Module 2.3 Inflammation, Tissue Repair and Wound Healing. Flashcards
Purpose of inflammation
Eliminate cause of injury
Generate new tissue
Acute Inflammation Summary
- Short duration
- Aim is removal of injuring agent and limiting tissue damage
- Infiltration of NEUTROPHILS
- Produces EXUDATE
Chronic Inflammation summary
- Lasts days to years.
- Infiltration of MACROPHAGES AND LYMPHOCYTES
- Proliferation of FIBROBLASTS - scarring
Types of chronic inflammation
Recurrent or progressive
How to differentiate between chronic and acute inflammation in a patient.
look at the WBC’s in the area. lymphocytes not seen in early stages, only in chronic.
Leukocytes of inflammation
Monocytes
Neutrophils
Basophils
Eosinophils
When an Eosinophil moves into the tissue it becomes a
Mast cell
When a Monocyte moves into the tissue it becomes a
Macrophage
Connective tissue cells of inflammation
Fibroblasts
Macrophages
Mast cells
Vascular phase of inflammation
Vasodilation (after very brief constriction).
causes Rubor and Calor
Increased vascular permeability > swelling (tumor)
Rubor
redness
Calor
Heat
Tumor (in inflammation)
swelling due to vascular permeability
Dolor
Pain
Functio Laesa
Loss of Function
5 Hallmark signs of inflammation
- Rubor
- Calor
- Tumor
- Dolor
- Functio Laesa
Immediate Transient response
Lasts 15-30 minutes.
Minor burns/bumps
Immediate Sustained response
May last several days.
Usually result of vascular injury
Delayed hemodynamic response
occurs 2-24 hours after exposure to radiation.
Sunburn, radiation therapy
Margination
Accumulation of leukocytes caused by cytokines (ie selections, integrins) which recruit WBC’s.
Adhesion
leukocytes slow down and role until they find site of high cytokine activity. (verify/read up on?)
Transmigration
Leukocytes extend foot and squeeze through vessel wall. into tissue spaces
What causes transmigration
Chemotactic factors
Why are chemokines important in early inflammation
They attract and direct leukocytes to needed areas
What immune cell secretes chemokines
macrophages
Stages of Phagocytosis
Recognition and adherence (detection of cells covered in opsin)
Engulfment (opsinization)
Intracellular killing
LISTEN TO 13 MINUTE MARK
LISTEN TO 13 MINUTE MARK
Bacterial infections generally result in what WBC change?
Increased neutrophils
Parasitic infections and allergies generally result in what WBC change?
Increased Basophils
Effect of inflammation/infection on erythrocyte sedimentation rate
increased ESR
Overwhelming infection may cause
Leukopenia - decreased WBC’s
What cell releases histamines?
Mast Cells
Role of histamines in inflammation
Vasodilation and increased permeability of venules
What are the 2 arachidonic acid metabolites and where do they come from
Prostaglandins
Thromboxane
From cell membranes
Effects of Prostaglandins
vasodilation
Bronchconstriction
potentiates Histamine (associated with anaphylaxis)
Uterine contractions during menstruation
Effects of Thromboxane
Vasoconstriction
Bronchoconstriction
Promotes Platelet function
Effects of Platelet Activation Factor
Activates Neutrophils
Attracts Eosinophils
Activates Platelets
Plasma proteins as inflammatory mediators
Promotes blood clotting
Activates compliment system.
Vasoactive Peptides
Bradykinin (vasoactive peptide)
increased vascular permeability
Dilation of blood vessels, contraction of smooth muscle
Nitric Oxide as inflammatory mediator
Think free radicals!!
Platelet Aggregation
Causes increased tissue injury (can become never ending cycle)
STUDY FIGURE 9.3
STUDY FIGURE 9.3
Acute phase response of cell mediated response (TQ!)
Fever Anorexia Hypotension Tachycardia Corticosteroid and ACTH released
Serous Exudate
Watery
Low in protein content
Plasma entering the inflammatory site
Hemorrhagic exudates
Severe tissue damage involving vessels or severe leakage of red cells from capilaries
Membranous or Pseudomembranous exudates
Develop on mucous membrane surfaces.
Composed of necrotic cells enmeshed in fibro-purulent-exudate.
Seen in burns!
Purulent or Suppurative Exudates
contain pus (WBC’s, proteins, tissue debris)
Fibrinous Exudates
Large amount of fibrinogen
Form thick sticky meshwork
READ INFO ON SLIDE 23! WILL BE ON TEST
READ INFO ON SLIDE 23! WILL BE ON TEST
What is an abscess
A walled off inflamed area filled with purulent exudate.
What are characteristics unique to chronic inflammation.
Granulomas
Infiltration with Macrophages and LYMPHOCYTES
proliferation of Fibroblasts
What is chronic gramulomatous inflammation associated with
Foreign Bodies
Splinters, sutures, asbestos, silica
Microbes
TB, Syphilis, sarcoidosis, Deep fungal infections, brucellosis
Parenchymal Tissue
Tissue containing the functional cells of the organ (hepatocytes, renal tubular cells)
Stromal Tissue
Supporting tissue (Nerves, ECM, Blood Vessels, etc.)
Labile Cells
Replaceable cells (skin, mucosa, GI tract)
Stable Cells
Normally stop dividing when they reach maturity. May start again if damaged (partial liver removal)
Example of stable cells
Parenchymal cells of liver and kidneys. smooth muscle cells, vascular endothelium.
Permanent cells
Cannot undergo mitotic division.
Nerves, skeletal muscle, cardiac.
Stages of wound healing
Inflammatory phase
Proliferative phase
Maturational (remodeling) phase
inflammatory phase of healing
Injury
Blood clots and WBC’s migrate to site
Neutrophils arrive first, then macrophages.
Proliferative phase
Fibroblasts are predominant cell.
Secrete reconstruction material (collagen, vascular growth factors for angiogenesis)
Maturational or remodeling phase
~3 weeks post injury.
Scar formation
Healing by primary intention
Small clean wound, well approximated, no tissue lost.
Healing by secondary intention
great tissue loss, contamination, left open to heal.
Still minimal scarring if properly cared for
What may delay wound healing
DM Corticosteroid use Malnutrition Impaired circulation/perfusion Age Infection
Issues with healing in children
Electrolyte imbalances
Temp Instability
Immune insufficiency in very young kids
Nutritional needs (Short gut syndrome, DM)
