Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/117

Click to flip

117 Cards in this Set

  • Front
  • Back
inflammatory reponse
a sequential reaction to cell injury

neutralizes and dilutes inflammatory agent

removes necrotic materials

establishes an environment suitable for healing and repair
vascular response to injury
arterioles in the area briefly undergo transient vasoconstriction

after release of histamine and other chemicals by the injured cells, the vessels dilate

which results in hyperema, which raises filtration pressure
hyperemia
increased blood flow to the area
neutrophils
the first leukocytes to arrive, usually within 6-12 hours

results in elevated WBC
shift to the left
increased numbers of band neutrophils in circulation

commonly found in pts with acute baterial infections
monocytes
second type of phagocytic cells that migrate from circulating blood

usually arrive within 3-7 days after onset of inflammation
lymphocytes
arrive later at the site of injury

primary role is related to humoral and cell-mediated immunity
eosinophils
released in large quantities during an allergic reaction

release chemicals that control the effects of histamine and serotonin

involved in phagocytosis of the allergen-antibody complex
basophils
the histamine and heparin that basophils carry in their granules are released during inflammation
complement system
major mediator of inflammatory reponse

functions are
enhanced phagocytosis
inreased vascular permeability
chemotaxis
cellular lysis

each activated complex can act on the next, creating a cascade effect
prostaglandins
substances that can be synthesized from the phospholipids of cell membranes of most body tissues, including blood cells

can be converted to arachidonic acid, which is then oxidized by two different pathways
cyclooxygenase metabolic pathway
leadds to the production of PGs of the D, E, F, and I series and thromboxanes

E and I series are potent vasodilators and inhibit platelet and neutrophil aggregation
exudate formation
fluid and electrolytes that move from tthe circulation to the site of injury
clinical manifestations of response to inflammation
redness, heat, pain, swelling, and loss of function
acute inflammation
the healing occurs in 2-3 weeks and usually leaves no residual damange

neutrophils are the predominant cell type at the site of infection
subacute inflammation
has the features of the acute process but lasts longer

ie infective endocarditis is a smoldering infection with acute inflammation but lasts for weeks
chronic inflammation
lasts for weeks, months or years

injurious agent perisists or repeatedly injures the tissue
serous exudate
results from the outtpouring of fluid that has low cell and protein content

seen in early stages of inflammation or when injury is mild

skin blisters, pleural effusion
catarrhal exudate
found in tissues where cells produce mucous

mucous production is accelerated by inflammation response

runy nose assoc with upper respiratory tract infection
fibrinous exudate
occurs with increasing vasclar permeability and fibrinogen leakage into intersitial spaces

excessive amts of fibrin coating tissue surfaces may cause them to adhere

adhesions
purulent exudate
consits of WBCs, microorganisms (dead or alive), liqifeied dead cells, and other debris

furuncle (boil)
abscess
cellulitis
hemorrhagic exudate
results from rupture or necrosis of blood vessel walls

it consists of RBCs that escape into tissue

ie. hematoma
healing process
includes two major components:

regeneration
repair
regeneration
the replacement of lost cells and tissues with cells of the same type
repair
healing as a result of lost cells being replaced by connective tissue

repair healing occurs by primary, secondary or teriary intention

the more common type of healting and usually results in scarring
primary intention
healing takes place when wound margins are neatly approximated

ie surgical incision or paper cut

initial phase, grantulation phase, maturation phase and scar contraction
initial phase of primary intention
lasts 3-5 days

the edges of the incision are first aligned and sutured in place

an acute inflammatory response occurs
granulation phase of primary intention
granulation (fibroblastic, proliferative, reconstructive) is the second step

lasts from 5 days to 3 weeks
components of granulation tissue
proliferating fibroblasts
proliferating capillary sprouts (angioblasts)
various types of wBCs
exudate
loose, semifluid, ground substance
maturation phase and scar contraction
the maturation phase, during which scar contraction occurs, overlaps with the granulation phase

it may being 7 days after injury and continue for several months or years
secondary intention
wounds that occur from trauma, ulceration and infection have large amounts of exudate and wide, irregular wound margins with extensive tissue loss

may have edges that can be approximated

the debris may have to be cleaned away (debrided) before healing can take place
Primary to secondary intention
a primary incision may become infected creating additional inflammation

the wound may reopen, and healing by secondary intention takes place
tertiary intention
(delayed primary intention)

when a contaminated wound is left open and sutured closed after the infection is controlled

also occurs when a primary wound becomes infected, is opened, allowed to granulate, and is then sutured

usually results in a larger and deeper scar than primary or secondary intention
wound classification
by cause
surgical or nonsurgical
acute or chronic

depth of tissue affected
superficial
partial thickness
full thickness
superficial wound
involves only the epidermis
partial thickness wounds
extend into the dermis
full thickness wounds
have the deepest layer of tissue destruction because they involve the subcutaneous tissue and sometimes extend nto the fascia and underlying structures such as muscle, tendon or bone
Red Wound - Characteristics
traumatic or surgical wound
possible presence of serosanguineous drainage
pink to bright or dark red healing
or chronic wounds with granulating tissue
Red Wound - TPurpose of reatment
protection and gentle atraumatic cleansing
Red Wound - Dressings and Therapy
tranparent film dressing
(tegaderm, opsite)
hydrocolloid dressing
(duoderm)
hydrogels
(tegagel)
gauze dressing with antimicrobial ointment or solution
telfa dressing with antibiotic ointment
Yellow Wound - Characteristics
presence of slough or soft necrotic tissue

liquid to semiliquid slough with exudate ranging from
creamy ivory to yellow-green
Yellow Wound - Purpose of treatment
wound cleasing to remove nonviable tissue and absorb excess drainage
Yellow Wound - Dressings and Therapy
wound irrigations
hydrotherapy
moist gauze dressing
with or w/out antibiotic
or antimicrobial agent
hydrocolloidal dressing
hydrogel covered with gauze
absorptive dressing
Black Wound - Characteristics
black, gray or brown adherent necrotic tissue

possible presence of purulent drainage
Black Wound - Purpose of Treatment
debridement of eschar and nonviable tissue
black wound - dressings and therapy
topical enzyme debridement
surgical debridement
hydrotherapy
chemical debridement
moist gauze dressing
hydrogel covered with gauze
absorptive dressing covered with gauze
Vitamin C deficiency
delays formation of collagen fibers and capillary development
Protein deficiency
decreases supply of amino acids for tissue repair
Zinc deficiency
impairs epithelialization
inadequate blood supply
decreases suppy of nuttrients to injured area

decreases removal of exudative debris

inhibits inflammatory response

-diabetics on extremities
further from the heart
Corticosteroid drugs
impair phagocytosis by WBCs

inhibit fibroblast proliferation and function

depress formation of granulation tissue

inhibit wound contraction
Infection
increases inflammatory response and tissue destruction

have to get infection and nonviable tissue out
Smoking
nicotine is a potent vasoconstrictor and impeds blood flow to healing process
mechanical friction on wound
destroys granulation tissue

prevents apposition of wound edges
Advanced Age
slows collagen synthesis by fibroblats
impairs circulaton
requires longer time for epithelialization of skin
alters phagocytic and immune responses
Obesity
Decreases blood supply in fatty tissue
Diabetes Mellitus
Decreases collagen synthesis
retards early capillary growth
impairs phagocytosis
(result of hyperglycemia)
reduces supply of o2 and nutrients
secondary to vascular disease
Poor general health
causes generalized absence of factors necessary to promote wound healing
anemia
supplies less oxygen at tissue level
factors delaying wound healing
vitamin C deficiency
protein deficiency
zinc deficiency
inadequate blood supply
corticosteroid drugs
infection
smoking
mechanical friction on wound
advanced age
obesity
diabetes mellitus
poor general health
anemia
hypertrophic scar
inappropriately large, red, raised and hard

remains confined to the wound edges and regresses in time
Keloid
a greater protursion of scar tissue that extends beyond the wound edges and may form tumorlike masses

permanent, without tendency to subside
contracture
wound contraction is necessary for healing but this process can become abnormal when there is excessive contraction reulting in deformity or contracture
dehiscence
the separation of disrupttion of previously joined wound edges
three possible contributing causes of dehiscence
1) an infection may cause an inflammatory process

2) the granulation tissue may not be strong enough to withstand the forces imposed on the wound

3) obese individuals are at high risk for wound dehiscence because adipose tissue interferes with healing
evisceration
occurs when wound edges separate to the extend that intestings protrude though the wound
excess granulation tissue
may protrude above the surface of the healing wound

if the granulation tissue is cauterized or cut off, healing continues in a normal manner
adhesions
bands of scar tissue between or around organs

may occur in the ab cavity, or betwen the lungs and pleura
adhesions in the abdomen
may cause an intestinal obstruction
adhesions between the lungs and pleura
require decortication, or stripping of pleura, to permit normal ventilation
drug therapy
used to decrease the inflammatory response

antihistamines may also be used to inhibit the action of histamine
nutritional therapy
a high fluid intake is needed to replace fluid loss from perspiration and exudate formation
antipyretic drugs
salicylates (aspirin)
acetaminophen
nsaids (ibuprofen, motrin, advil)
antiinflammatory drugs
salicylates
corticosteroids
nsaids
Vitamins
vitamin a
vitamin b complex
vitamin c
salicylates
lower temp by action on heat regulating center in hypothalamus
resulting in peripheral dilation and heat loss

interfere with formation and release of PGs

selectively depress CNS

reduce capiallary permeability
acetaminophen
lowers temperature by action on heat-regulating center in hypothalamus
nsaids
inhibit syntheses of PGs
corticosteroids
interfere with tissue granulation
induce immunosuppressive effects (decreased synthesis of lymphocytes)
prevent liberation of lysosomes
vitamin A
accelerates epithelialization
Vitamin B complex
acts as coenzymes
Vitamin C
assists in synthesis of collagen and new capillaries
Vitamin D
facilitates calcium absorption
inflammation - implementation
best management of inflammation is prevention of infection, trauma, surgery and contact with potentially harmful agents

adequate nutrition is essential
observation and vitals
ability to recognize the manifestations of inflammation is important

classic manifestations in immunosuppressed may be masks

vital signs important
moderate fevers
up to 103 usually produce few problems in most patients

if the patient is very young or very old, is extremely uncomfortable or has a significant medical problem, antipyretics should be used
RICE
rest
ice
compression
elevation

key concept in treating soft tissue injuries
rest
helps the body better use its nutrients and oxygen for healing
cold and heat
cold appplication appropriate initially to cause vasoconstriction and decrease swelling, pain and congestion from increased metabolism in area of inflammation

heat used later (after 24-48 hrs) to promote healing by increasing the circulation to the inflamed site and subsequent removal of debris
compression and immobilization
promote healing by decreasing the inflammatory process
assisting in the repair process
decreasing metobolic needs
elevation
will reduce the edema at the inflammatory site and incease venous return

helps reduce pain and improve ciculation of blood, which provides the oxygen and nutrient needed for healing
wound healing - assessment
Use clock form

wound should be measured

the consistency, color, and odor of any drainage should be recorded and reported if abnormal for the situation
purposes of wound management
1) cleaning a wound to remove any dirt and debris from wound bed

2) treat infection to prepare the wound for healing

3) protect a clean wound from trauma so it can heal normally
wound healing management by primary intention
common to cover the incision with a dry, sterile dressing that is removed as soon as the drainage stops or in 2-3 days
wound healing managment by secondary intention
depends on the wound etiology and type of tissue in the wound (red, yellow, black)
Debridement methods
surgical
mechanical
autolytic
enzymatic
negative pressure wound therapy
vacuum assisted wound closure -

uses suction to remove drainage and speed wound healing

for acute or traumatic wounds, surgical wounds that have dehisced, pressure ulcers and chronic ulcers
hyperbaric oxygen therapy
deliver of O2 at increased atmospheric pressure or by creating chamber around the limb

90-120 minutes long
infection prevention and control
pt should not touch wound
keep free from contamination
antibiotics may be given
if infection developsl, culture
psychological implications
pt needs to understand they healing process and normal changes that occur as wound heals
patient teaching includes
how to care for wound
it might take 4-6 weeks
adequate rest
good nutrition
observe for complications
report abnormal healing
drug-specific side effects
pressure ulcer
localized area (usually over a bony prominence) of tissue necrosis caused by unrelieved pressure that occludes blood flow to the tissues

fall under category of healing by secondary intention
pressure ulcer common sites
sacrum and heels
factors that influence development of pressure ulcers
amount of pressure (intensity)
lenth of time pressure is exerted on the skin (duration)
ability of patient tissue to tolerate the pressure
shearing force
friction
excesive moisture
shearing force
pressure exerted on the skin when it adheres to the bed and the skin layers slide in the direction of body movement
Stable eschar on heels
stable (dry, adherent, intact) eschar on the heels serves as the body's natural biological cover, and should not be removed
braden scale
risk assessment
scores range from 6-23
the lower the numeric score, the higher the patient's predicted risk of developing a pressure ulcer
braden scale scores
19-23 no risk
15-18 at risk
13-14 moderate risk
10-12 high risk
9 or below very high risk
overall goals for patient with pressure ulcer
1) have no deterioration of the ulcer stage

2) reduce or eliminate the factors that lead to pressure ulcers

3) not develop an infection in the pressure ulcer

4) have healing of pressure ulcers

5) have no recurrence
local care of pressure ulcer may involve...
debridemet
wound cleaning
applicaion of dressing
relief of pressure
pressure ulcer with necrotic tissue or eschar (except dry, stable, necrotic feet or heels)
must have the tissue removed by either surgical, mechanical, enzymatic or autolytic debridement methods
After pressure ulcer has been debrided
the goal is to provide an appropriate wound environment that supports mose wound healing and prevents disruption of the newly formed granulation tissue
Solutions for pressure ulcers
Dakin's solution (sodium hypochlorite solution), acetic acid, povidone-iodine, and hydrogen peroxide are cytotoxic and should not be used
irrigation pressure for pressure ulcers
use enough irrigation pressure to adequately clean the pressure ulcer (4-15 psi)without causing traumka or damate to the wound

can use 30ml syringe with 19-gauge needle
pressure ulcers and selection of dressing
mainenance of moist environment
prevention of wound desiccation (drying out)
ability to absorb the wound drainage
location of wound
amount of caregive time
cost of dressing
presence of infection
clean vs sterile dressing
care delivery setting
wet-to-dry dressings and pressure ulcers
should never be used on a clen granulating pressure ulcer

this type of dressing should be used only for mechanical debridement of the wound
contaminated pressure ulcers
stages II through IV pressure ulcers are considered to be contaminated or colonized with bacteria