Acute and chronic, wound healing, eyes and ears

patho final

Acute skin conditions

Bacterial or fungal infection

Contact with offending organism or allergen

Medications

Pain from first layer of skin

Alterations in tissue perfusion can lead to damage or necrosis

Chronic skin conditions

Long term, may or may not resolve

Viral infection

May or may not resolve

Cellulitis

Diffuse painful inflammation of skin and subcutaneous layers induced by a bacterial infection that enters through a break in the skin (cut, scrape, burn, or surgical incision, or bug bite)

Cellulitis clinical man

Painful, red, swollen area of skin; hot, tender to touch.

Fever and chills

Vesicles, bullae, plaques (with Staphylococcus)

Tachycardia, hypotension, confusion, headache

Lymphadenitis and lymphangitis

Impetigo

Superficial acute, highly contagious skin infection

Impetigo etiology and patho

Colonization facilitated by high temperature, humidity, preexisting skin disorders, young age (ages 2-5), recent antibiotic treatment

Furuncle

Extension of folliculitis or infection of sebaceous gland. spreads down hair shaft through follicle and into dermis

Carbuncle

Cluster of infected hair follicles. the cluster coalesces to form lesion filled with pus, dead tissue, fluid

Candidiasis

Infection of skin or mucous membranes with any species of Candida (C. albicans most common)

• Mouth, throat, lungs, vagina, folds of skin, bowel

• Usually secondary condition

Candidiasis etiology and patho

Candida normal in skin and mucous membranes

• Warmth, moisture, breaks in epidermis can cause infection

• Life threatening if in bloodstream

Candidiasis clinical man

Thrush: white covering of tongue, mouth, throat

Vaginal yeast infection: itching; foul odor; white discharge

Balanitis: flattened pustules, edema, burning, tenderness

Diaper rash: dark red patches in skin folds; fluid-filled spots

Tinea

Contagious infection by different types of fungus

Superficial infections; called dermatophytosis

Named by location on body

Necrotizing Fasciitis

‘Flesh-eating disorder”

Rapidly spreading infection caused by aerobic and anaerobic bacteria

Necrotizing Fasciitis etiology and patho

Starts from contagious ulcer, wound, untreated skin infection, complication of surgery, abscess

Occlusion of small subcutaneous vessels; tissue ischemia, infarction, necrosis

Stevens-Johnson Syndrome

Rare skin and mucous membrane disorder

• cell death causes epidermis to separate from dermis

Stevens-Johnson Syndrome etiology

More than 200 meds

Infectious causes

Delayed hypersensitive rxn

Stevens-Johnson Syndrome clinical man

Flulike symptoms

Symmetric burning rash, red, purple lesions

Toxic Epidermal Necrolysis (TEN)

Inflammation of skin caused by poison

TEN with spots

Widespread with detachment of epidermis, erosion

More than 30% of body surface area

TEN without spots

Widespread with erythema, no lesions

More than 10% of body surface area

TEN etiology

Reactions to drugs; bacterial infection; malignancy; graft-versus-host disease; vaccinations

TEN Clinical Man

Flulike symptoms

Rash; large blisters in center rash; ruptures; skin peels off

Chronic viral skin infection examples

Herpes simplex virus

Varicella-zoster virus

Human papillomavirus

Herpes simplex virus type 1 (HSV-1)

Affected body regions

• herpes labialis (lip, cold sores)

• Herpetic keratitis (eye)

• Herpetic whitlow (digits or hands)

• Herpes gladiatorum (torso of wrestlers)

• Herpetic sycosis (beard follicles)

Usually contracted during childhood

Recurrences persist into old age

Herpes simplex virus T2 (HSV-2)

Causes most sexually-transmitted anogenital herpes

• lesions on genitals, perineum, or anus

May cause cold sires

• less common cause than HSV-1

Likely contracted via sexual contact

5th most common US transmitted infection

• 1/6 

HSV cause and patho

• Virus enters skin or mucous membrane via microscopic tear

• Virus travels to sensory root ganglion

• Virus becomes dormant and permanent resident of ganglion

• Cell-mediated immune system is triggered

• Viral activation occurs

• Virus travels from neuron to skin innervated by neuron

• Virus enters dermal and epidermal cells

• Viral replication causes recurrent rash outbreak

HSV clinical man

May have asymptomatic herpes or mild fever

• Usually begins with prodrome - Fever or flu-like symptoms

• Red, swollen area of skin or mucous membrane develops

• Eruption of painful vesicles

• Regional lymph nodes swell

• Lesions open and form painful ulcers that crust and begin healing

• Primary genital herpes

• May cause dysuria and urinary retention, especially in women

Herpes Zoster

Chronic viral skin condition

Affects abt 1 million people

AKA shingles

Caused by varicella zoster virus (VZV)

• member of the herpesvirus family

First VZV infection causes chickenpox

Potential complications of HZ

• Postherpetic neuralgia (PHN) (most common complication)

• Transient ischemic attack (TIA) and stroke

• Encephalitis and aseptic meningitis

• Chronic eye disorders and retinal necrosis

• Bacterial superinfection of lesions

• Cranial or peripheral nerve palsies

• Pneumonitis

• Hepatitis

HZ diagnosis

History and physical exam

• usually sufficient for diagnosis after rash appears

Lab testing

• PCR or direct immunofluorescent assay

Warts cause

Various types of HPV

Warts site of occurrence

Anywhere on skin or mucous membranes

Warts malignancy

Most lesions caused by HPV are benign

Some HPV types linked to dysplasia and cancer

• Genital HPV

  • Most frequently occurring sexually transmitted infection in US

Warts patho

HPV

• Enters skin via small openings

• Infects epidermal basal layer

• Viral replication occurs in cell nuclei

HPV causes nuclear atypia

• Structural abnormality in a cell

Nuclear atypia triggers epidermal cell changes

• Replication and hyperproliferation of keratinocytes

Wart develops

Family history

Most important risk factor for certain chronic skin diseases

Chronic skin conditions that have genetic component

Atopic dermatitis

Psoriasis

Hidradenitis suppurativa

Eczema

General term

Describes inflammatory skin disorders

Includes atopic dermatitis (AD)

• most severe form of eczema

Atopic Dermatitis

Chronic, recurring, itchy, inflammatory disorder

Associated with increased serum IgE

Affected individuals often have other atopic disorders

• E.g., asthma, allergic rhinitis

Most often affects children

May persist into adulthood

Dysfunctional epidermal barrier

AD and susceptibility to infection is due to this

Atopic dermatitis clinical man

Exacerbation and remission of dry, itchy, red skin

Begins in infancy

Constant pruritus

• Prevailing symptom

• Precedes eczematous rash

Skin excoriations and lichenification

Negative impact on overall quality of life

• E.g., sleep disturbances, depression

Psoriasis cause

Immune mediated disease

Genetic and environmental causation

Psoriasis patho

Hyperproliferation of keratinocytes

Decreased epidermal cell turnover rate

Inflammation

Proliferation of keratinocytes

Thickening of dermis and epidermis

Psoriasis clinical man

Plaque psoriasis – Skin lesions usually round or oval, well-

demarcated plaques

Hidradenitis Suppurativa cause

Genetic, immunologic, hormonal, and environmental factors

Hidradenitis Suppurativa patho

Occlusion of hair follicle via infundibular hyperkeratosis

Hyperplasia of follicular epithelium

Collection of cellular wastes

Cyst forms in apocrine sweat gland adjacent to hair follicle

Nodule opens beneath the skin and spreads laterally

May lead to abscess formation and sinus tract formation

Keloid-like scarring may occur

Hidradenitis Suppurativa clinical man

Painful nodules, abscesses, and sinus tract formations

Lesions develop in skinfold areas

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