chapter 9 - exam #1

stage 1 of acute inflammation

vascular phase:

blood vessels near the site of injury briefly constrict and then widen and become “leaky” —> fluid then leaks into tissues causing swelling (edema)

signs: redness, warmth, swelling

stage 2 of acute inflammation

cellular phase:

WBC’s (especially neutrophils) move out of the blood and into the tissue (chemotaxis) —> WBC’s then “eat” bacteria/debris (phagocytosis)

signs: pus (if infection), pain, possible fever

external signs of inflammation

• redness

• swelling

• heat

• pain

• loss of fnx

outcomes of acute inflammation

• complete healing w/ return to normal

• scar formation (if tissue damage is significant)

• abscess (pus filled pocket)

• chronic inflammation if injury/pain persists

neutrophils

first responders; fight bacteria

if elevated —> acute infection, inflammation

lymphocytes

fight viruses; regulate immune response

if elevated —> viral infection

monocytes

become macrophages; clean up debris

if elevated —> chronic inflammation

eosinophils

fight parasites; involved in allergies

if elevated —> allergies, parasites

basophils

release histamine during allergic rxn

if elevated —> severe allergies (these are rarely elevated)

elevation of C- reactive protein (CRP) and erythrocyte sedimentation rate indicates …

active inflammation

WBC differential lab

part of a complete blood count (cbc); shows the percentage of each type of WBC

fever

a common sx of inflammation; pyrogens are the substances that cause it by telling the brain (hypothalamus) to raise body temp.

why does the body create a fever

a higher body temperature is theorized to increase the efficiency of WBC’s in their defenses

signs and sx of fever

• warm skin

• sweating/chills

• HA/fatigue

• increased HR

lymphadenopathy

enlargement of lymph nodes due to inflammatory process

why do lymph nodes swell

lymph nodes trap and filter out bacteria, viruses, or abnormal cells

WBCs multiply inside the node to fight infection —> causes swelling

common causes of lymphadenopathy include

• viral infections (cold, mono)

• bacterial infections (strep throat)

• cancer or immune disorders

chronic inflammation

long lasting, can cause on-going damage

acute inflammation

short, strong and healing focused

chronic vs. acute outcomes of inflammation

best outcomes:

chronic - tissue repair or control of cause

acute - healing, resolution, return to normal

worst outcomes:

chronic - ongoing tissue damage, fibrosis, or organ damage

acute - abscess, scarring if damage is bad

wound healing - phase 1

hemostasis —> clotting of the blood

wound healing - phase 2

inflammation —> WBC’s (especially neutrophils and macrophages) remove dead tissue and bacteria

wound healing - phase 3

proliferative —> tissue growth; fibroblasts create collagen, granulation tissue fills up the wound

wound healing - phase 4

remodeling —> strengthen tissue, scar tissue forms, healed epidermis and dermis

primary intention

no gap in the tissue, regrowth of basal epidermis, re-epithelialization, restoration to intact skin (little to no scarring)

secondary intention

gap w/ blood clot, regeneration of the same to replace the lost tissue is not possible and granulation tissue fills the wound

tertiary intention

wound is missing a large amount of deep tissue and is contaminated

primary intention ex.

healing of a clean, surgical laceration

pressure injuries and severe burns are examples of

wounds that require secondary and tertiary intention healing

debridement

removal of necrotic tissue on the wound to promote healing and new growth of tissue

factors that help healing

• good nutrition (especially protein, vitamin C, and zinc)

• good blood flow/oxygen

• clean wound (low infection risk)

• proper moisture balance (not too wet or dry)

• controlled blood sugar (especially in DM pts)

factors that delay or impair healing

• infection

• poor circulation (e.g., from DM, smoking, vascular disease)

• malnutrition

• chronic diseases (e.g., diabetes, cancer)

• steroids or immunosuppressant medications

• excessive movement or pressure on the wound

dysfunctional healing

excessive scarring

• hypertrophic scar —> thick raised, stays within wound edges

• keloid —> grows beyond original wound

wound dehiscence

• dehiscence —> opening of wounds suture line

• evisceration —> opening of wound w/ extrusion of tissues and organs

margination (in the cellular phase)

WBC’s go to injury and the site starts to close with platelets and WBC’s line up in the area