Acute and chronic, eyes and ears, wound healing

patho final

Skin

Largest organ in the body

9-11 lbs

Skin functions

Serves as first line of defense; waterproof barrier

Minimizes excessive water loss

Maintains thermoregulation

Contains receptors for somatic sensations

Participates in metabolism and activation vitamin D

Epidermis

Upper layer of the skin

Stratified squamous epithelial cells; keratinocytes

Contains melanocytes, dendritic cells, tactile cells; are sensory receptors for touch

Keratinization

Keratin is water-insoluble protein

Keratocytes filled with keratin; dead to surface

Dermis

Contains:

Blood vessels, skin appendages, sensory receptors, and smooth and skeletal muscle cells

Dermis 2 layers

Papillary layer (superficial)

Reticular layer (thicker and deeper)

Papillary layer

Loosely and irregularly organized connective tissue

Fibroblasts, macrophages, plasma, mast, endothelial, and adipose cells

Reticular layer

Dense connective tissue

Dermal-epidermal junction (DEJ)

Barrier against passage of substances into and out of body

Framework to restore architecture of the tissue

Extracellular matrix (ECM)

Ground substance

Tissue growth and wound healing

Fibrous structural proteins: Collagen and elastin

Adhesive glycoproteins

Glycosaminoglycans (GAGs)

Cell interactions

Integrins and cytokines and growth factors

Integrins

Transmit information bidirectionally

Bind extracellular substances

Adhesion molecules

Acute wound

Occurs suddenly or over brief period

Restoration of structural and functional integrity in 4-6 weeks

Chronic wound

Occurs over long period

Does not heal in organized and timely manner

Impairment of structural and functional integrity

Partial thickness wound

Damage extends through epidermis; dermis intact

Reepithelialization occurs

Reepithelialization

Epithelial cells migrate to area and replicate by mitosis

Full thickness wound

Damage extends through epidermis and dermis

Possibly extends into subcutaneous tissue, muscle, bone

Scar formation

Wound healing phases

Hemostasis

Inflammation

Proliferation/granulation

Remodeling/maturation

Chemical mediators

Neutrophils, macrophages, lymphocytes, platelets, keratinocytes, fibroblasts, endothelial cells

Growth factors

Cytokines

Cytokines

Initiate healing process

Produce and simulate growth factors and cytokines

Develop the ECM

Coordinate the intracellular communication

Wound healing

Depends on:

Type of injury

Extent of tissue loss

Infection, necrotic tissue, or secondary tissue breakdown

Type of cells involved

Primary intention (primary closure)

Surgical closure of wound

Repair: formation of new ECM

Regeneration: reepithelialization

Little granulation tissue

Secondary intention (secondary or spontaneous closure)

Full thickness wound heals without closure attempt

Large amount of granulation tissue

Longer healing time; larger scar

Skin grafting; skin substitutes

Tertiary intention (delayed primary closure)

Full thickness wound heals without closure attempt

Large amount of granulation tissue

Longer healing time; larger scar

Skin grafting; skin substitutes

Growth factors

Stimulate growth, division, differentiation of other cells

Regulate intercellular communication

Nitric oxide

Direct effect: Bacterial killing

Indirect effect: Modulate cytokine and growth factor activity

Hemostasis

Prevent additional tissue injury

Prepare wound for healing and regeneration

Hemostasis phases

1: vessel constriction, platelet formation

2: Platelet clot (primary hemostasis)

3: Coagulation factors (secondary hemostasis)

4: Fibrin clot

Inflammatory response goals

To clean wound

Prevent additional tissue injury

Prepare wound for healing and regeneration

Recruitment of phagocytic cells and wound debridement

Proliferative phase of wound healing

Wound healing guided towards tissue repair

Granulation tissue: foundation for collagen- based matrix that replaces fibrin-based provisional matrix

Fibroblasts: produce collagen, adhesive proteins for ECM

Myofibroblasts

Endothelial cells: angiogenesis (neovascularization)

Reepithelialization: regeneration of keratinocytes

Remodeling phase of wound healing

Restores structural and functional integrity of skin

Dermal matrix not regenerated; mended

Steps:

—Wound contraction and closure

–Continuous turnover of collagen

–Decreased capillary density

–Declining cellular content

–Mature scar tissue devoid of skin appendages

–Maturation of scar tissue continues for minimum of one year

Local factors that impede wound healing

Blood flow and hypoxia

Infection and contamination

Radiation exposure

Movement/tension

Desiccation

Excessive edema

Denervation

Systemic factors that impede wound healing

Advanced age

Malnutrition

Nutritional status

Immune deficiency

Smoking

Medications

Metabolic status

Hypoxia

Delays or stops wound healing process, leading cause of wound infection, inhibits fibroblast activity, collagen deposition in matrix

Infection and contamination

Badly contaminated wounds may overwhelm host defenses. Surgical wound handling

Contamination

Necrotic tissue, foreign or exogenous material, endogenous substances

Nutritional status

Major role in wound healing

Essential macronutrients: Carbs and fats

Effect of negative nitrogen balance

Impaired immune and inflammatory responses

Delayed wound healing; increased wound infection

Diminished angiogenesis

Vitamin and mineral deficiencies

Associated with chronic, nonhealing wounds in nutritionally debilitated individuals

Corticosteroids

Promote breakdown of carbohydrates, fats, proteins

Anti-inflammatory action impedes inflammatory phase of wound healing

Various negative effects

Antineoplastic drugs

Potent immunosuppressants

Impair reepithelialization, granulation tissue formation, angiogenesis

Diabetes mellitus

Insufficient insulin, insulin resistance, or both

• Hyperglycemia with untreated diabetes

  • Chronic macrovascular disease

  • Atherosclerosis; tissue ischemia and hypoxia

  • Thickening of basement membranes: diabetic lesions

• With impaired perfusion

  • Impaired granulocyte function and chemotaxis

  • Reduced ability to fight infection

• Sensory neuropathy

  • Reduces pain sensation associated with wounds

Excessive wound healing

Abnormally high connective tissue deposition resulting in altered tissue structure and function

Fibrosis

Replacement of normal tissue excessive, nonfunctional collagen or scar tissue

Excess synthesis and/or delayed degradation

Keloids

Lesions of dermal scar or fibrotic tissue

Hypertrophic scars

Excess fibrotic tissue

Raised above level of surrounding skin

Grow within boundaries or original injury; regress spontaneously

Contractures

Abnormal exaggeration of wound contraction

Shrinking scars severely deform wound; reduce mobility

Compromise mobility of involved joints

Deficient

Insufficient deposition of dermal connective tissue matrix weakens tissue to wound failure

Wound dehiscence

Extrafascial: partial or complete separation of outer layers of sutured wound; underlying fascial layer remains intact

Fascial: evisceration; separation of fascial layers

Clinical manifestations of impending wound disruption

Signs of infection

Absence of healing ridge by fifth to ninth postoperative day

Seroma or hematoma formation

Increase in serous discharge

Chronic nonhealing wounds

Do not proceed through healing process

Progress through healing process but cannot maintain structural and functional integrity

Arrest in inflammatory phase

Harbor bacteria; imbalance between neutrophilic proteolytic enzymes and their inhibitors

Increased levels of inflammatory mediators; chronic inflammation, necrosis, fibrosis

Structures in Ear

Hear and interpret sounds

Provide info about position and movement of head in space

Receptors within eye

Shapes and colors conveyed in light energy

Impairments to ear and eye

Alter information available to cortex to process

Disease, aging, medications, environmental factors, genetics

Disorders of hearing, balance and vision

Have a negative effect on quality of life

Children will have developmental, communication, and mobility delays

Adults will have mobility, nutrition, stress, coping, and mood problems

• increased susceptibility to environmental issues

Hearing process

Sound waves transformed into neural impulses

Pitch, loudness, timing preserved at each step, allowing brain to perceive sound accurately

Auditory system pathologies

Disrupt normal sound transmission process

Types of hearing loss

• Sensorineural

▪Conductive

▪Mixed

INNER EAR AND PERIPHERAL BALANCE DO slides 11-13

Conductive Hearing Loss Disorders

Sound unable to travel normally to inner ear

Reflect audibility problem

Types of Conductive hearing loss

Outer ear disorders

Otitis media

Otosclerosis

Outer ear disorders

Highly treatable

Typically do not involve hearing loss

• exception is congenital outer ear malformations

Some common disorders

• Cerumen impaction

• Collapsed ear canal

• External otitis

• Stenosis of ear canal

Otitis Media (OM)

Inflammation of middle ear space

• Associated with Eustachian tube dysfunction

• Commonly diagnosed in children

OM Clinical man

Cold like symptoms and/or upper respiratory problems

Acute Otitis Media

Inflammation of middle ear with acute onset

Moderate to severe bulging of TM and middle ear effusion

Complications

• Rupture of Tm

• Conductive hearing loss (temporary)

Treatment

• Antibiotics

Recurrent Acute Otitis Media

3+ episodes of AOM in 6 months

4+ episodes in 12 months

Factors that increase risk

• male

• Passive exposure to smoking

• Winter

Chronic Otitis Media

Infection longer than 6 weeks with persistent effusion in middle ear space

Mild to moderate conductive hearing loss

Treatment:

• Topical antibiotics and/or steroids

• Frequent cleaning of ear

Severe cases:

• Surgery

• PE tubes (pressure equalization)

Otosclerosis

Abnormal bone growth in middle ear space

Associated hearing loss

• bilateral

• Slowly progressive 

• Conductive

Otosclerosis cause and patho

Alternating bone resorption and formation

Genetic component as autosomal dominant

Viral factors

Autoimmune system disorders

Otosclerosis diagnosis

History

Otoscopy

Audiologic results

Radiologic studies

Otosclerosis treatment

Annual hearing tests

Surgery

Hearing aids

Presbycusis

Hearing loss due to aging

Most common form of hearing loss

Various contributing factors

4 types of Presbycusis

Sensory

Neural

Metabolic/strial

Mechanical/cochlear conductive

Presbycusis clinical man

Progressive decrease in hearing thresholds

Decreased ability to understand speech

Presbycusis diagnosis

History and complete audiologic assessment

Presbycusis treatment

Hearing aids

Assistive listening devices

Cochlear implants

Ménière Disease (inner ear disorder)

Inner ear disorder with both auditory and vestibular symptoms

• Excess endolymph within membranous labyrinth of

inner ear

Ménière Disease

Intense vertigo with accompanying nausea and vomiting

Tinnitus

Pressure or fullness in the ear

Fluctuating hearing loss

Ototoxicity

Side effect of some meds

• damage to sensory cells of inner ear

Cochleotopic meds

Damage to sensory cells of cochlea

Cause sensorineural hearing loss

Typically bilateral

Vestibulotoxic medications

Damage sensory cells of peripheral balance system

Effects typically bilateral

Factors that affect Ototoxicity

Age

Coexisting medical conditions

Genetic predisposition

Drug

Genetic hearing loss

One of the most common birth defects

Caused by genetic mutation

Genetic hearing loss clinical man

Nonsyndromic hearing loss: Hearing loss only

Syndromic hearing loss: Accompanied by pattern of

other clinical abnormalities

Genetic hearing loss diagnosis

Physical attributes related to syndrome

Genetic testing for definitive diagnosis

Genetic hearing loss treatment

Regular audiologic monitoring

Sensorineural hearing loss

• hearing aid or cochlear implant

Conductive hearing loss

• hearing aid or osseointegrated hearing implant

Myopia

Nearsightness, image focused in front of the lens

Hyperopia

Farsightness, eyeball is too small, image focused behind the retina

Presbyopia

Farsightness associated with aging, loss elasticity reduce accommodation

Ciliary muscles weakening and the eye’s lens becoming less flexible with age

Astigmatism

Irregular curvature in the cornea or lens

Strabismus

Result from deviation of one eye, double vision (diplopia)

May cause by weak or hypertonic muscle, short muscle or neurological defect

In children - must be treated immediately to prevent development of amblyopia

Nystagmus

Rapid, involuntary eye movement

Develops in some individuals with amblyopia and strabismus.

May result from neurological causes, inner ear or cerebral

disturbance, drug toxicity

Acquired diplopia

Result from neurological causes (stroke), paralysis of extraocular muscle

Loss depth perception

Color blindness

Types

▪ Red/green color blindness (most common)

▪ Blue/yellow color blindness

▪ Achromatopsia (most severe)

Congenital or acquire

Hordeolum (stye)

Tender, red, often pus-filled bump along edge of eyelid

Bacterial infection in oil glands at base of eyelash

Resolve in week without treatment

Conjunctivitis (pinkeye)

Symptoms

▪Redness, discharge, itching, burning of eyes

▪Increased tearing; blurred vision, Light sensitivity

Viral Conjunctivitis

Most common

Adenoviruses; herpes simplex virus

Resolves 7-21 days

Bacterial Conjunctivitis (chlamydia)

Resolves in 1 week

Symptoms persist up to 3 weeks

Topical antibiotics

Allergic Conjunctivitis

Not contagious

Treated with saline and/or oral and topical meds

Pterygium

Benign growth on Conjunctiva; may extend to cornea

Risk factors:

• High levels of UV exposure, wind

Causes for removal

• Unsightly

• Interferes with vision

• Causes discomfort

Keratitis

Severe pain and photophobia: Develops when cornea is infected or irritated

• Transfer from herpes lesion around month.

• Increase the risk of ulceration eroding the cornea.

• Scar formation damages the cornea

Cause: Damage from chemicals, splashes and fume