Lecture 7 - Integumentary System (Skin) Pathologies Flashcards

1
Q

skin anatomy review

A
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2
Q

Terminology

A
  1. Papule (mụn sẩn): is a solid elevation of skin with no visible fluid, 1-10 mm in size, may be brown, purple, pink or red and may cluster causing a papular rash. phát ban sẩn
  2. Pustule (mụn mủ): small bumps or blisters on the skin that fill with fluid or pus, usually appear as white bumps surrounded by red skin, look like pimples but larger.
  3. Nodule (nốt sần): a growth of abnormal tissue, similar to a papule, but is greater than 5-10 mm in both width and depth, and most frequently found in the dermis, deeper tissues and internal organs.
  4. Cyst: an enclosed sac like pocket of membranous tissue that contains fluid, air or other substances. They can occur anywhere in the body and are mostly benign, vary in size. If a cyst is filled with pus it is a sign of infection and may turn into an abscess.
  5. Bullae (bóng nước): a fluid filled sac or lesion, a type of blister, fluid is trapped between layers of the skin, larger than 10mm, seen in bullous impetigo.
  6. Abscess (also called a boil or a furuncle): a collection of pus causing redness, pain, warmth and swelling. Mostly caused by infection around a hair follicle entering through the skin barrier. Most common sites are the skin of the armpits, base of spine and groin.
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3
Q

Bullous
Impetigo (Bệnh chốc lở)

A

Description: bacterial infection on skin, often around nose, mouth, hands or feet, very contagious (especially in children), blisters are up to 2 cm that crust over when healing.

Etiology: staphylococcus aureus, or less often streptococcus pyogenes

Pathogenesis: pathogenic organism produces a toxin that causes loss of cell adhesion in the superficial layers of the skin causing dissociation of epidermal cells and eventually forming blisters.

Clinical Features: may affect intact skin or damaged skin, epidermis separates from the dermis and fluid collects in between the layers forming blisters, reddened area develops pustules that rupture and crust over, often around nose, mouth, hands or feet and it is very contagious.

Treatment: antibiotics oral and topical and good hygiene

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4
Q

Non-Bullous
Impetigo

A

Description: bacterial infection on skin, often around nose, mouth, hands or feet, very contagious (especially in children), macule or papule becomes a vesicle that quickly ruptures and forms a honey coloured crust

Etiology: staphylococcus aureus, or less often streptococcus pyogenes

Pathogenesis: a disturbance in skin barrier allows pathogen to enter and come into contact with fibronectin for colonization and overgrowth

Clinical Features: reddened area develops pustules that rupture and crust over, may clump together, often on damaged skin, found around nose, mouth, hands or feet and it is very contagious,

Treatment: antibiotics oral or topical

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5
Q

Ecthyma

A

Description: infection forms a pustule that crusts over an ulcer, a deeper form of impetigo

Etiology: staphylococcus aureus, or less often streptococcus pyogenes

Pathogenesis: a disturbance in skin barrier allows pathogen to enter and come into contact with fibronectin for colonization and overgrowth

Clinical Features: painful deeper lesions, like impetigo except the pustules further form into ulcers that may scar

Treatment: antibiotics oral or topical and good hygiene

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6
Q

Cellulitis

Viêm mô tế bào

A

Description: infection causing inflammation of the lower layers of the skin and subcutaneous tissues, skin appears swollen and red and is warm to the touch, margins are not elevated and it is painful.

Etiology: staphylococcus aureus or streptococcus

Pathogenesis: a disturbance in skin barrier allows pathogens to enter, overwhelming the immune system’s defence cells that would normally contain the inflammation and accumulation of cellular debris.

Clinical Features: often on the skin of the lower legs, but may occur on face or arms. common, pain, swelling, tenderness, warmth, erythema, fever, chills, ulcerations, pustules and possibly systemic symptoms such as fever or chills.

Treatment: antibiotics, if untreated may lead to abscess, destruction of tissue or lymphangitis.

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7
Q

Erysipelas

Viêm quầng

A

Definition or description: infection causing inflammation of the upper layer (dermis) of the skin and subcutaneous tissues, margins are elevated with clear borders. Infection enters lymphatic vessels where it stimulates a response from the immune system.

Etiology: group A streptococcus

Pathogenesis: a disturbance in skin barrier allows pathogens to enter lymphatic vessels where they release toxins causing an immune response and an inflammatory response, contact with fibronectin allows colonization of bacteria

Clinical Features: red raised patches, warm and painful, may blister, streaking, rash, lymphadenoma, malaise, chills and fever, mostly on legs and face.

Treatment: antibiotics

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8
Q

Folliculitis

Viêm nang lông

A

Description: infection causing inflammation of a hair follicle forming a pustule. If in the eye it is called a “sty” or folliculitis on the eyelid also occurs on hairy skin of the face, scalp, thighs, axilla and inguinal area.

Etiology (cause): staphylococcus or fungal infection, trauma or idiopathic

Pathogenesis: a disturbance in skin barrier allows pathogens to enter a hair follicle causing immune response of inflammation.

Clinical Features: may be itchy, painful, clusters of small swollen red bumps or white heads, may be pus filled blisters that break open and crust over, occurs face, scalp, thighs, axilla and inguinal area

Treatment: antibiotic topical, antifungal topical, anti inflammatory topical, laser hair removal or minor surgery.

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9
Q

Folliculitis Complication
Furuncle nhọt and Carbuncle Nhọt độc

A

Furuncle: also known as a boil, a painful bacterial infection (staphylococcus aureus) around a hair follicle with pus. Becomes inflamed and is red and raised. It soon ruptures and drains cloudy fluid or pus. Most commonly on the face, neck, thigh and buttocks.

Carbuncle: many furuncles grouped together under the skin

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10
Q

Hidradenitis
Suppurativa

viêm tuyến mồ hôi mưng mủ

A

Description: chronic inflammation of the hair follicular epithelium causing small painful lumps to form under the skin where skin rubs together or is rich in apocrine glands such as the armpits, groin, buttocks and under the breasts.

Etiology: unknown, possible combination of genetic, endocrine and environmental factors, hair follicles become blocked

Pathogenesis: blockages contribute to accumulation of cellular debris causing an inflammatory response and the formation of cysts and abscess formation.

Clinical Features: blackheads, painful pustules or nodules (pea sized) and scarring, if folliculitis results in obstruction of the apocrine gland, chronic inflammation, pustules can be large and are often painful.

Treatment: anti inflammatories and good hygiene

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11
Q

Fungal - Tinea Infections
(Dermatophytosis)Q

A

Description: a group of infectious fungus (mysosis) called dermatophytes invade human epidermis and live off keratin. There are many forms named by where it occurs followed by “tinea” (example tinea capitis is dermatophytosis of the scalp). It is contagious,
Etiology (cause): fungus spread by direct contact
Pathogenesis: enters through a break in the skin barrier and adheres to keratinocytes, fungi live of keratin and reproduce, infection causes a hypersensitivity type immune response Clinical Features: contagious, all forms cause itching (except tinea versicolour)
Treatment: topical antifungals

  1. Tinea capitis: scalp, ringworm, causes hair loss
  2. Tinea corporis: general body regions, ringworm, causes scaly, reddish plaques or pustules in a ring
  3. Tinea pedis - athlete’s foot, most common, fissuring, maceration
  4. Tinea cruris - jock itch, groin
  5. Tinea barbae: beard and neck region
  6. Tinea faciale: face
  7. Tinea unguium: nails, causes nail discolouration, malformation, loss of the nail
  8. Tinea manus: hand
  9. Tinea versicolour: only tinea that does not cause itching, covers chest back and proximal extremities, flat scaly rash with different pigmentation, treated with topical antifungals.
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12
Q

Parasitic - Pediculosis - Lice
(Capitis, Corporis, Pubis)

A

Description: tiny insects live in skin with hair and feed off blood. Their saliva irritates the skin and causes an immune reaction that causes itching, highly infectious spread on contact or with shared items. Very common in school age children. Very small but eggs (nits) are more visible.
3 types: Head-pediculosis capitis: common in school
Body-pediculosis corporis: over the body or trunk
Pubic-pediculosis pubis: “crabs” spread via sexual contact

Etiology: parasite called lice

Pathogenesis: lice breaks the skin barrier and lives off blood. Their saliva irritates the skin and causes a hypersensitivity immune reaction causing itching.

Clinical Features: pruritus or itching

Treatment: parasite-killing soaps and shampoos, wash bed clothes and laundry well and good hygiene.

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13
Q

Mites or ScabiesVe hoặc ghẻ

A

Description: tiny mites related to ticks and spiders live in the epidermis for about 30 days, females also lay eggs ther. As they move around they leave wavy trails and create tiny red pustules (dermatitis) which causes intense itching (pruritus). Common locations are interdigital web spaces, extensor aspect of wrist, dorsum of feet, axilla, elbows, waist and pubic region. Infection by skin to skin contact. Do not survive well outside of the skin, laundering clothes and sheets kills them.

Etiology: mites in the family arachnida

Pathogenesis: tiny mites break the skin barrier and feed off skin. Their saliva irritates the skin and causes a hypersensitivity immune reaction causing itching.

Clinical Features: itchy and red skin, wavy trails, commonly affected include the interdigital web spaces, extensor aspect of the wrist, dorsum of the feet, axillae, elbows, waist, and genitalia. Symptoms are worse at night. Children affected on face, soles and palms only.

Treatment: topical antiparasitic cream, laundry of clothes and sheets.

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14
Q

Viral
Molluscum
Contagiosum

U mềm lây do virus

A

Description: common viral infection of the skin that causes benign, round, firm bumps (1-8mm), warts. Spreads through skin to skin contact or with contact with fomites. More common in children

Etiology: molluscum contagiosum virus

Pathogenesis: this virus replicates in and infects keratinocytes, inhibits the immune response and it causes the infected cells to grow and swell eventually making them burst spreading infectious debris

Clinical Features: raised, round, firm bumps that are approximately 1 - 8 mm in size, warts, may become itchy or inflamed, common on face, neck, armpits, genitals and tops of hands in children. Disappears within a year without treatment

Treatment: may be unnecessary, cryotherapy (liquid nitrogen) to remove, laser therapy, curettage, oral medication, topical cream.

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15
Q

Viral
Common Warts

A

Description: small, grainy skin growths often on fingers or hands. May also have tiny black dots from clotted blood vessels. Transmitted skin on skin. Harmless, usually painless and disappear on their own

Etiology: human papillomavirus (HPV) (with many subtypes)

Pathogenesis: virus enters through break in skin, hangnail, minor scrape or nail biting.

Clinical Features: small fleshy grainy bumps, flesh colored, white pink or tan in colour, rough to the touch, may have tiny black dots.

Treatment: may be unnecessary, cryotherapy (liquid nitrogen) to remove, laser therapy, minor surgery, oral medication or topical cream.

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16
Q

Acne Vulgaris

Mụn trứng cá

A

Description: hair follicle with accompanying sebaceous glands are obstructed or clogged with sebum and dead skin. This causes inflammation that forms papules, pustules, nodules, comedones (white and blackheads) and cysts. The bacteria cuti bacterium acnes colonizes in the debris and reproduces causing an inflammatory reaction. It is triggered by hormones of puberty when sebum production increases in the face, neck, arms and back. Cysts may cause scarring.

Etiology: cutibacterium acnes bacteria is colonized in the accumulation of sebum caused by an obstruction of the hair follicle and sebaceous gland.

Pathogenesis: the obstruction (filled with dead cells and sebum) is colonized by bacteria which then forms papules, pustules, nodules or cysts, comedones (whiteheads and blackheads) and causes an inflammatory reaction.

Clinical Features: papules, pustules, nodules, comedones (white and blackheads) and cysts.

Treatment: topical and oral antibiotics and medications.

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17
Q

Acne Rosacea Mụn trứng cá đỏ

A

Description: skin irritation with erythema, small pustules and telangiectasiasQ over malar area of face, common in 30-50 yo women, often triggered by a stressor.

  • Has 4 phases:
    Phase I: flushing, stinging, caused by triggers: spicy foods, stress or hot weather
    Phase II: erythema and telangiectasias develop
    Phase III: papules and pustules develop
    Phase IV: thickening of the skin occurs

Etiology: unknown, possible genetic component, venous drainage abnormalities, mites in the skin or idiopathic.

Pathogenesis: a triggered immune response
Clinical Features: facial redness, flushing, stinging, erythema, telangiectasias (spider veins) over face (malar areas), small pustules, thickened skin especially on nose. Common triggers: hot drink, spicy food, red wine, alcohol, sunlight, emotions, exercise or cosmetics.

Treatment: manage symptoms and avoid triggers, gentle cleansers and moisturizers, sun protection, topical medications

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18
Q

Pseudofolliculitis Viêm nang lông giả Barbae
(Shaving Rash or Razor Bumps)

A

Description: inflammation reaction of facial hair, just shaved hair growing backwards. It is caused by shaving also called razor burn

Etiology: irritation causes an immune response, possibly a bacterial infection

Pathogenesis: the hair breaks the skin barrier and causes an immune response with inflammation.

Clinical Features: predominantly affects african men (curly hair), in the beard and neck region, mild to moderate redness and irritation of skin causing red bumps that are itchy and painful.

Treatment: antibacterial topical, warm compresses, steroid topicals.

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19
Q

Alopecia (Hair Loss)

A

Description: hair loss affecting scalp or entire body, may be temporary or permanent and is more common in men.

Etiology: genetics, hormone changes, medical conditions, medications like chemotherapy, radiation therapy to the head, normal aging and extreme stress.

Pathogenesis: unknown, but immune response is triggered.

Clinical Features: gradual thinning, receding hairline or circular, patchy bald spots.

Treatment: some medications may help, hair transplant

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20
Q

Psoriasis

A

Description: chronic scaly silver coloured patches caused by overgrowth of epidermis and dermal papillae. Macules, papules and plaques (mildly itchy) are formed. The plaques form scales that may bleed and are mildly itchy. Breeding ground for staph and strep infections. Often affects scalp, extensor surfaces, sacrum, buttocks, knees and elbows and sometimes face. May cause nail deformities. Periods of flare ups and remission. Common triggers: infections, weather, sunburn, stress, smoking, alcohol and medications. Very common, affects 1-5% of population.

Etiology: genetic component

Pathogenesis: immune response that causes epidermis of skin to overgrow causing plaques.

Clinical Features: macules, papules,pustules, plaques are mildly itchy, affects scalp, extensor surfaces, sacrum, buttocks, face and nail deformities.

Treatment: no cure, sun exposure, topical creams, moisturizers, intense UV light therapy,

21
Q

Inflammatory Reactions to Drugs

Stevens-Johnson Syndrome

Phản ứng viêm do thuốc Hội chứng Stevens-Johnson

A

Description: much more severe reaction than erythema multiforme. A severe reaction to medications with flu like symptoms followed by rash. Larger proportion of the body is affected and there is more frequent involvement of mucous membranes, which can be severely affected and impair eating or urination. Lesions are similar to those of erythema multiforme but more likely to cause ulcers and vesicles/bullae.

Etiology: autoimmune disease, drug allergic reaction

Pathogenesis: altered drug metabolism triggers a severe immune response releasing perforins and granzymes that kill nearby cells and tissues.

Clinical Features: a more severe reaction than erythema multiforme, target shaped lesions on skin near or in mucous membranes, macular, vesicles, flu like symptoms, joint pain, malaise, fatigue, sore mouth or throat and may be fatal if more than 10% of body involved.

Treatment: medical emergency, hospitalization, immunosuppressants and steroids.

21
Q

Inflammatory Reactions
to Drugs

Erythema Multiforme

Phản ứng viêm do thuốc Ban đỏ đa dạng

A

Description: target-shaped lesions on the skin and mucous membranes, center is darker, with a lighter-colored periphery, usually macular, but can also exhibit papules and vesicles. Asymptomatic (no itching, pain) and tends to resolve on its own.

Etiology: autoimmune disease (50% from infection of herpes simplex virus) and possibly from a drug allergic reaction

Pathogenesis: hypersensitivity reaction triggered by infection

Clinical Features: target shaped lesions on skin near or in mucous membranes, macules and papules gradually enlarging to plaques, mild itching and burning, often on backs of hands, tops of feet and spreading to limbs and trunk, often asymptomatic, resolves quickly

Treatment: none required

22
Q

Types of Dermatitis (Eczema)

A
  1. Primary Irritant Contact
  2. Atopic
  3. Allergic Contact
  4. Nummular Dermatitis
  5. Dermatitis Stasis (Venous)
  6. Neurodermatitis
  7. Dermatitis Seborrheic
  8. Perioral Dermatitis
  9. Phototoxic or Photoallergic
23
Q

Dermatitis

Primary Irritant Contact

A

Primary Irritant Contact:

Description: inflammation of the skin characterized by edema, erythema and scaling. Itching, burning or stinging are also common. A nonspecific response of the skin to chemical damage.

Etiology: chemicals, microtrauma from frequent hand washing or dry atmosphere.

Pathogenesis: triggering of a nonspecific immune system response to chemical damage releases mediators of inflammation from epidermal cells.

Clinical Features: edema, erythema (redness), scaling, itching, burning, stinging and blisters

Treatment: removal of cause, lotions, moisturizers and topical steroid cream.

24
Q

Atopic Dermatitis

(Eczema)

Viêm da dị ứng (Bệnh chàm)

A

Description: chronic skin irritation, begins in early childhood, with pruritis, redness, mild edema, cracking as well as lichenification (skin thickening) as common symptoms. Found on hands, feet, ankles, wrists, neck, eyelids, inside elbow, knees and upper chest. Often accompanied by asthma or allergic rhinitis. Has periods of remission and flare ups.

Etiology: defect in genetic skin barrier functions allowing allergens into the dermis setting off a type I hypersensitivity reaction from the immune system.

Pathogenesis: allergens in the dermis cause an allergic reaction and inflammation.

Clinical Features: itching or pruritus, eczema, lichenification, redness, edema, accompanied by asthma or allergic rhinitis. Found on hands, feet, ankles, wrists, neck, eyelids, inside elbow, knees and upper chest.

Treatment: avoidance of irritants, anti inflammatories, steroid creams, moisturizers and light therapy.

25
Q

Allergic Contact
Dermatitis

A

Description: exposure to an allergen causes sensitization, but takes 48 - 72 hours to develop the response (antibodies), next exposure causes a Type IV delayed hypersensitivity reaction. Skin becomes intensely itchy with erythema, vesicle formation and sometimes bullae formation.

Etiology: allergen enters the skin breaking through the defensive barrier and cause a Type IV delayed hypersensitivity reaction. Common allergens are poison ivy, hair dye, nickel, leather, latex citrus peel.

Pathogenesis: allergen penetrates stratum corneum and activates Langerhans cells that then migrate to the lymph nodes where they initiate the immune response and inflammation.

Clinical Features: at site of exposure; intense itching or pruritus, erythema, vesicles and bullae formation.

Treatment: topical antibiotics, avoidance of irritant

26
Q

Nummular Dermatitis

Viêm da đồng tiền

A

Description: itchy, red rash over trunk and buttocks, may form small vesicles or scales. Lesion is macular or coin shaped. Affects middle-aged people, is exacerbated by dry skin, insect bites, scrapes or burns and is worse in the winter.

Etiology: idiopathic

Pathogenesis: environmental factors initiate an inflammatory reaction.

Clinical Features: itchy, burning, red rash comprised of coins shaped coloured lesions with scattered small vesicles.

Treatment: steroid topical cream

27
Q

Stasis (Venous) Dermatitis

Viêm da ứ đọng (tĩnh mạch)

A

Description: chronic condition that causes inflammation,ulcers and itchy skin on the lower legs. Affects sufferers with underlying vascular conditions like chronic venous insufficiency, varicose veins, deep vein thrombosis (DVT), hypertension, obesity, multiple pregnancies, kidney failure and congestive heart failure. Affects people over 50.

Etiology: poor blood circulation in lower legs due to faulty valves, blood pools in lower legs causing increased pressure and swelling in the veins.

Pathogenesis: swelling veins are damaged and become inflamed

Clinical Features: irritated and red, itchy swollen skin especially over a varicose vein, scaling and dryness, swollen ankles.

Treatment: compression stockings, sleeping with legs elevated, medications,

28
Q

Neurodermatitis

Viêm da thần kinh

A

Description: begins with one itchy patch of skin, when scratched causes more itch and a cycle of itching eventually causing thick leathery skin with scaly patches. Common sites are in the neck, wrist, forearms, legs or anal region. Itching may be intense and recurrent.

Etiology: unknown

Pathogenesis: irritant of any kind begins the scratch/itch cycle/

Clinical Features: itching may be intense, itchy patch or patches, leathery scaly skin, raised rough patches, common sites are in the neck, wrist, forearms, legs or anal region.

Treatment: anti itch medication, corticosteroid injections, anti anxiety drugs, light therapy and psychotherapy.

29
Q

Seborrheic Dermatitis

Viêm da tiết bã

A

Description: skin irritation close to sebaceous glands found on face, scalp (mostly) and trunk. Also known as dandruff. Symptoms include pruritus, scaly patches, dandruff, red skin, flaking and a yellow greasy scale. Often more severe with certain neurological disorders like Parkinson’s disease.

Etiology: idiopathic but may be linked to bacteria: pityrosporum ovale or to a fungus called malassezia, an abnormal immune response

Pathogenesis: defective barrier allowing penetration and immune response with inflammation.

Clinical Features: pruritus or itching, scaling or flaking and yellow greasy scales, found commonly on face, scalp (mostly) and trunk.

Treatment: anti inflammatory (corticosteroids) topical, antifungal topical and medicated shampoos or lotions

30
Q

Phototoxic or Photoallergic Dermatitis

Viêm da nhiễm độc ánh sáng hoặc dị ứng ánh sáng

A

Description: skin irritation from sunlight UV - A, sun exposure can cause conversion of a non-irritating substance to an irritating one, this is known as photosensitivity.

Etiology: sunlight UVA causes an immune reaction

Pathogenesis: an enzyme in the skin absorbs radiation in the UVA range and converts this into a photo-allergen which triggers an immune reaction.

Clinical Features: blister, itch, redness, inflammation, pain and a burning sensation, hyperpigmentations lasting weeks to months.

Treatment: avoidance, cold compresses and corticosteroids.

31
Q

Perioral Dermatitis

Viêm da quanh miệng

A

Description: inflammatory rash on skin around mouth, may spread to nose, eyes, forehead or chin. Rash consists of small red bumps that may contain fluids or pus, may look like acne.

Etiology: unknown, common triggers: use of topical steroids or nasal sprays for treatment of other conditions, cosmetics, bacterial or fungal infections, constant drooling, fluoridated toothpaste, oral contraception and sunscreens.

Pathogenesis: above substances cross the skin barrier which activates the innate immune response with inflammation

Clinical Features: scaly red bumpy rash around mouth, may spread to nose, eyes, forehead or chin, may have clear fluid discharge, slight burning or itching.

Treatment: topical or oral antibiotic, immunosuppressive and acne medication.

32
Q

Skin Cancer
Basal Cell Carcinoma

Ung thư biểu mô tb basal

A

Description: skin cancer of the basal cells. Basal cells are the stem cells of our skin, they sit on the basement membrane (innermost layer) and produce new skin cells as old ones die. Many different appearances on the skin and occurs on skin that is exposed to sun (UV radiation) especially the head and neck. Occurs more often in fair skinned and the elderly.

Etiology: long term exposure to UV radiation from sunlight or tanning beds, radiation therapy, exposure to arsenic, these damage the DNA of our basal cells and causes a mutation in the gene, also unknown, or genetics.

Pathogenesis: the mutation in the gene produces cancerous cells with uncontrolled cell growth and reproduction of dysfunctional cells that never die. They eventually form a mass or a tumour.

Clinical Features: develops on sun exposed parts of the body especially the head and neck. It is a change in the skin’s appearance, like a growth that won’t heal. May have one of the following characteristics: pearly white skin coloured or pink bump, a brown, black or blue lesion, a flat scaly reddish patch or a white waxy scar like lesion

Treatment: removal of cancer: surgery with radiation therapy, liquid nitrogen (cryosurgery), topical creams, avoidance of sun and sun screens.

33
Q

Basosquamous Cell Carcinoma

Ung thư biểu mô tế bào đáy

A

Description: skin cancer of the squamous cells of the skin (these cells form the middle and outer layers of the skin) and skin cancer of the basal cells (these cells form the innermost layer of skin or the basement membrane) combined. A rare form of skin cancer. Very invasive and metastatic. Found often in the head and neck and in the elderly.

Etiology: long term exposure to UV radiation from sunlight or tanning beds, radiation therapy, exposure to arsenic, these damage the DNA of our basal cells and causes a mutation in the gene, also unknown, or genetics.

Pathogenesis: the mutation in the gene produces cancerous cells with uncontrolled cell growth and reproduction of dysfunctional cells that never die. They eventually form a mass or a tumour.

Clinical Features: develops on sun exposed parts of the body especially the head and neck. It is a change in the skin’s appearance, like a growth that won’t heal. May have one of the following characteristics: pearly white skin coloured or pink bump, a brown, black or blue lesion, a flat scaly reddish patch or a white waxy scar like lesion

Treatment: removal of cancer with surgery followed by radiation and/or chemotherapy.

34
Q

Skin Cancer
Malignant Melanoma

Ung thư da Khối u ác tính

A

Description: skin cancer that develops from pigment producing cells in the skin called melanocytes. Sometimes starts in an existing mole. More common in fair skinned people with a history of sunburn and excessive sunlight exposure.

Etiology: unknown, exposure to UV radiation from sunlight or tanning beds increases risk.

Pathogenesis: the above causes damage to the genes of the DNA of melanocytes causing them to grow uncontrollably forming a mass. These cells are dysfunctional and never die.

Clinical Features: most often develops in sun exposed areas of body (but can also develop elsewhere), 1st symptoms is a change in an existing mole or the development of a new pigmented growth. The appearance is highly variable, we use the following acronym:
A: asymmetrical shape
B: borders that are irregular
C: changes in colour
D: diameter, larger than 6mm
E: evolving, changes over time

Treatment: surgery to remove melanoma and affected lymph nodes followed by radiation and chemotherapy.

35
Q

Cancer
Sebaceous Gland Neoplasm

Ung thư tuyến bã nhờn

A

Description: cancer of the sebaceous gland (produce an oil called sebum) of the skin (surrounding the hair follicle), glands of the eyelid are called meibomian glands often affects the eyelid and causes a firm, painless lump or skin thickening, it is rare, highest rate with elderly women, recurs often.

Etiology: unknown, damage to genes in the DNA
Pathogenesis: gene mutation causes uncontrolled cell growth, dysfunctional cells that do not die, they form a mass or tumour that spreads via continuous growth, through bloodstream and through lymphatic vessels.

Clinical Features: upper eyelid (specifically) upper tarsal plate) is most commonly affected, but could be anywhere sebaceous glands exist on the body. Tumour formed is a nodule that is hard and immobile and yellowish in colour, may metastasize to the orbits or to the parotid gland.

Treatment: surgery

36
Q

Cutaneous Papilloma (U nhú ở Da)

(Skin Tag or Acrochordon)

A

Description: a noncancerous skin tag or benign growth, may have a stalk or peduncle. May appear anywhere but common on eyelids, neck armpits, upper chest and groin. Especially common where skin rubs together or in a skin fold. Usually asymptomatic, do not spread and do not have aggressive growth. Linked to a higher risk of cancer.

Etiology: from skin rubbing together and aging, also possibly from low risk human papillomavirus (HPV), genetics, associated with lipidemia, type 2 diabetes, obesity and cardiovascular disease.

Pathogenesis: epidermis is hyperkeratotic with basal cells that are flattened out which increases pigmentation with extra mass of loose fibrous tissue.

Clinical Features: asymptomatic skin coloured or hyperpigmented benign growths, may be 2-5 mm in size or larger. May appear anywhere but common on eyelids, neck armpits, upper chest and groin. Especially common where skin rubs together or in a skin fold.

Treatment: liquid nitrogen (cryosurgery), removal with scissors or scalpel.

37
Q

Urticaria (Hives)

Mề đay (Mề đay)

A

Description: known as hives, are swollen, pale red, bumps, welts or plaques, on the skin that are itchy, they usually form batches, heat, exercise and stress triggers a flare.

Etiology: unknown or allergens

Pathogenesis: allergens cause a release of histamine from a mast cell and other inflammatory chemicals into the bloodstream causing itching, redness and swelling.

Clinical Features: skin rash with swollen pale red bumps or welts, can be intensely itchy and is triggered by allergens, heat, exercise and stress.

Treatment: antihistamines, anti itch and anti inflammatory medications.

38
Q

Pathology - Skin
Corns

A

Description: hard thickened areas of skin typically occurring on the feet. They develop in areas of high friction and pressure as a protective mechanism. They are similar to a callus, but harder, smaller and more painful.

Etiology: mechanical trauma, wearing shoes that don’t fit or wearing no socks.

Pathogenesis: constant friction and pressure instigate focal or localized hyperplasia of the epidermis or abnormal growth.

Clinical Features: a hard centre (bump) surrounded by inflamed skin, it is tender under the skin, most common in feet and develop where there is high friction or pressure spots.

Treatment: soak in warm water, sand with a pumice stone, use padding, wear loose fitting shoes, if possible.

39
Q

Callus

mô sẹo

A

Description: hard thickened areas of skin typically occurring on the feet. They develop in areas of high friction and pressure as a protective mechanism. Larger than corns.

Etiology: mechanical trauma, wearing shoes that don’t fit or wearing no socks.

Pathogenesis: constant friction and pressure instigate focal or localized hyperplasia of the epidermis or abnormal growth.
Clinical Features: a thick, rough area of skin, most common in soles of feet where there is high friction or pressure spots. Larger than corns.

Treatment: soak in warm water, sand with a pumice stone, use padding, wear loose fitting shoes, if possible.

40
Q

Bunion

A

Description: a bony bump that forms at the base of your metatarsophalangeal (MTP) or big toe joint. Skin may be red and tender. Possibly caused by wearing tight, narrow, high heels.

Etiology: improper shoe wear, foot stresses or injuries or congenital anomalies

Pathogenesis: genetics, lateral bursa at the MTP joint swells causing the bones to move inward towards the second toe

Clinical Features: bulging bump at the outside base of the big toe, swelling, redness and tenderness, corns and calluses sometimes develop between the big toe and the second toe, pain that is intermittent or continuous causing limited motions.

Treatment: change shoes, padding, orthotics, ice, medications or surgery.

41
Q

Pathology - Skin
Ichthyosis (Vulgaris)

Bệnh vảy cá

A

Description: a genetic disorder characterized by dry, thickened scaly skin due to dead skin cells accumulating on the skin’s surface. Appears during early childhood and ranges in severity from very mild to severe. Often found on elbows and lower legs especially the shins. Worse in cold dry environments.

Etiology: genetic mutation

Pathogenesis: slowing of the skin’s natural shedding process

Clinical Features: dry scaly skin, scales are white, grey or brown, may have deep painful cracks in the skin and a flaky scalp.

Treatment: no known cure, management of symptoms, exfoliating creams or retinol creams.

42
Q

Pathology -

Skin Vitiligo

bệnh bạch biến

A

Description: skin loses pigment cells called melanocytes resulting in discoloured patches of skin, hair and mucous membranes. Often begins on hands, forearms, feet and face but may be anywhere and can change over time. Common with people age 10 to 30.

Etiology: autoimmune, genetics, toxic substances or stress may be triggers.

Pathogenesis: autoimmune reaction that destroys melanocytes and their function of skin colour production.

Clinical Features: painless loss of skin pigmentation usually in patches.

Treatment: no cure, camouflage therapy (using differing sunscreens or makeup & hair dye), repigmentation therapy, light therapy or surgery (skin grafts).

43
Q

Pathology - Skin

Burns

A

Description: severe skin damage causing skin cells to die, from excessive heat, chemicals, fire, electricity.
First Degree: dermis only affected, red non blistered skin, minimal damage, inflammation or swelling, pain, dry peeling skin, heal within 7-10 days, treated at home with cool water

Second Degree: dermis and part of epidermis affected, blisters, red and painful with thickening of skin, heal within 3 weeks, cool water and analgesics.
Third Degree: dermis, epidermis and hypodermis all affected, most severe, widespread thickness with white leathery appearance, heals with scarring without surgery, requires immediate medical attention, high risk of infection.

Etiology: contact on skin with hot liquid, chemicals, electricity, fire, or excessive sun exposure.

Pathogenesis: skin destroyed by damage releases systemic inflammatory mediators and cytokines that increase capillary permeability causing severe leakage. Interleukin and tumor necrosis factor are also released causing inflammation and starting the wound healing process.

Clinical Featurs: blisters, pain, peeling and red skin, swelling and scarring if severe.

Treatment: cool water, if severe immediate medical attention.

44
Q

Open Wounds
or Ulcer & Sores

A

Description: break in the skin barrier, open wound or ulcer, risk of infection.

Abrasion: rubs against or scrapes a hard surface like road rash)
Laceration: deep cut or tearing of skin-knife, tools, bleeding may be severe)
Puncture: small hole-long pointy object-may damage internal structures)
Avulsion: partial or complete tear of the skin away from the tissues underneath, bleeding may be severe

Etiology (cause): injury, poor circulation or too much pressure.

Pathogenesis: damage causes blood loss and the beginning of the wound healing phases with inflammation.

Clinical Features: break in the skin with redness, pain and bleeding depending how severe.

Treatment: if deeper than ½ inch or bleeding doesn’t stop seek immediate medical attention, risk of infection is high.

45
Q

Scars

A

Description: fibrous tissue replaces normal skin tissue after an injury and after the normal process of wound healing.

Etiology: normal byproduct of the healing process in wound repair

Pathogenesis: collagen fibres are produced and replace damaged tissue forming the scar.

Clinical Features: at the site of a previous injury, different texture and colour as surrounding skin tissue. Usually flat and pale but may be more severe and become hypertrophic or keloid scars.

Treatment: topical creams, surgery, steroid injections, dermabrasion, laser resurfacing, cryosurgery, filler injections.

46
Q

Pathological Scars

Keloid

A

Definition or description: a raised scar comprised of excessive fibrous tissue that forms over a wound to protect the injury site. They are larger than the original wound. Most common in chest, shoulders, earlobes and cheeks. Not harmful but may be itchy.

Etiology: overgrowth of fibrous scar tissue at the site of acne, burns, chickenpox scars, ear piercing, scratches, surgery and vaccination site or genetics.

Pathogenesis: imbalances occur in the healing process that produces more collagen that it degrades causing the scar to excessively grow.

Clinical Features: scar that is larger than original wound, take weeks to months to develop.

Treatment: surgery

47
Q

Pathological Scars

Hypertrophic

A

Definition or description: a thickened, wide and raised scar comprised of excessive fibrous tissue that forms over a wound to protect the injury site (to a lesser degree than keloid scars), may form after burns, piercings, cuts or acne. Does not grow beyond the boundaries of the original wound (unlike keloid).

Etiology (cause): overgrowth of fibrous (collagen) scar tissue at the site of injury, an abnormal response.

Pathogenesis: imbalances occur in the healing process that produces more collagen that it degrades causing the scar to excessively grow.

Clinical Features: scar over an original wound, asymptomatic usually except some mild itching.

Treatment: laser therapy, corticosteroid injections, cryotherapy or surgery.