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Introduction to Pathophysiology
Dr. Bini Thomas, PT, MSA, DPT

Tissue Injury & The Healing Process

Mechanisms of Tissue Injury

Ischemia Infection Trauma/Physical Factors Immune Reaction Genetic Factors Nutritional Factors Chemical Factors

Mechanisms of Injury I
Ischemia
Hypoxia
Resp. obstruction Inadequate transport lung l Inadequate transport blood Inability within the cell

Infectious Agents
Bacteria
Exo- & Endotoxins Inflammatory response

Viruses Fungi Mycoplasmas, others Sepsis Septic Shock

CV collapse

Anoxia Thrombus Necrosis

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Mechanisms of Injury II
Viruses
Complete redirection of cell towards replication RNA Viruses DNA Viruses HIV

Immune System
Antibody attachment Complement activation Inflammatory cell activation

Mechanisms of Injury III

Genetic
Chromosomal Damage
Downs Syndrome Huntingtons

Nutritional
Protein Insufficiency
Kwashiorkor Marasmus

Single gene mutation altering protein(s)

Sickle Cell Anemia

Obesity Essential Insufficiency

Vitamin C Vitamin D Iron Ca

Multiple gene mutations +environmental factors

DM Type II

Vitamin Overdose

Mechanisms of Injury IV
Phys. Trauma
Blunt Trauma
Falls MVA

Chemical
Direct injury by toxin
Heavy metals like lead Mercury Chemotherapy

Extremes of PhysicalAgents Thermal

Burns Frostbite

Indirect inj. By toxin

metabolism
Many, if not most drugs

Radiation Electricity

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Necrosis
Necrosis is usually from ischemic injury Lack of oxygen causes mitochondrial failure, calcium

overload, membrane lipid peroxidation, and rupture

Necrosis releases intracellular components into the

extra cellular fluid

Inflammation and tissue damage are apparent

Mechanism of Necrosis

Types of Necrosis
Coagulative Liquifactive Caseous Fat Gangrenous necrosis

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Inflammation
Definition: a local response to cellular injury that is

marked by capillary dilatation, leukocytic infiltration, redness, heat, and pain and that serves as a mechanism initiating the elimination of noxious agents and of damaged tissue

4 Cardinal Signs of Acute Inflammation

Erythema Warmth Edema Pain

Plus Necrosis, Pus and loss of Function

Acute vs Chronic
Acute inflammation
Of relatively short duration; nonspecific early response to injury Aimed primarily at removing the injurious agent and limiting tissue damage

Chronic inflammation
Longer duration, lasting for days to years A recurrent or progressive acute inflammatory process or a low-grade smoldering response that fails to evoke an acute response

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Signs of inflammation
Rubor (redness) Tumor (swelling) Calor (heat) Dolor (pain) Functio laesa (loss of function)

Systemic Signs of Acute Inflammation:

Fever Tachycardia Hypermetabolic state

Elev. Serum protein levels Elev. WBC

Purposes of Inflammation
Inactivate the injurious agent Break down & remove dead cells
Initiate healing Starts within 1 minute & continues for months

Destroy and remove pathogens If destruction is not possible, to limit effects by

confining the pathogen and its products.

Repair and replace tissue damaged by pathogen and

its products.

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The Process

Inflammatory Response
Blood vesselsbecome leaky Circulating blood cells- The Cavalry! Connective/Interstitial cells Fibroblasts, mast cells, macrophages Chemical mediators Extracellular matrix Collagen, basement membrane

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Inflammatory Exudates

Inflammatory Exudates
Sanguinous-bright red, bloody, RBC Serosanguinous-red-tinged yellow, RBC Serous-yellow, albumin, immunoglobulins Purulent-cloudy, pus Catarrhal-thin,clear mucus Fibrinous-thin, clear to cloudy, pink to yellow

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Signs of Chronic Inflammation

Low grade fever Malaise Weight loss Anemia Fatigue Leukocytosis/Lymphocytosis Detected by ESR

Chronic Inflammation
Sx are the result of persistent injuryLeads to accumulated WBC, plasma cells & macrophages Fibrosis leads to: Progressive tissue damage Progressive loss of function

The Art of Healing

Local factors Systemic factors Nutrition Treatment

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Local Factors in Healing

Presence/absence of Infection Blood Supply Extent of Necrosis Presence of Foreign Bodies Protection from Trauma or Movement

Systemic Factors in Healing

Nutritional Status Well-being Hx CVD Hx CA Hematologic Disorders Systemic Illness DM Immunosuppression

Fluid & Electrolyte Imbalance

Acidemia arterial blood pH<7.35 Acidosis- blood pH < normal ( H ions) Alkalemia-arterial blood pH>7.45 Alkalosis blood pH > normal (H ions) Dehydration negative fluid balance Hypercalcemia high blood Ca level Hypocalcemia-low blood Ca Hyperkalemia-high K in blood Hypernatremia-high Na in blood Hypervolemia-abn. inc. blood volume

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Pain
Acute Pain Less than 6 wks Chronic Pain Old theory: More than what is considered anatomically indicated Now: More than 6 wks

Pulse
Is there circulation to the area of trauma or healing?

Blood Pressure
Can the body maintain normal function: Moving blood Reacting to changing position Reacting to stress

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Respirations
Can the body provide adequate oxygen to the tissues? Can the body remove excess waste products from

respiration process?

Nutrition and Healing

Can the Body provide the raw materials to make new tissue and regain biochemical homeostasis?
Proteins Water Vitamins Minerals Fats

Treatment to Boost Healing

Psychological Physical Emotional Medical

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Psychological
Hope Counseling Education Control Others?

Physical
Relaxation Response Sit quietly Close your eyes Breathe in slowly thru nose Breathe out slowly thru mouth Focus on one sound Do for three minutes PRN Can be augmented by pets, music, yoga, tai chi,

gardening.

Emotional
Nurturing Unconditional acceptance Love Kindness TLC May require intervention

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Medical
Examination Treatment Medical Surgical Medicinal Osteopathic Holistic

Phases of Tissue Repair

Inflammatory Response Proliferation Phase Contraction Phase Remodeling

Inflammatory Phase (minutes)

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Proliferation Phase (Days)

Contraction Phase (Weeks)

Remodeling Phase (Months)

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Healing Formation of Scar Tissue

Complications of Scar Tissue

Loss of function: there is a loss of normal cells Contractures and obstructions: scar tissue tends to

shrink over time and restrict movement

Adhesions: bands of scar tissue joining two surfaces

that are normally separated

Hypertrophic scar tissue: an overgrowth of fibrous

tissue
Ulceration: blood supply may be impaired around the

scar resulting in further tissue breakdown

Stages of Bone Healing

Healing occurs in three distinct but overlapping

stages: 1) early inflammatory stage 2) repair stage 3) late remodeling stage

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Bone Inflammatory Phase

Hematoma develops at fracture Within hours to days Inflammatory cells infiltrate bone under prostaglandin mediation. Results in the formation of granulation tissue, ingrowth of vascular tissue, & migration of mesenchymal cells. Anti-inflam & cytotoxic meds during 1st week can alter healing

Bone Repair Phase

Fibroblasts begin to lay down a stroma that helps

support vascular ingrowth.

At this time nicotine in the system can inhibit this

capillary ingrowth.
A significantly decreased union rate had been

consistently demonstrated in tobacco abusers.

Bone Repair Phase II

Callus very weak in the first 4 to 6 weeks
Requires adequate protection in the form of bracing or internal fixation.

Callus ossifies and bridges gaps If improper immobilization: may develop unstable fibrous union instead.

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Bone Late Remodeling

Returns to original shape, structure, and

mechanical strength
Months to years Axial loading assists

Adequate strength is typically achieved in 3 to 6

months
Add 1 week+ per decade

The Process.

Bone Healing

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Open Reduction and External Fixation

ORIF

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The journeys of Life

Acknowledgements
SU Tampa PTA Faculty

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