Class 6 - Inflammation Flashcards
What is inflammation?
A protective process that is initiated to minimize or remove the pathologic agent or stimulus triggering the inflammation and to promote healing
Inflammation and infection relationship
Inflammation is always present with inflammation, but inflammation can occur in the absence of infection
Causes of inflammation
Infection and immunity
Inflammation can be:
Acute or Chronic or Repair/Restorative
Local or Systemic
Inflammation is triggered by:
- Mechanical trauma
- Thermal, electrical or chemical injury
- Radiation damage
- Biological assault (infection)
The goal of a normal inflammatory response
- Restore normal cell function
- Fibrous repair when cells can’t be restored
Physiological process of a normal inflammatory response
White blood cells and chemicals that serve to protect the body from invaders or cellular/tissue damage are involved
Types of WBCs
Granulocytes (mature, around 8-15 days = segmented [segs], immature = bands)
Agranulocytes
Granulocytes
Neutrophils (helps in phagocytosis)
Eosinophils (fights against parasitic infections)
Basophils (produces inflammatory and allergic reactions)
Tissue mast cells (signal for more neutrophils)
Agranulocytes
Lymphocytes (produce specific immune responses - B lymphocytes, T lymphocytes, Natural Killer Cells)
Monocytes (fights off bacteria, viruses, and fungi)
Chemotaxis
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
Proinflammatory hormones
Prostaglandins
Histamines
Cytokines
Functions of proinflammatory hormones
- 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
Stage 1 of vascular response
- Injured tissues, local granulocytes, and tissue masts secrete proinflammatory hormones
- Macrophages secrete proinflammatory hormones
What do injured tissues, local granulocytes, and tissue masts secreting proinflamamtory hormones do?
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)
What do macrophages that secrete proinflammatory hormones do?
Mature WBCs quicker and promote neutrophil invasion
Stage 2 of vascular response
Cellular response
- Granulocytes and tissue mast cells become activated
- Exudate forms
- Macrophages increase and stimulate monocyte production
- Arachidonic acid cascade
Granulocytes and tissue mast cells become activated
- Neutrophilia occurs 12 hrs after injury & Phagocytosis
- Eosinophils, basophils, and mast cells promote continuous inflammatory response
Exudate forms
Dead WBCs, necrotic tissue, leaked cell fluid
Arachidonic acid cascade
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
Stage 3 of vascular response
Tissue repair and replacement
- 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
Local responses
Swelling
Pain
Heat
Redness
Exudate/impaired function - serous/fibrinous/purulent/hemorrhagic
Chronic inflammation
- 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
What is subclinical?
- No overt symptoms (more systemic manifestations)
- Investigate through blood tests: CRP and ESR
- May need a WBC scan to identify areas of inflammation
Systemic responses
Neutrophilia
Fever
Malaise
Loss of appetite
Muscle catabolism
What is ESR?
Fibrinogen levels go up in the serum which causes RBCs to clump.
**CHRONIC INFLAMMATION MARKER **
Erythrocyte sedimentation rate
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
Drugs that reduce inflammation
Steroidal agents = glucocorticoids (Prednisone)
Non-steroidal anti-inflammatory drugs (NSAIDs) = Ibuprofen
Drugs that manage fever
Antipyretics
- Acetaminiphen
- Aspirin (almost never because of anti-coagulant properties)
- NSAIDs
Drugs for pain relief
Analgesics
- Acetaminophen
- Aspirin (rarely)
- NSAIDs
- Opioids for severe pain
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
Glucocorticoids (Prednisone) adverse effects
Hyperglycemia
Fluid and electrolyte imbalances (Na/K)
Psychological disturbances (anxiety/agitation/insomnia)
Peptic ulcer disease
Adrenal insufficiency
Osteoporosis
Cushings
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
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
