wounds and inflammation

Injury to cellular tissue that can be external or internal

Wound

Because inflammation and healing depend on cellular structure and function

Why review normal cell structure

Activity limitation and disrupted routines

Impact of wounds on occupational performance

Size, location, severity, healing stage

Factors influencing wound impact

Diabetic ulcers and pressure injuries

Examples of chronic wounds

Nucleus, cytoplasm, plasma membrane

Main cell components

Contains DNA and RNA; controls gene expression

Nucleus function

Differential gene expression

Cause of cell specialization

Specialized cells with unique functions

Differentiated cells

Embryonic unspecialized cells

Undifferentiated cells

Area containing organelles

Cytoplasm

Larger with more organelles

Characteristic of differentiated cytoplasm

Mitochondria, Golgi, ER, lysosomes

Major cytoplasmic organelles

Energy production (ATP)

Mitochondria function

Protein modification and transport

Golgi apparatus function

Protein and lipid synthesis

Endoplasmic reticulum function

Breakdown of waste and damaged components

Lysosome function

Separates intracellular and extracellular space

Plasma membrane function

Balanced internal cellular environment

Homeostasis

Equilibrium with adequate nutrients and oxygen

Steady state

Increase metabolism

Cell response to increased demand

When the cell cannot adapt further

Point of no return

Reversible and irreversible

Types of cell injury

Injury within homeostatic limits allowing recovery

Reversible cell injury

Cell swelling due to water influx

Hydropic change

Decreased ATP, protein synthesis, increased autophagy

Changes in reversible injury

Yes if stressor removed

Recovery from reversible injury

Severe toxins or prolonged hypoxia

Cause of irreversible injury

Nuclear damage or membrane rupture

Key features of irreversible injury

Cell death

Outcome of irreversible injury

Predictable tissue response to injury or pathogens

Inflammation definition

Trauma, toxins, microbes, pathological stimuli

Causes of inflammation

No

Inflammation in necrotic tissue

Multicellular organisms only

Where inflammation occurs

Dynamic with predictable stages

Nature of inflammation

Acute and chronic

Types of inflammation

Heat, redness, swelling, pain

Four cardinal signs

Celsus

Who described four signs

Loss of function

Fifth cardinal sign

Virchow

Who added fifth sign

Blood flow, WBCs, permeability, mediators

Components of inflammation

Brief vasoconstriction then vasodilation

First vascular response

Increased blood flow

Hyperemia

Warmth and redness

Cause of heat and redness

Plasma leakage

Cause of edema

Stacking of RBCs

Rouleaux

WBC adhesion to endothelium

Pavementing

Cytokines

Activator of adhesion molecules

Soluble inflammatory mediators

Cytokines definition

Platelets, endothelial cells, leukocytes, macrophages

Cytokine sources

Histamine, bradykinin, leukotrienes, cytokines

Chemical mediators

Vasodilation and increased permeability

Primary mediator effects

Plasma protein cascade

Complement system

Nine proteins

C1–C9 count

Increases permeability and oxidative response

C5a function

Opsonization and phagocytosis

C3b function

Fluid leakage causing edema

Transudation

Protein

rich fluid with inflammatory cells

Exudate

Neutrophils

Early inflammatory cells

Directed leukocyte movement

Chemotaxis

Bacteria, tissue damage, complement

Chemotaxis triggers

Engulfment of debris

pathogens

Resolution and return to steady state

Outcome of phagocytosis

Endogenous pyrogens acting on hypothalamus

Cause of fever

Elevated WBC count

Leukocytosis

5,000–10,000 per µL

Normal WBC range

11,000 per µL

Leukocytosis threshold

Fatigue, weakness, anorexia, pain

Systemic inflammation symptoms

Continuously dividing stem cells

Mitotic cells

Skin basal layer and mucosa

Mitotic cell locations

Divide when stimulated

Stable cells

Liver and kidney

Stable cell examples

Postmitotic non

dividing cells

Permanent cells

Neurons and myocardial cells

Permanent cell examples

Produce cytokines and growth factors

Macrophage role in healing

Contract wound and produce matrix

Myofibroblast function

Form new blood vessels

Angioblast function

Produce extracellular matrix and collagen

Fibroblast function

Type III collagen

Initial collagen

Type I collagen

Final collagen with tensile strength

Hemostasis, inflammation, proliferation, remodeling

Phases of wound healing

Clot formation stops bleeding

Hemostasis phase

Neutrophils and macrophages

Inflammatory phase cells

Vascular red tissue with fibroblasts and angioblasts

Granulation tissue

Beefy red

Healthy granulation appearance

Collagen replacement and scar formation

Remodeling phase

Wound edges approximated

Primary intention

Faster healing and minimal scarring

Benefits of primary intention

Wound edges cannot close

Secondary intention

Visible granulation and larger scar

Secondary intention characteristics

Delayed closure after contamination

Tertiary intention

Negative pressure wound vacuum

Tertiary intention treatment

Chronic wounds remain inflamed

Chronic vs acute wounds

Infection, poor circulation, diabetes, nutrition, age

Delayed healing factors

Movement disrupts repair

Why joints heal slower

Age

related skin changes

Why older adults heal slowe