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106 Cards in this Set
- Front
- Back
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Layers of the Skin:
1. Epidermis |
*First line of defense
*Most superficial layer *Continually shedding *3 different types of cells in the epidermis that help the skin function effectively: Melanocytes, Langerhans Cells and Merkel Cells |
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3 Types of Cells in the Epidermis:
1. Melanocytes |
*Synthesizes and secrets the pigment melanin in order to shield the skin against UV radiation
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3 Types of Cells in the Epidermis:
2. Langerhans Cells |
*Sit in the dermal layer and initiate the immune response that provides a defense against environmental antigens which come into contact with the skin surface
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3 Types of Cells in the Epidermis:
3. Merkel Cells |
*Serve as pressure sensors that sit on top of the dermal layer and activate when pressure is applied to the epidermis
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Layers of the Skin:
2. Dermis |
*Hair follicles, sebaceous glands, sweat glands, BV, lymphatic vessels and nerves
*Made up of collagen, elastin and reticulin, which are forms of connective tissue to allow the skin to be mobile, stretch and contract |
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Layers of the Skin:
3. Subcutaneous |
*AKA Hypodermis
*Made up of fat, adipose cells, BV, sweat glands, sebaceous glands, nails and hair *Macrophages, Mast cells and Fibroblasts live in the dermis |
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The Skin and Aging
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*Genetic and environmental factors lead to changes such as UV from the sun and other irritants and pollutions
*Skin becomes thinner, drier, wrinkled and has changes in pigmentation *Fewer Melanocytes and Langerhans cells *Decrease vascular pressure, decreased temp regulation and delayed wound healing, which can lead to an increased risk of hypothermia and stroke |
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Pressure Ulcers
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*Ischemic ulcers resulting in pressure and shearing forces
*Factors associated with formation: Elderly in hospital or LTC, neurological disorders, chronic disease and coarse sheets *Top 3: Nutritional status, skin moisture and immobilization *Causes coagulative necrosis |
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Pressure Ulcer Stages:
1. Stage 1 |
*Non blanching erythemea of the skin
*No tearing of the skin *The non blanching is due to underlining ischemia and damage to the dermal and possibly the subcutaneous tissue |
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Pressure Ulcer Stages:
2. Stage 2 |
*Partial thickness loss involving the epidermis and dermis
*Broken through the skin, and wound is as deep as the epidermis and dermis but has NOT reached subcutaneous |
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Pressure Ulcer Stages:
3. Stage 3 |
*Full thickness loss involving the subcutaneous layer
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Pressure Ulcer Stages:
4. Stage 4 |
*Involves tissue necrosis of the muscle layer, bone and supporting structures
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Pressure Ulcer Stages:
5. Unstagable |
*Primary reason we cant stage an ulcer is if you can not visualize the wound bed
*Anytime there is eschar over the tissue, you cannot tell how deep the wound is, and therefore it cannot be staged |
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Deep Tissue Injury
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*May be confused with a bruise or stage 1 ulcer, but in reality it is an injury well below the skin surface, hidden due to the epidermis remaining in tact.
*Generally occurs over bony prominences and is caused by pressure/ischemia in the area |
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Inflammatory Skin Disorders:
1. Dermatitis |
*AKA Eczema
*Most common skin disorder *Characterized by pruritus, lesions with indistinct borders and epidermal changes |
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Inflammatory Skin Disorders:
2. Allergic Contact Dermatitis |
*Caused by hypersensitivity IV (T Cells) reaction, causes a delayed reaction over a few hours
*The allergen comes in contact with the skin, binds to a carrier protein to form a sensitizing antigen, Langerhans cells process the antigen and carry it to T cells, which becomes sensitized to the antigen *Causes erythema, swelling, pruritus, and vesicular lesions *Ex: Poison Ivy, latex, topical antibiotics and anesthetics |
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Inflammatory Skin Disorders:
3. Atopic Dermatitis |
*Very common among childen
*Type I Hypersensitivity (IgE mediated and Histamine) *Activation of mast cells, eosinophils, T lymph and other inflammatory cells *Causes red, weeping crusts and chronic inflammation *Most have family history with asthma and allergies *Treatment: Avoiding irritants, moist skin and wet compresses |
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Inflammatory Skin Dermatitis:
4. Irritant Contact Dermatitis |
*Non-immunological inflammation of the skin
*Chemical irritation from acids or prolonged exposure to irritating substances *Often due to soaps or detergents *Symptoms similar to allergic contact dermatitis *Treatment: Remove stimulus |
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Inflammatory Skin Disorders:
5. Stasis Dermatitis |
*Occurs due to poor circulation (Due to congested heart failure) in the legs.
*Can occur from poor heart contractility/ decreased pressure, fluid overload or narrowing of the arteries *Occurs as a result of venous stasis, edema and vascular trauma *Appearance is varicose veins, erythema, darkness, waxiness of skin *Can lead to venous ulcers if not treated *Treatment: Elevating legs, compressions for edema and treatment of heart condition |
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Inflammatory Skin Disorders:
6. Seborrheic Dermatitis |
*Inflammation of the skin involving skin folds such as the scalp, eyebrows, eyelids, nasolabial fold and ear canals
*Also known as cradle cap *Scaly white and yellow plaque *Unknown cause, occurs from birth to old age intermittently and treated with steroids and sulfur based shampoos *Has periods of remission and exacerbation |
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Psoriasis
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*Chronic, relapsing, proliferative skin disorder that can occur at any age
*Idiopathic cause although genetics, immunologic and biochemical have been investigated *Epidermis and Dermis are thickened with erythema *Lesions are usually thick, silvery, scaly, erthematous plaque surrounded by normal skin *Found in face, knee, elbow, nails and scalp |
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Psoriasis Continued...
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*Skin lesions are caused by inflammatory cytokines, particularly TNF-Alpha
*Increased mitotic division of the cells causes plaques to form, bc there are too many skin cells *Treatments: Emollients, corticosteroids, antimetabolites *Also Methotrexate is used as a treatment, which is an immune suppressant, and retards the cell growth |
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Vesiculo-Bullous Disroder: (Vesicle and Blister Formation)
1. Pemphigus |
*Autoimmune blistering disease of skin and oral mucous membrane from circulation autoantibodies
*IgG (Also IgM) and C3 complement (Atigen-Antibody Complex) bind to adhesion molecules destroying cell-to-cell adhesion in epidermis with fluid build up, causing the blister *Can range from benign to fatal, need to be aware of infection from blisters and cellulitis *Treatment: Steroids and immunosupressive therapies |
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Vesiculo-Bullous Disroder: (Vesicle and Blister Formation)
2. Bulous Phemphigoid |
*Benign disease, presence of IgG in the serum leads to blistering in the subepidermal layer of skin
*Usually occurs in people over the age of 60 *Starts with localized erythema and pruritic plaques *Can grow into bulla that will burst and then heal rapidly *Treatment: Anti-puritic medication and steroids to immunospress and prevent further blistering |
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Vesiculo-Bullous Disroder: (Vesicle and Blister Formation)
3.Erythema Multiforme |
*Inflammation of skin and mucous membranes associated with immune or toxic reaction to drugs or herpes virus.
*20-40 yrs old are most at risk *C3, IgM and fibrinogen deposition around superficial dermal blood vessels causing edema and then vesicles and bullae |
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Vesiculo-Bullos Disorders:
3. Erythema Multiforme... Steven Johnson Syndrome |
*Severe bullos formations generally caused by IV drug reaction.
*Causes fever, headaches, malaise, sore throat and coughing *Occurs on skin and epithelial lining of the mouth, air passages, esophagus, urethra and conjunctiva *Blidness can result if it reaches eyes, and death can occur if it affects air passages and can cause renal failure *"Target" lesions are the first external symptom |
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Vesiculo-Bullos Disorders:
3. Erythema Multiforme... Toxic Epidermal Necrolysis (TEN) |
*Medication related
*Causes the epidermis to separate from the dermis *Affects mucosa membranes, mouth, eyes and vagina *Can be fatal and is very rare |
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Skin infections:
1. Folliculitis |
*Bacterial infection of the hair follicles caused mostly by Staphylococcus Aureus
*Lesions appear as pustules with surrounding are of erythema *Treatment: Cleaning with soap and water and use of antibacterial are effective |
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Skin Infections:
2. Furuncles |
*Boils, inflammation of the hair follicles following folliculitis
*Deep, firm, red, painful nodules around 1-5cm *Can lead to cellulitis *Most common on scalp and extremities |
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Skin Infections:
3.Carbuncles |
*Collection of infected hair follicles occuring most frequently on the back of the neck, upper back and lateral thighs
*Begin in subcutaneous tissue and lower dermis *May become painful and swollen as the press the skin up and may turn into abscess which then require debridement |
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Skin Infections:
4. Cellulitis |
*Infection of the dermis and subcutaneous tissue caused by bacteria
*Can occur as an extension of a skin wound, an ulcer or furuncles/carbuncles *Treatment: Antibiotics bc we are concerned with the infection spreading throughout the system bc it affects deep into the subcutaneous layer |
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Fungal Skin Infections
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*Predisposing Factors: Local environment of moisture, warmth, maceration, systemic administration of antibiotics, diabetes mellitus, low immune system states
*Treated with anti-fungal |
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Fungal Skin Infections:
1. Tinea Infections |
*Fungal infections of the skin by dermatophytes and are classified according to their locations
*Treated with local or systemic anti-fungal *Systemic anti-fungal can be very dangerous bc it is very toxic to the liver, so local is much more preferred |
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Tinea Capitis
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*Superficial infection of the scalp
*More common in children then adult *Scaly, pruritic scalp with bald patches bc the hair breaks easily |
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Tinea Corporis
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*Ringworm infection
*More common in children then adults *Circular elevated ring-link border with mildly erythematous scaly patches |
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Tinea Cruris
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*Jock Itch
*Small, erythematoys and scaling esicular patches with well defined borders *Spreads over inner and upper surfaces of the thigh *Occurs with high heat and humidity |
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Tinea Pedis
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*Chronic, superficial fungal infection of the skin of the foot, common in adults
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Tinea Manus
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*Dry scaly erthematous lesions of the hang
*Causes itching |
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Tinea Ungium
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*Superficial or deep inflammation of the nail that develops yellow-brown accumulations of brittle keratin overall or portions of the nail
*Also known as onchomycosis *Difficult to treat and besides the loss of normal nail function, it is not harmful and does not spread beyond the nail bed |
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Fungal Skin Infections
2. Candidiasis |
*Caused by yeast like fungus Candida Albicans
*Found in normal flora of the GI system, skin, vagina and mucosa membrane but can cause disease if the immune system is depressed *Found in wet skin folds such as breast, groin, axialla and immunocompromised patients in the mouth (Thrush) *Bacteria flourish with the wet/moist area *Treated with anti-fungal |
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Viral Infections:
1. Herpes SImplex |
*Caused by 2 viruses:
A. HSV-1 Generally Oral (Cold Sores B. HSV-2 Generally Genital (STD) |
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Viral Infections:
2. Herpes Zoster (Shingles) |
*Causes pain and parasthesias on localized effected dermatome
*Attacks the spinal cord nerves *If treated with antiviral within 72 hours, can prevent post herpetic neuralgia, which is the pain that occurs in the dermatome (Cutaneous are innervated by a single spinal nerve) *Affects Specific Dermatomes: Spinal, facial, cervical, thoracic and lumbar *If not treated it can lead to Herpes Zoster Encephalitis, which is inflammation of brain tissue |
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Viral Infections
2. Herpes Varicella (Chicken Pox) |
*Mostly in children
*Causd by the same herpes virus as herpes zoster.... Varicella-Zoster Virus (VZV) |
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Viral Infections
2. HSV and VZV |
*One develops lifelong latency in the dorsal root ganglion
*UV light, skin irritation, fever, fatigure, and stress can reactivate it *Zoster can also stay dormant in trigeminal ganglia |
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Skin Cancers:
1. Basal Cell Carcinoma (BCC) |
*Most common human cancer
*Originates in interfollicular basal cells, hair follicles and sebaceous glands *Depressed shape, and rolled borders *Usually do not metastasize, but can cause severe localized destruction of tissue |
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Skin Cancers
2. Squamous Cell Carcinoma (SCC) |
*Mostly found in head, neck and hands
*Invasive SCC can arise from premalignant lesions in the skin or damaged skin *Almost never arises from healthy skin *2 Types: A. In Situ: Easy to treat if taken care of early B. Invasive: Which can be more rapidly growing than BCC, and can spread to lymph nodes |
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Skin Cancers:
3. Malignant Melanoma |
*From Melanocytes
*Young to middle age adults are most at risk *RIsks include UV light exposure, genetic predisposition, steroid hormone activity, fair hair, light skin, and freckles *Highly malignant, if local and not invasive it can be surgically removed *Once it has become invasive, generally requires chemotherapy or biotherapy |
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Skin Cancers :
4. Kaposi Sarcoma |
*Associated with AIDS
*Caused by KSHV *Occurs in endothelial cells and is easily treated if no immune deficiency is present |
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Skin Cancer Identifications
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A: Asymmetry
B: Border Irregularity C: Color Variation D: Diameter Larger then 6mm E: Elevation |
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Viral Conjunctivitis
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*Caused by adenovirus
*Symptoms can be mild to severe including eye strain, watering, redness, photophobia (Light sensitivity) *Contagious *Treatment: Manage symptoms, not curative, need to wait it out |
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Acute Bacterial Conjunctivitis
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*Highly contagious
*Caused by gram + bacteria *Mucopurulent (Mucous + pus) drainage is present, can be in one eye or both eyes *Spreading is prevented by hand washing *Self limiting and resolves in 10-14 days , antibiotic drops can speed up the process |
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Allergic Conjunctivitis
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*From pollens or other antigens
*Symptoms: Itching, photophobia, burning and gritty sensation in the eye *Treatment: By symptom |
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Trachoma Conjunctivitis
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*Chlamydial Conjuctivits is the leading cause of preventable blindness
*Contracted at birth, prevented by treating mother with antibiotics prior to birth and give babies antibiotics eye drops right after birth *Causes inflammation and vascularization of the cornea, leading to scarring and thus blindness |
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Visual Disorders:
1. Cataract |
*Opacity of the lens
*Develops due to an alteration of metabolism and transport of nutrients within the lens *Causes decreased acuity, blurriness, glare, and decreased color perception *Treated by removing the lens and replacement with an artificial lens |
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Visual Disorders:
2. Glaucoma |
*Increased interocular pressure that can cause ischemia and degeneration of the optic nerve
*3 Types: Acute, Chronic and Chronic-Acute |
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3 Types of Glaucoma
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1. Chronic: Occurring over time, can be treated with hypersensitive eye drops. If untreated, loss of peripheral vision and then central vision and then blindness
2. Acute: Caused by extreme pressure, within hours or days it can lead to blindness. Emergency and needs to be treated right away 3. Chronic-Acute: Someone develops glaucoma on top of a pre-existing chronic glaucoma. Emergency. |
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Visual Disorders:
3. Retinal Detachment |
*Separation of the retina (Painless as it occurs)
*Caused by trauma or post cataract surgery. Also caused by photoreceptors or the retina being separated from the rest of the retina, causing oxygen deprivation and eventually death of those cells *Pt will describe vision as if a curtain is slowly coming down, there are holes in the image they are seeing or missing parts of the image *Emergency and needs to be treated right away, can lead to blindness |
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Hearing Disorders:
1. Conductive Hearing Loss |
*Impaired sound conduction
*Due to sound not being able to make it to the inner ear to interpreted *Examples: Outer, and middle ear infections, and impacted cerumen (Ear Wax) *Treat the condition and hearing should return |
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Hearing Disorders:
2. Sensoriuneural Hearing Loss |
*Impairment of the organ of corti in the inner ear or its central connections
*Usually due to to exposure to loud noise over time or caused by congenital or heredity disease early on in life or b several medications or diseases *Example: Presbycusis (Age related hearing loss) |
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Pain
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*Subjective experience for each patient, and there for much rely on the patients explantion
*Cannot be judged by looking at a patient *Cultural and individual differences in pain tolerance |
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3 Systems Involved in Pain:
1. Sensory/Discriminative: |
*Processes info about the strength intensity and temporal and spatial aspects of pain
*Sensations are mediated through afferent nerve fibers, the spinal cord, brain stem and higher brain cents *Results in prompt withdrawal from painful stimuli |
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3 Systems Involved in Pain:
2. Motivational/Affective: |
*Motivational determines individuals conditioned or learned approach and avoidance behaviors
*Occurs through interaction of the reticular formation limbic system and brain stem |
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3 Systems Involved in Pain:
3. Cognitive/Evaluative: |
*Individuals learned behavior concerning the experience of pain
*Cultural preferences, gender, life experience Etc. *Cognitive can block or enhance pain perception |
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Pain Pathway:
1. Afferent Pathways |
* Peripheral Nervous System (PNS) travels through the spinal gate in teh dorsal horn and ascends to higher centers in the CNS
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Pain Pathways:
1. Afferent.... Nociceptors |
Free nerve endings that respond to chemical, mechanical and thermal stimuli.
*Found under the epidermis and within joint bone surfaces, deep tissue, muscles, tendons and subcutaneous tissue *2 Types: 1. C Fibers: Unmyleniated and thus are slow, diffuse, burning or aching pain 2. A Gamma: Myelinated, and more sharp, fast pain sensations |
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Pain Pathways:
2. Interpretive Center |
*Located in brain stem, midbrain, diencephalon and cerebral cortex
*Processes the pain signals from nerves |
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Pain Pathways:
3. Efferent Pathways |
*Descends back to the dorsal horn of the spinal cord providing feedback to the location
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Theories of Pain:
1. Gate Control Theory |
*Pain transmission is modulated by a balance of impulses transmitted to the spinal cord/ substantia gelatinosa by A Gamma and C fibers
*There cells function as a gate regulation transmission of impulses to the CNS *Stimulation of non-nociceptive large A fibers such as touch vibration and thermal causes cells to close the gate, diminishing the pain perception so that stimuli that shouldn't cause pain, don't *This does not explain chronic pain, or neuropathic pain such as phantom limb pain |
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Theories of Pain:
2. Neuromatrix Theory of Pain |
*Where there is no discernible cause of chronic pain, brain produces patterns of nerve impulses from widely distributed neural networks causing pain where no nociceptive element exists
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Pain Neurochemistry
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*Multiple factors effect pain response
*Bradykinin, prostaglandins and leukotrienes signal pain where there is tissue damage *Substance P, is invovled in nociecptive pain, due to tissue damage, signaling C fibers to fire *Plays a role in chronic disease such as arthritis, and fibromyalgia *Can be inhibited by using capcasin, which is what makes hot peppers spicy |
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Other Modulators of Pain: Opiate Receptors
1. Endorphins |
* Released by stress, exercise, acupuncture and sex.
*Also release serotonin and norepinephrine. These all raise the pain threshold *Endorphins act upon 3 opioid receptors: Mu, Kappa and Delta *Opioid medication, such as morphine, attach to the mu receptor to reduce pain |
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Other Modulators of Pain: Opiate Receptors
2. Enkephalin |
*Found in the brain and spinal cord neurons
*Weak analgesic (Pain Killer), but longer lasting then morphine or endorphins |
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Other Modulators of Pain: Opiate Receptors
3. Dynorphin |
*Can be 5-50x more powerful then endorphins
*Impedes pain signals but can also incite pain *Repeated exposure to cocaine increases dynorphin levels in the brain causing addiction |
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Other Modulators of Pain: Opiate Receptors
4. Endomorphins |
*A group of peptides found in the brain that block nociception due to high affinity for morphine receptors
*They also cause vasodilation by releasing nitric oxide |
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Other Modulators of Pain: Opiate Receptors
5. Inhibitory Neuromodulators |
*Prevent pain signaling from occurring in the brain
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Clinical Types of Pain:
1. Somatogenic |
*Pain with physical cause
*Visceral: From internal organs or skeleton, is poorly localized, diffused, often accompanied by N/V hypotension, restlessness and shock *Often spreads away from acute site of injury |
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Clinical Types of Pain:
2. Psychogenic |
*No physical cause, but can be just as painful
*Patients suffering from this type of pain tend to be stigmatized by medical providers *It is thus impt to be conscious that pain is still pain, and should be treated |
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Clinical Types of Pain:
3. Neuropathic |
*Chronic and results from abnormal processing of sensory information
*Difficult to treat, traditional analgesics generally do not work, tricylic antidepressants are first line of treatment |
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Clinical Types of Pain:
4. Acute vs. Chronic |
*Chronic: At least 3-6 months, related to tissue damage, inflammation or injury of the NS. Can be persistant, like lower back pain or intermittent like migraines. Caused by decreased endorphines and C neuron stimulation. Strongly associated with depression.
Acute: Due to present stimulus related to tissue damage |
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Clinical Types of Pain:
1. Somatogenic |
*Pain with physical cause
*Visceral: From internal organs or skeleton, is poorly localized, diffused, often accompanied by N/V hypotension, restlessness and shock *Often spreads away from acute site of injury |
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Clinical Types of Pain:
2. Psychogenic |
*No physical cause, but can be just as painful
*Patients suffering from this type of pain tend to be stigmatized by medical providers *It is thus impt to be conscious that pain is still pain, and should be treated |
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Clinical Types of Pain:
3. Neuropathic |
*Chronic and results from abnormal processing of sensory information
*Difficult to treat, traditional analgesics generally do not work, tricylic antidepressants are first line of treatment |
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Clinical Types of Pain:
4. Acute vs. Chronic |
*Chronic: At least 3-6 months, related to tissue damage, inflammation or injury of the NS. Can be persistant, like lower back pain or intermittent like migraines. Caused by decreased endorphines and C neuron stimulation. Strongly associated with depression.
Acute: Due to present stimulus related to tissue damage |
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Pain Threshold
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*Lowing intensity at which a stimulus is perceived as painful
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Pain Tolerance
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*Amount of time or intensity of pain
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Types of Lesions:
1. Macule |
*A flat circumscribed area that is a change in the color of the skin
*Less then 1 cm *Ex: Freckles, flat moles, petechiae, measles and scarlet fever |
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Types of Lesions:
2. Papule |
*An elevated, frim, circumscribed area
*Less then 1 cm *Ex: Wart, elevated moles and linchen planus |
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Types of Lesions:
3. Patch |
*A flat, non palpable, irregular shaped macule
*More then 1 cm *Ex: Virilgo, port-wine stains, Mongolian spots and cafe au lait spots (Skin Stains) |
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Types of Lesions:
4. Plaque |
*Elevated, firm, and rough lesions with flat top surfaces
*More then 1 cm *Ex: Psoriasis, seborrheic and actinic keratoses |
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Types of Lesions:
5. Wheal |
*Elevated, irregular shaped area of cutaneous edema.
*Solid and transient (Temporary) *Variable diameter *Ex: Insect bites, urticaria and allergic reactions |
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Types of Lesions:
6. Nodule |
*Elevated, firm, circumscribed lesion
*Deeper in dermis then a papule *1-2 cm in diameter *Ex: Erythema nodosum, and lipomas |
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Types of Lesions:
7. Tumor |
*Elevated, solid, lesions
*Deeper in dermis *More than 2 cm *Ex: Neoplasms, benign tumor, lipoma and hemangioma |
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Types of Lesions:
8. Vesicle |
*Elevated, circumscribed, superficial
*Not in the dermis *Filled with serous fluid *Less then 1 cm *Varicella, and shingles |
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Types of Lesions:
9, Bulla |
*Vesicle but more then 1 cm
*Ex: Blister, pemphigus vulgaris |
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Types of Lesions:
10. Pustule |
*Elevated, superficial lesion, similar to a vesicle but filled ith purulent fluid
*Ex: Impetigo, and acne |
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Type of Lesions:
11. Cyst |
*Elevated, circumscribed, encapsulated lesion
*In dermis or subcutaneous layer *Filled with liquid or semisolid material *Ex: Sebaceous cyst and cystic acne |
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Type of Lesions:
12. Telangiectasia |
*Fine, irregular red lines produced by capillary dilation
*Telangiectasia in rosacea |
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Type of Lesions:
13. Scale |
*Heaped up, keratinized cells, flaky skin, irregular, thick or thin, dry or oily
*Variation in size *Ex: Flaking of skin with seborrheic dermatitis, following scarlet fever, flaking of skin from drug reaction or dry skin |
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Type of Lesions:
14. Lichenification |
*Rough, thickened epidermis secondary to persistent rubbing, itching, or skin irritation
*Flexor surface of extremity (Bending parts of body) *Ex: Chronic dermatitis (Eczema) |
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Type of Lesions:
15. Keloid |
*Irregular shaped, elevated progressively enlarging scar
*Grows beyond borders of the wound, caused by excessive collagen formation during healing *Ex: Keloid formation after surgery |
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Type of Lesions:
16. Scar |
*Thin to thick fibrous tissue that replaces normal skin following injury or laceration to the dermis
*Ex: Healed wound or surgical incision |
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Type of Lesions:
17. Excoriation |
*Loss of the epidermis
*Linear hollowed out, crusted out area *Ex: Abrasion, scratch and scabies |
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Type of Lesions:
18. Fissure |
*Linear crack or break from the epidermis to the dermis, may be moist or dry
*Ex: Athletes foot or cracks in the corner of the mouth |
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Type of Lesions:
19. Erosion |
*Loss of part of the epidermis, depressed, moist, glistening
*Follows rupture of a vesicle or bulla *Ex: Varicella or variola after rupture |
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Type of Lesions:
20. Ulcer |
*Loss of epidermis and dermis, concave
*Varies in size *Ex: Decubiti and stasis ulcers |
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Type of Lesions:
21. Atrophy |
*Thinning of the skin surface, and loss of skin markings
*Skin appears translucent and paper like *Ex: Aged skin and striae |
