Inflammation/Healing Flashcards
Acute + Chronic + Wound Healing
Acute Inflammation
Acute Inflammation
Rapid & Exudate
Eliminate/prevent/remove necrotic tissue from spreading
Results: Complete resolution, chronic inflammation, fibrosis/scarring
Acute Inflammation
Hallmarks
Red (rubor)
Heat (calor)
Swelling (Tumor)
Pain (Dolor)
Loss of Function (funcitonal lasse)
Acute Inflammation
Cellular infiltrates in inflammation
PMN/PMNLs (neutrophil) and cause apoptosis + macrophages enter
Acute Inflammation
Steps
Vasodilation (redness/warmth) and permeability (inflammation), macrophages (phagocytosis)
Diapedesis is PMS migrating across to where they need to go and cheokines push them to the site, they activate pain followed macrophages
Short life for neutrophils, macrophages clean it up so the dead neutrophils do not cause pus to form
Acute Inflammation
Serous Inflammation
Copius Effusion from plasma/mesothelial cells –> seperation of layers (blister)
Acute Inflammation
Fibrinous inflammation
Meshwork of fibrin (pink strands) exuded out of the blood
Examples: fibrinous pericarditis/emningitis, can be broken down by fibrinolysis
Acute Inflammation
Purulent Inflammation
Localized vicous exudate - pus, dying neutrophils
Results: Complete Resolution/abcess (pus), sinus, fistula (w/liquefactive necrosis)
Microscope: Capillary walls congested –> yellow exudate
Acute Inflammation
Vasoactive Amines
Vasodilation/vascular permeability
Mast cell - histamine
Platlet - histamine/serotonin
Acute Inflammation
Complement
Mast Cell stimulation, chemotaxis
Acute Inflammation
Kinins
Vascular permeability, pain, smooth muscle contraction (vasodilation)
Kallikren: attract neutrophils
Acute Inflammation
APP
Made by liver released in blood
Acute Inflammation
Coagulation Factors
Clot pathways to activate kinins
Chronic Inflammation
Fibrinous and Fibrous Inflammation
Fibrinous and fibrous inflammation from fibrin deposition fibromas chronic fibrous inflammation (fibroblast surrounding collagen fibers in dense connective tissue)
Chronic Inflammation
Granulomatous Inflammation
Granulomatous Inflammation is the collection of cells that can’t eliminate: multinucleated cells, activated macrophages, lymphocytes
Microscope: pale nuclei, pink cytoplasm, palisading
Chronic Inflammation
Transudate vs. Exudate
Transudate is clear, low protein, low cell content/ low gravity caused by starling forces
Exudate opaque, high protein, high protein count, high gravity caused by damage to endothelial wall
Chronic Inflammation
Acute vs. Chronic Pneumonia
Acute Bronchopneumonia is acute bacterial infection of terminal bronchioles extending into alveoli, leads to outpouring of PMNs and red blood cells pus created macrophages eat up exudate removed
Chronic Pneumonia is inflammation w/I alveoli and distal bronchioles is inflammatory exudates that fill alveoli and may be transformed into nodules (no necrosis + neutrophil infiltration) and is secondary to injury via drugs
Chronic Inflammation
Acute vs. Chronic Bronchitis
Acute Bronchitis: viral infection, desquamated cells, infiltrates in bronchial mucosa, predominantly neutrophilic
Chronic Bronchitis: Inflammatory swelling and mucous production, never healed from acute (>3 mnths), ↑ size of mucus-secreting gland, goblet cells, , squamous epithelial cell, mononuclear consist of lymph and plasma cells
Chronic Inflammation
SIRS + Sepsis
SIRS (massive release of cytokines in blood, HPA axis, high RR/HR, acute phase response) +Infection = SEPSIS + EOD = Severe Sepsis + Hemodynamic instability = Septic Shock
Chronic Inflammation
Labatory Markers
Acute phase proteins (APPs) – trigger release of cytokines (alpha 1, 6),
C reactive proteins increases 100-1000x,
procalcitonin commonly used for if a patient responds to antibiotics,
ESR tells if a blood sample has how many RBCs and relies on fibrinogen which if there is a lot of it can mask the RBCs,
high fibrinogen will mask the RBCs if it comes down quicker it is being masked and is an inflammatory response.
CBC will have high or low leukocytes, high bands (bandemia), leukemoid reaction is increase in WBC count that limits leukemia, leukopenia=neutropenia
Left shift – increase in immature form of neutrophils
Wound Healing
Define Regeneration vs Repair
Regeneration (same replacement), Repair (fibrous scar tissue replacement)
Wound Healing
Describe the basic elements of regeneration and repair (Liable, Stable, Permanent Cells)
a. Liable Cells are continuous exfoliation and replacement (lining of the uterus)
b. Stable Cells regenerate when prompted (parenchymal cells – liver, kidney, pancreas)
c. Permanent Cells are least likely to regenerate/lost their ability to divide (neurons, cardiomyocytes, no CNS, no PNS)
d. Complete resolution can occur with stable/liable cells whereas with permanent cells leads to scarring.
Wound Healing
Indicate factors that favor resolution versus repair; note exceptions
Factors favoring complete resolution include proteolytic digestion and respobrtion of exudates & absence of necrosis. Exceptions include the accumulation of exudate in large volumes
Wound Healing
Recognize the contribution of granulation tissue to wound healing
a. WOUND HEALING
b. Specialized tissue of repair that is highly vascularized/leaky/lacking epithelial coverage, angiogenesis (new capillary buds) contains glycosaminoglycans/collagen fibers/myofibroblasts, appearance wet and exudate
Wound Healing
Compare primary and secondary union
Primary Union is the first intention, few cells die, scab forms quickly (small cut, surgical incision)
Secondary Union is second intention, intense inflammatory rxn, necrosis (MI, inflammatory ulceration, abscess formation)
Wound Healing
List the phases of cutaneous wound healing and events in each stage
Homeostasis (vasoconstriction, release of clotting factors, platelet plug, thrombus) Inflammation (ROS , neutrophil, macrophages release) Proliferative (“filling the covered wound” – angiogenesis, fibroblasts Remodeling-Maturation (collagen, scar tissue formation)
Wound Healing
Distinguish among the different forms of an ulcer
Infection can cause abnormal wound healing causing ulcer
Non-healing wounds will become chronic due to multiple factors
Pressure – immobile, pressure on bony area
Diabetic foot - damage to sensory, autonomic, and motor nerves
Venous – hydrostatic pressure increase, slow capillary blood flow
Arterial insufficiency – reduced blood flow to affected limb
Wound Healing
Identify and describe aberrant responses to wound healing, including dehiscence, keloids, incisional hernias, contracture, adhesions, and fistula
Aberrant response
Deficient scar formation
Dehiscence – splitting open of a wound
Evisceration – dehiscence with exterior exposure of organs
Incisional hernias – big area without external appearance
Keloids – scars beyond the borders of the injured site
Contracture – exaggeration of normal contraction
Adhesions – fibrous bands between tissues, commonly caused by surgery, becomes fibrinous tissue they will not break down but can cause strangulation of an intestine
Fistula – abnormal passage between two organs, typically via arterial/vein formation that previously did not exist
Bone spur – osteophytes, osteoarthritis can be caused by wear and tear damage
Wound Healing
Define: Organization, Granulation, Scarring, Abrasion, Laceration, Puncture, Erosion/ulcer, infarct, infarction
Organization – intermediate of healing and repair
Granulation – vascularized wound repair
Scarring – repair with fibrous tissue replacement
Abrasion – surface damage
Laceration – jagged wound
Puncture – wound that forces debris/bacterium in
Erosion/ulcer – craters on tissue surfaces
Infarct – localized dead tissue
Infarction – ischemic necrosis
