Inflammation Two Flashcards
Inflammation
A non-specific response to any agent that causes cell injury.
Absolutely necessary for healing, but potentially harmful to body as well.
Agents of inflammation
Can be:
Physical
Chemical
Biologic
Non-Specific Response
Same response regardless of cause
Amount of response can vary
Variable to: Virulence of agent Size Severity Host factors
Suffix for -itis
Inflammation
Are cardinal signs on inflammation always visible?
No, not always.
Presentations of Loss of Function
Decreased ROM
Decreased performance
Decreased ability
PRICE
Old theory to treatment of inflammation
Some studies still support
Protect Rest Ice Compress Elevate
SHARP Mnemonic
S - Swelling H - Heat A - Abnormal function R - Redness P - Pain
PT Actions When Swelling Presents
Generally, do not treat.
If significantly worsens, very uncomfortable, puts pressure on other structures, or makes ADL’s too challenging then should be treated for.
Acute = leave it, chronic = treat it
Local Manifestations of Inflammation
Exudate formation; many potential types
Abscess formation
Ulceration
Exudate
& Types
A local manifestation of inflammation
Appearance associated with name
Serous Fibrinous Sanguinous Serosanguinos Seropurulent/Prurulent
Serous Exudate
Clear
Healthy response, normal
Fibrinous Exudate
Yellow
Occurs later in healing, normal
Sanguinous Exudate
Red
Indicative of blood, normal
Serosanguinous Exudate
Pink
Indicative of minor blood, normal
Seropurulent/Prurulent Exudate
Pus
Indicative of infection, abnormal
Abscess formation
A local manifestation of inflammation
When exudate occurs in solid tissue
“Walled off” by fibroblasts & macrophages
Inhibits body from releasing infections
Ulceration
A local manifestation of inflammation
When inflammation erodes epithelial surface
May require surgical intervention
Hypothalamus function in inflammation
Directs body to increase temperature to fight off infection
Systemic manifestations in inflammation
Occurs only in large injuries, infections, or autoimmune diseases
Signs of systemic manifestations
Fever Leukocytosis Malaise Lymphadenitis Leukopenia
What is the hallmark sign of systemic inflammation?
Fever
Leukocytosis
Sign of systemic manifestation of inflammation
WBC growth
Potential leukopenia if overwhelming condition
Malaise
Sign of systemic manifestation of inflammation
Unwell feeling
Lymphadenitis
Sign of systemic manifestation of inflammation
Lymph nodes swelling
Leukopenia
Sign of systemic manifestation of inflammation
Low WBC count
Fight is using more cells than can produce
Leuko-
white
Cyto-
cells
-osis
growth of
Categories of Inflammation
Acute = short (less than a week)
Subacute = closer to healing, sign that still in inflammatory process but progressing
Chronic = long, need to intervene
Acute on Chronic = has existence of a chronic disease
Self-perpetuating
Viscous cycles of inflammatory response
Individual leaks cells to fight off
Usually severe exposure
Lasts weeks, months, years
Why can self-perpetuating cycles occur?
Cause still present
Chronic low intensity irritant, infection
Altered function of inflammatory/immune system response
How is chronic inflammation identified?
May result in further tissue destruction
More macrophages, lymphocytes, plasma cells
More fibroblasts
Little/no edema, exudate
Greater fibroblast proliferation
Scar tissue Lack original tissue properties Can interfere with tissue function ROM decreased Lack of function
Medical concerns with chronic inflammation
"Recurring systemic inflammation" Alzheimers Diabetes Mellitus Athersclerosis (heart disease) Some cancers Some autoimmune disease
Atherosclerosis
Wearing down on lumen and plaque forms
Parenchymal Tissue
Actual function tissue
Stromal Tissue
Support structures
Give stability
Tissue regeneration
Repair by same parenchymal type cells
Depends on cell proliferation and ability to move through cell cycle:
Labile, Stable, Fixed cells
Labile cells
Always replicating
They are used to dividing and do it easily
Ex: smooth tissue repair
Ex: skin, GI tract
Stable cells
Can be triggered to replicate/re-grow
Ex: liver
Permanent or Fixed Cells
Will never proliferate or re-grow
Ex: neurons, cardiac, and skeletal
Think “expensive”
Phases of tissue healing and repair
Inflammatory phase
Proliferation phase
Maturation phase
Proliferation phase
“Fibroblastic phase”, Granulation, Granular phase
If better vasculature, better healing
Generally days 3-20
Rebuilding stage done by fibroblasts
Has four major components
*First phase PT’s can start to really help
Maturation phase
“Remodeling phase”
Can last months or years
New tissue laid down, but changing
MOST progress occurs here
Day 7 - or Years 1-2
Longest phase in healing # of macrophages, fibroblasts, capillaries decrease Scar whitens and collagen aligns Capillaries decrease Collagen fiber synthesis
No pain
No swelling
Components of Proliferative phase
Collagen production
Wound contraction
Revascularization
Epithelialization
Collagen production
in Tissue Regeneration
First gets laid down
Basis for nearly all tissues
Produced by fibroblasts
Provides support/strength to tissue
Encourages correct “lay down”
Wound contraction
in Tissue Regeneration
Make wounds smaller Only for large defects Edges of wound pull together Similar to the way sutures work From outside in
Revascularization
in Tissue Regeneration
Good blood supply returns to area "Angiogenesis" Vessels from wound periphery migrate inward, providing blood New scars often pink or bright red Blood provides nutrients, O2
Bone fractures = quick
Ligaments = long
Epithelialization
in Tissue Regeneration
Wound edges start to heal
Cells start at wound edge and migrate along granulation tissue
Stages of healing in proliferation phase
Epidermal layer reestablished Epithelialization Collagen & fibroblasts proliferation continues WBC leave Edema decreases Small blood vessels degenerate Tissue blanches Collagen production Wound contraction Revascularization
Variable time based on size of wound
Primary intention
Small wound
Easy to heal
Minimal scar tissue
No initial tissue loss
Little or no scar formation
Secondary intention
Larger injuries
Occurs if:
larger amount tissue loss
contamination or infection
Larger amount of scar/fibrotic tissue
Collagen fiber synthesis
Occurs in maturation phase
Reaches homeostasis during phase
Collagen fiber orientation resembles original tissue
Synthesis and lysis of collagen to reorient scar to increase tensile strength
70-80% of normal tissue strength at best
Maturation phase: regeneration
Injured tissue replaced with new tissue of same kind and properties
Begins with granulation tissue
Maturation phase: fibrosis
Scar tissue present
With more severe inflammation or larger tissue insults
Scar tissue not same as original tissue:
Lacks original strength
Lacks flexibility
Lacks original function
Impaired healing can occur due to what 12 factors?
Impaired blood flow, O2 Cardiac conditions Respiratory conditions Vascular conditions Blood conditions Malnutrition Edema Age (extremes = young and old) Impaired inflammatory function Impaired immune function Foreign bodies Some medications
Malnutrition
Many micro and macro nutrients needed for adequate tissue function and healing
Impaired inflammatory and immune function
Too much or too little action
Can be primary or secondary conditions
What kind of system does the body work on?
Negative Feedback Mechanism
Anti-Inflammatory medications
Common prescription for inflammation
Is inflammation normal?
Yes - normal response to cellular injury
Vital for normal healing
Dangers of excessive inflammation
Prolonged or excessive inflammation can cause more damage than the initial cellular injury
Types of Anti-inflammatory meds
Analgesics
Non-steroidal anti-inflammatories
Corticosteroids
DMARD’s
Analgesics
Strictly pain inhibitors
Symptom relief
“Not feeling”
Ex: acetaminophens, opiates, narcotics
Non-Steroidal Anti-inflammatories
Prescription or OTC
Interrupt pathway to prostaglandin production
NSAID, non-NSAID’s, anti-feveretics
Ex: aspirin, ibuprofen, naprosyn, Celebrex
Corticosteroids
Sugar based NOT anabolic Either hormone from adrenal cortex (cortisol) or a synthetic derivative Very potent anti-inflammatory properties Many different kinds
-one’s
Ex: cortisone, prednisone, hydrocortisone, dexamethasone
DMARD’s
Disease modifying anti-rheumatic drugs
Symptom relief
Affect underlying disease processes
Most common for autoimmune conditions
Ex: methotrexate, Enbrel, Humira
Corticosteroid Potential Adverse Effects in Major systems
Muskuloskeletal Immunological Cardiovascular Integumentary Metabolic & Endocrine Psychological
How are corticosteroids delivered?
Injection (tissue or IV)
Topical
Inhaled (nebuligens)
Conditions corticosteroids used for
Reduce inflammation for local OR systemic
Especially chronic
Allergies
Autoimmune disorders
-itis conditions (arthritis)
Adverse Musculoskeletal Effects Corticosteroids
Muscle, tendon, cartilage weakening
Myopathy, muscular atrophy
Osteoporosis
Osteonecrosis
Adverse Immunological Effects Corticosteroids
Immunosuppression
Bone marrow suppression
> intervene with RBC, WBC, platelet production
Adverse Cardiovascular Effects Corticosteroids
HTN
Elevated blood lipids
Atherosclerosis
High blood pressure
Adverse Integumentary Effects Corticosteroids
Acne Stretch marks (breakdown of collagen) Hair loss Easy bruising/bleeding Skin atrophy Poor wound healing "skin tears" - friction causes skin to rip
Adverse Metabolic & Endocrine Effects Corticosteroids
Fluid retention Electrolyte imbalances Obesity Growth retardation in children Elevates BP (cause diabetes)
Excess sugar means pancreas malfunction
Adverse Psychological Effects Corticosteroids
Mood changes
Behavioral changes
Can occur even in short doses;
anger, can’t sleep, hungry
Adverse Psychological Effects Corticosteroids
Mood changes
Behavioral changes
Can occur even in short doses;
anger, can’t sleep, hungry
PT Implications for Corticosteroids
Be aware of adverse effects with long term use
Systemic effects more likely when used for systemic conditions
Four major effects
Four major effects for PT implications and corticosteroid usage
1) Weakness, may not tolerate activity well
2) Immunosupression
Standard precautions, risk of infection, may need neutropenic precautions
3) Poor skin quality, poor wound healing
4) Edema, weight gain
= Everything with awareness!
Intra-cellular injections
Few months of effectiveness
Control acute pain and inflammation
Not to treat muscular, tendinous, or ligamentous injury
Less likely to result in systemic effects
Used as a bridge prior to surgery
Ex: cortisone shots
Erythrocyte Sedimation Rate (ESR)
“sed rate”
Nonspecific test for inflammation
Positive result if elevated
C-reactive protein (CRP)
Nonspecific test for inflammation
Positive result if elevated
Current Considerations for Inflammation
Traditional Rx
-Halt/Limit inflammation following injury
Some newer proponents
- Calling RICE into question
- Allow normal inflammation to occur
