Understand the pathophysiology, signs and symptoms, and complications of the following:
Wound healing -
Keloid –fibrous tissue overgrowth consisting of excessive collagen deposits, hard ridges of scar tissue.
Contractures – Restricting motion due to scar tissue
1st Intention healing –...
Understand the pathophysiology, signs and symptoms, and complications of the following:
Wound healing -
Keloid –fibrous tissue overgrowth consisting of excessive collagen deposits, hard ridges of scar
tissue.
Contractures – Restricting motion due to scar tissue
1st Intention healing – Incised- closed wound, suture/fragile, fibroblasts, granulation tissue/scab
formation
2nd Intention healing – Open wound, no fibroblasts, large scab/blood clot, left to heal on its own,
large scar.
Cellular healing (types) –
Resolution – minimal damage, scrapes, resolves quickly.
Regeneration – tissue regeneration if cells are able, i.e. liver.
Replacement – normal cells replace cells that cannot regenerate, grafting
Promoting healing:
Youth, good nutrition (protein, vit. A & C), adequate hemoglobin, effective circulation, clean &
undisturbed wound.
Delayed healing:
Advanced age, dehydration, poor nutrition, anemia, circulatory problems (DM, PAD),
irritation/excessive mobility of the area, infection, foreign body, prolonged use of
glucocorticosteroids.
5 Complications of healing:
Loss of function, contractures, adhesions, ulcerations, metaplasia
Inflammation process – 1. Injury> Histamine release> Vasodilation to get more fluid to area,
increase capillary permeability to allow more fluid including proteins to shift into the interstitial
space >Phagocytes engulf material, the large space allows WBC’s to get into the fluid to locate
injury to begin phagocytosis, collects debris> debris dumped into lymph system>Healing begins
Inflammation-
Local S/S:
Redness (rubor) & warmth (calor)
Swelling or edema
Pain
Loss of function
Complement system – A cascade of proteins that circulate in the blood; when activated, they destroy
bacteria or antigens, “tags”? cells in massive infections
Chronic inflammation – less swelling and exudate than acute, more lymphocytes and macrophages,
more fibroblasts, more collagen production/larger scar formation.
Exudate: Fluid collection at the site of increased vascular permeability.
TYPES:
Serous – Clear yellow fluid
Fibrous – High amount of fibrin (clotting factor)
Purulent – Many dead WBC’s (pus)
Abscess – “Walled off”, protected purulent exudate, protects spread but keeps antibiotics from
arriving to site. Usually needs to be incised and drained.
Burns
Classification of burns:
Partial Thickness (1st degree) – Does not penetrate past the epidermis, no blisters, resolves quickly,
example – sunburn
Deep Partial Thickness (2nd degree) - Compete epidermis and partial dermis, blistering, heals slower
& will leave scar, higher risk of infection, increased future risk of cancer at the site in some
individuals.
Full Thickness (3rd degree) – Damage through epidermis and dermis, extending into
connective tissue, nerves, bones, vasculature. High risk of infection causes increased cap perm,
vaso dil, massive swelling.
Electrical – Burn is interior, may only see exit “wound”, effects heart conduction.
Burn determination – Rules of 9
Treating burns - Keep pt hydrated to keep BP up, monitor for infection, encourage skin
regeneration/grafting, return function.
, Homeostasis – (Definition) – The state of equilibrium, (balance between opposing pressures) in the
body with respect to various functions and to the clinical compositions of the fluids and tissues.
Stable, “normal”, consistent environment in the body.
Hypersensitivity reactions
Type I – Allergic – Histamine, IgE mediated, Mast Cell reaction; basophil release reaction.
Vasodilation, cap perm (edema), airway obstruction, hypoxia.
Causes – insect stings, foods (nuts, shellfish), antibiotics, anesthesia.
1st exposure – usually no reaction 2nd exposure- allergic reaction.
Anaphylaxis is life threatening because: systemic vasodilation > low BP > tissue edema > bronchial
edema.
Type II – Cytotoxic Think Blood Typing – ABO incompatibility. If incompatible blood is given in
transfusion, host blood will attack donor blood. Reaction results in donor blood destruction
(hemolysis) (IgG-mediated complement), inflammatory response.
A: RBC has A antigens; blood serum has B antibodies. Can only receive A or O blood
B: RBC has B antigens; blood serum has A antibodies. Can only receive B or O blood
O: RBC has no antigens; blood serum has A & B antibodies. Can only receive O
blood. Rh: If RBC has antigen Rh+, no antigen Rh-
S/S – SOB, CP, diaphoresis, jaundice, death
Type III: Immune complex – Ag-Ab Complex immune reaction. If after an infection the
antigen/antibody complex is not removed completely, it will deposit in the tissues, damages host
tissue/organs. Example: Rheumatic fever – fever goes away and returns later w/ chest & joint pain.
Heart valves become perm damages. Example: Autoimmune disorders – Lupus (SLE), Rheumatoid
arthritis, MS
Type IV: Cell Mediated - AKA – delayed sensitivity due to exposure. T-cells become sensitized to
antigens, causing cell destruction mediated through cytokines. Example: TB skin test (Mantoux)
delayed reaction to previously exposed antigen. Example: Contact dermatitis (i.e. latex, nickel,
poison ivy) Example: Graft-host rejection, transplant rejection.
Cancer: etiology, stages, methods of spread
Uncontrolled growth (neoplasms) which no longer respond to normal controls, consist of
undifferentiated, atypical or immature cells. Useless cells continue to grow & deprive nutrients to
other cells. Causes pressure on surrounding structures.
Cancer-Malignant neoplasms-
Cells – vary in size and shape w/lg nuclei, undifferentiated, atypical, increased mitosis.
Growth – Rapid growth, cells not adhesive, infiltrate tissue, no capsule.
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