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Inf & Wound Healing
Chapter 13-Infection & Wound Healing
| Question | Answer |
|---|---|
| What is inflammatory response and what is the goal? | Reaction to cell injury. Goal: remove necrotic debris and make suitable for healing |
| What is an infection? | Organism-bacteria, protozoa, fungus--invades tissues |
| What is intensity of response? | The degree of response depends on degree of injury; immune suppression decreased = decreased response |
| Types of inflammatory response systems? | Vascular Response & Cellular Response |
| Vascular Response (what the arteries will do?) | Arteries initially dilate, to allow chemoreceptors into area=redness & warmth |
| Cellular Response (what do the different cells do?)Neutrophils | Neutrophils: 1st line of defense, immature WBC "shift to the left", arrive in 6-12 hours, only around 24-48 hrs. Puss=accumulation of dead neurtrophils |
| Cellular Response (what do the different cells do?)Monocytes | 2nd WBC to arrive, arrive in 3-7 days, transform into macrophages to eat debris |
| Lymphocytes | 3rd WBC to arrive, involved in humoral and cell-mediated immunity--how vaccines work |
| Chemical Mediators: Complement System, Protaglandins, Leukotrienes | Complement system: chemical reaction, multiple enzymes react in sequence that cause more inflammation to occur. Get appropriate cells to area to clean it out and allow healing to occur |
| Prostaglandins | Produced by injured cells; cause vasodilation and sensitive pain receptors (why we hurt) |
| Leukotrienes | active in anaphylactic reaction, cause smooth muscle contraction of bronchi, increase capillary permeability--get bronchial restriction and pulmonary edema |
| Clinical manifestations: 1) local response, 2) systemic response, 3)Fever | local response: redness, pain, swelling systemic: incr WBC, fever, malaise Fever: triggered by protaglandins & cytokines; response to chem agts being sent out; incr temp creates a "bad" envir; treat fever >101.5; lower fever part of immune resp |
| Inflammation | Acute: comes on & resolves in 2-3 wks; temp, no long damage Chronic: weeks to months to yrs; Lupus pts, RA pts |
| Nursing Management: vitals, fever, meds, RICE | Sympts of inflam response: initial bp incr, systemic sepsis decrease bp; temp incr,hr incr, RR incr Fever: not damaging until >104; treat for comf., 105.8=brain damage; "rate" of incline-rapid incrs=seizures Meds:tylenol, ibuprofen, aspirin |
| Two types of healing: regeneration & repair | Regeneration: replacement of lost or damaged cells w/same cell type Repair: replacement of damaged cells w/ connective tissue-leads to scar tissue |
| Primary repair-wound edges well approximated (i.e. surgical incision) | Primary Repair: Initial-neutrophils, platelets form clots,meshwork Granulation-start of new tissue; bright red Fibroblasts-immature connective tissue cells; secrete collegen and form scar tissue Maturation&scar-can last 7 days to years |
| Secondary repair-wound is open | healing from sides in & bottom up; must keep wound bed clean |
| Tertiary repair-delayed primary repair | wound too swollen to close, surgically come back to put together |
| Complications of scars | Hypertrophic Scars & Keloids Contracture Dehiscence Excess granulation tissue Adhesions |
| Hypertrophic Scars & Keloids | Hypertrophic: over abundance of collegen--red-raised scars, excessive scar formation Keloids: protusion of scar tissue; huge over growth, expands beyond boundary of wound; pt. may complain of pain & tenderness,hereditary, more common in dark skin people |
| Contracture | Connective tissue doesn't skin to expand; burns of injuries over joints--must keep moving to keep mobility, always have in functional position |
| Dehiscence | wound opens Risk factors: infection, diabetes, obesity, too much pressure on wound/surgical site (split w/pillow) |
| Excess granulation tissue | "proud flesh" granulation tissue that protrudes above surface of wound--surgically removable, will not grow back |
| Adhesions | most common area=abdominal cavity; attaches to greater omentum & organs Scar tissue in abd cavity, can cause small bowel obstruction |
| Wounds: need to make note of closure device | sutures (7-10 days), staples (head, abdomen, hips), glue (open heart), retention sutures (trying to bring edges together) |
| Wound colors | Red: Good!!granulation tissue, pink, a little bleeding, wet wound Yellow: needs to be debrided for wound to heal; wet-to-dry & pack to pull of slough Black: eschar tissue, surgically removed, debride in order for healing to occur |
| nutrition management | high protein, high calorie, Vit. A,B,C,D NG tube first option for feeding--want to use "gut" first; TPN next |
| Infection prevention | use cleanest technique possible (aseptic tech,) watch MD order Culture-ID microorganism (ideal before 1st dose of antibiotic) Sensitivity-IDs most effective antibiotic |
| Patient teaching | note change in drainage, wound color, adequate rest, good nutrition |
| What causes Pressure Ulcers? | Pressure, friction, sheering forces, moisture, length on side *pressure ulcers heal by secondary intention; significant PU can take months to years to heal |
| How many Stages of PUs? | Suspected deep tissue injury, Stages I-IV & unstagable |
| Suspected Deep Tissue injury | purple of maroon localized are of discolored intact skin or blood filled blister due to damage of underlying soft tissue from pressure and/or sheer. Area may be preceded by tissue that is painful, firm, mushy, boggy, warm or cool as compared to adj tissue |
| Stage I | intact skin w/nonblanchable redness of local area usually over bony prominence. Area may be painful, firm, soft, warm or cooler than adjac. skin |
| Stage II | partial-thickness loss of dermis manifesting as a shallow, open ulcer with a red-pink wound bed w/out slough. May look like serum-filled blister |
| Stage III | full-thickness tissue loss. subcut fat may be visible, but bone, tendon and muscle are not exposed. Slough may be present. May include undermining and tunneling |
| Stage IV | full-thickness tissue loss w/exposed bone, tendon or muscle. Slough and eschar may be present. Often includes undermining and tunneling |
| Unstageable | full-thickness tissue loss in which base of ulcer is covered by slough (yellow, tan, gray, green or brown) and/or eschar in the wound bed |
Created by:
divelmama
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