMMATION** | Highly sensitive C-reactive protein
28
Drugs that reduce inflammation
Steroidal agents = glucocorticoids (Prednisone) Non-steroidal anti-inflammatory drugs (NSAIDs) = Ibuprofen
29
Drugs that manage fever
Antipyretics - Acetaminiphen - Aspirin (almost never because of anti-coagulant properties) - NSAIDs
30
Drugs for pain relief
Analgesics - Acetaminophen - Aspirin (rarely) - NSAIDs - Opioids for severe pain
31
MOA of Glucocorticoids (Prednisone)
Inhibit synthesis of chemical mediators (prostaglandins, leukotrienes, histamines) - They suppress infiltration of phagocytes so damage from lysosomal enzymes is averted - The suppress proliferation of lymphocytes and therby reduce the immune components of inflammation
32
Glucocorticoids (Prednisone) adverse effects
Hyperglycemia Fluid and electrolyte imbalances (Na/K) Psychological disturbances (anxiety/agitation/insomnia) Peptic ulcer disease Adrenal insufficiency Osteoporosis Cushings
33
Glucocorticoids (Prednisone) Nursing Considerations
Monitor: BP Weight gain Lab values Abdominal pain Signs and symptoms of infection Adminster with antacid Tapering required Caution with NSAIDs Give in the morning
34
Sudden withdrawal and adrenal crisis
Exogenous cortisol stops pituitary release of ACTH which controls adrenal glands thus stopping them from working Adrenal crisis = hypotension, fly-like symptos, seizures, shock