Serm 2

Front 1

Essentials of Diagnosis Molluscum Contagiosum.

Back 1

(1) Caused by a pox virus.
(2) Lesions are autoinoculable and spread by wet skin-to-skin contact.
(3) Principle sites of involvement are the face, lower abdomen and genitals.

Front 2

General consideration of Molluscum Contagiosum

Back 2

Molluscum Contagiosum is a localized, self-limited viral infection of the skin. It is spread on the skin by autoinoculation and is transmitted to others by skin-to-skin contact.
May occur at any age.
Peaks in ages between 3-9 years and again between the ages of 16-24 years.

Front 3

Physical findings in regarded to Molluscum Contagiosum

Back 3

Most lesions are asymptomatic, although tenderness and itching can occur and are usually associated with mild local inflammation.
(2) Begins as a 1-2 mm shiny, white to flesh-colored, dome-shaped firm papule.
(3) Small central whitish umbilication that is best seen under magnification.
(4) Over the course of a few weeks, lesion maintains its discrete dome shape with central punctum, attaining a maximum size of 2-5 mm.

Front 4

Untreated lesions usually persist for 6-9 months before slowly involuting. Typically does not leave any mark, but rarely a minute, pitted scar remains.

Back 4

True

Front 5

Lab/Imaging Findings

Back 5

(1) Skin biopsy is rarely needed.

Front 6

Differential Diagnosis

Back 6

(1) Flat or Genital warts
(2) Herpes Simplex Virus

Front 7

Non medicinal treatment

Back 7

(1) Skin-to-skin contact should be avoided to minimize transmission of the virus
(2) Due to spontaneous resolution of lesions and risk of scarring from treatment, decision to treat must be made on individual basis.
(3) Genital lesions in sexually active adults should be treated.
(a) Sexual partners of affected individuals should be checked for lesions.
(4) Curettage to remove the central core of the lesions is fairly painless and clears the lesion immediately.
(a) Particularly useful for genital lesions.
(b) Some risk of scarring. Caution should be used, especially on the face.

Front 8

Treatment of Molluscum Contagiosum

Back 8

Cryosurgery with Liquid Nitrogen is effective and may produce scarring.
(a) Can be painful, especially for genital lesions.
(6) Canthardin 0.7% is painless, effective and well tolerated.
(7) Aldara or Tretinoin can also be applied to lesions to hasten resolution.

Front 9

Disposition

Back 9

Full Duty. Light duty may be warranted based on occupation, location of infection and treatment plan.

Front 10

Complications

Back 10

Secondary bacterial infection

Front 11

Recurrent small grouped vesicles on an erythematous base, especially in the orolabial and genital areas.
(b) May follow minor infections, trauma, stress or sun exposure; regional lymph nodes may be swollen and tender.
(c) Viral cultures and direct fluorescent antibody tests are positive.

Back 11

Herpes Simplex Virus (HSV)

Front 12

There are two immunologic types of HSV:

Back 12

HSV Type 1 – generally associated with vesicular ulcerative oral infections
HSV Type 2 – usually genital infections.

Front 13

HSV infections have two phases:

Back 13

1) Primary infection – the virus becomes established in a nerve ganglion.
2) Secondary infection - characterized by recurrent disease at the same site

Front 14

Virus remains dormant in the nerve ganglia and recurrent herpetic eruptions can be precipitated by:

Back 14

1) Overexposure to sunlight
2) Febrile illnesses
3) Physical or emotional stress
4) Immunosuppression
5) Certain foods/drugs

Front 15

Describe the genital HSV

Back 15

Common sexually transmitted disease caused by the HSV-2 virus.

Primary infection is followed by recurrent outbreaks of grouped vesicles on an inflamed red base.
Many cases transmitted by people who are unaware they have the infection or are asymptomatic when transmission occurs.

Front 16

Describe the primary infection of HSV

Back 16

2-20 days after exposure, influenza-like symptoms (fever, headache, malaise, myalgias) begin with complaints peaking 3-4 days after viral vesicles develop.
b) Tender lymphadenopathy occurs in the second and third weeks.

Front 17

Describe the Recurrent Infection of HSV

Back 17

a) Influenza-like symptoms are less intense or most often are absent.
b) Prodrome is described as burning or itching in the infected area.
c) Chronic, relapsing course is common.

Front 18

Physical findings of primary infection

Back 18

May be spread by respiratory droplets, direct contact with an active lesions or contact with virus-containing fluid (saliva, cervical secretions)
a) Symptoms occur from 3-7 days or more after contact.
3) Tenderness, pain, mild paresthesias or burning occurs before the onset of lesion at site of inoculation.

Front 19

Vesicles in primary HSV are more numerous and scattered than in recurrent infection.

Lesions last for 2-6 weeks and heal without scarring.
a) Virus enters the nerve endings in the skin directly below the lesions and ascends through peripheral nerves to the dorsal root ganglia, where it remains in a latent stage.

Back 19

True

Front 20

Physical findings of Recurrent Infection

Back 20

Recurrence rate is the same as for patients who had a symptomatic or asymptomatic primary infection.
Prodromal symptoms, lasting 2-24 hours can resemble those of primary infection. Tenderness, pain, mild paresthesias or burning occurs before the onset of lesions in the focal area of the primary infection.
3) Within 12 hours, group of lesions evolves rapidly from an erythematous base to form papules and then vesicles.

Front 21

Dome-shaped, tense vesicles rapidly umbilicate.
5) In 2-4 days, the vesicles rupture, forming aphthae-like erosions in the mouth and vaginal area or erosions covered by crusts on the lips and skin.
6) Crusts are shed in approximately 8 days to reveal a pink, re-epithelialized surface.
7) Systemic symptoms and lymphadenopathy are rare unless there is secondary infection.

Back 21

True

Front 22

Lab/Imaging Findings

Back 22

(a) Viral culture
(b) Serology testing - can be performed for virus types 1 and 2.

Front 23

Differential Diagnosis

Back 23

(a) Hand, Foot and Mouth disease

(b) Aphthous Stomatitis
(c) Erythema Multiforme
(d) Impetigo
(e) Herpes Zoster

Front 24

Topical agents can be used for relief of pain. Examples are:

Back 24

a) Tetracaine cream 1.8% reduces the healing time of recurrent herpes labialis lesions by about two days when applied frequently.
b) Abreva – non-prescription topical cold sore medication that shortens healing time by about ½ a day.
c) Penciclovir cream reduces the duration of herpes labialis by about ½ a day. It is very expensive

Front 25

Oral antiviral therapy is initiated at the first sign or symptom.
a) Most effective when administered within_______

Back 25

48 hours of the onset of signs and symptoms.

Front 26

Frequency and severity of episodes of untreated Herpes may change over time. After 1 year of suppressive therapy, the frequency and severity should be_______

Back 26

reevaluated to assess the need for continued therapy

Front 27

Valacyclovir therapy

Back 27

Initial episodes – 1 g PO BID for 10 days.
Recurrent episodes – 500 mg PO BID for 3 days.
Suppressive therapy – 1 g PO QD.

Front 28

Famciclovir therapy

Back 28

Recurrent episodes – 125 mg PO BID for 5 days.
Suppressive therapy – 250 mg PO BID for 1 year.

Front 29

Acyclovir therapy

Back 29

Initial episodes – 200 mg PO 5 times daily for 10 days.
Recurrent episodes – 400 mg PO TID for 5 days.
Suppressive therapy – 400 mg PO BID for up to 12 months.

Front 30

Counselling needed for the patient with hsv

Back 30

There is currently no permanent cure for Herpes Simplex virus.
b) The natural history of the disease, the potential for recurrent episodes, asymptomatic viral shedding and sexual transmission should be explained.
c) Patient should be instructed to use condoms during all sexual exposures with new or unaffected sex partners.

Front 31

Systemic Therapy

Back 31

Antiviral drugs partially control the symptoms and signs of herpes eruptions.
These drugs neither eradicate latent virus nor affect the risk, frequency or severity of recurrences after the drug is discontinued.

Front 32

Primary infection treatment

Back 32

Treatment should be initiated within 72 hours of the onset of signs and symptoms.
(2 Valacyclovir (Valtrex) 1 g every 12 hours for 10 days
(3 Famciclovir (Famvir) 250 mg can be administered every 8 hours for 10 days
(4 Acyclovir (Zovirax) on one of the following schedules for 10 days:
(a 200 mg every 4 hours
(b 400 mg every 8 hours
(c 800 mg every 12 hours

Front 33

Cool, wet water dressings may suppress inflammation.
Severe primary infections can be treated intravenously with Acyclovir 5 mg/kg every 8 hours for 7 days.

This regimen should be considered in immunocompromised patients.

Back 33

True

Front 34

Recurrent Infections treatment

Back 34

(1 Treatment with one of the following regimens is initiated within 24-48 hours of the onset of signs and symptoms.
(a Valacyclovir 500 mg every 12 hours for 5 days
(b Famciclovir 125 mg every 12 hours for 5 days
(c Acyclovir 400 mg every 8 hours for 5 days
(2 Patients should be provided with a prescription for the medication so that treatment can be started at the first sign of prodrome or genital lesion.

Front 35

Suppressive Therapy:

Back 35

Valacyclovir 500 mg - 1 g daily can be prescribed for fewer than 9 recurrences a year.
Famciclovir 250 mg BID

Acyclovir 400 mg BID

Front 36

Treatment is continued for at least 6-12 months.
(5 If treatment is successful, a trial without medication may be considered.
(6 Daily suppressive therapy reduces the frequency of genital herpes recurrences by 75% among patients who have frequent recurrences (6 or more recurrences per year).
(7 Suppressive treatment reduces but does not eliminate asymptomatic viral shedding.

Back 36

True

Front 37

Complications

Back 37

(a) Pyoderma
(b) Eczema Herpticum
(c) Herpetic Whitlow
(d) Ocular Keratitis

Front 38

Essentials of Diagnosis of Herpes Zoster (Shingles)

Back 38

(a) Pain along the course of a nerve followed by grouped vesicular lesions.
(b) Involvement is unilateral; some lesions (< 20) may occur outside the affected dermatome.
(c) Lesions are usually on the face or trunk.
(d) Direct fluorescence antibody positive, especially in vesicular lesions.

Front 39

Physical findings of Herpes Zoster (Shingles)

Back 39

Pre-eruptive tenderness or hyperesthesia throughout the dermatome is a useful predictive sign.
(b) Pain, itching or burning, generally localized to the dermatome, may precede the eruption by 4 or 5 days.
(c) Usually limited to the skin of a single dermatome, but may involve one or two adjacent dermatomes

Front 40

Eruption begins with red, swollen plaques of various sizes and spreads to involve part or all of a dermatome.
(e) Vesicles arise in clusters from the erythematous base and become cloudy with purulent fluid by the third or fourth day.
(f) Vesicles vary in size and either umbilicate or rupture before forming crusts, which fall off in 2-3 weeks.

Back 40

True

Front 41

Lab/Imaging Findings

Back 41

(a) Viral culture
(b) Tzanck smear

Front 42

Differential Diagnosis

Back 42

(a) Poison Oak dermatitis
(b) Herpes Simplex virus
(c) Eczema Herpeticum
(d) Smallpox
(e) Folliculitis

Front 43

Treatment plan

Back 43

(a) Topical therapy can be tried. Cool tap water dressings are applied for 20 minutes several times a day.
(b) Oral steroids decrease acute pain and result in a quicker rash resolution.
(c) Oral antivirals drugs decrease acute pain, inflammation, vesicle formation and viral shedding.
(d) Treatment is most effective when started in first 48 hours of infection.

Front 44

It is reasonable to use antiviral therapy more than 48 hours after vesicles appear if lesions are not completely crusted.

Back 44

True

Front 45

Recommended oral dosage for adults:

Back 45

1) Acyclovir – 800 mg PO 5 times a day for 7-10 days.
2) Valacyclovir – 1 g PO TID for 7-10 days.
3) Famciclovir – 500 mg PO TID for 7-10 days.

Front 46

Disposition of pt with Herpes Zoster (Shingles)

Back 46

Light duty – based on location, presentation of patient, symptoms, pain management and complications.
Patients with Herpes Zoster on the face should be referred to Medical Officer for further evaluation.

Front 47

Complications of pt with Herpes Zoster (shingles)

Back 47

(a) Postherpetic Neuralgia – common after involvement of the trigeminal region and patients over the age of 55.
(b) Neurogenic bladder – Sacral zoster may be associated with bladder and bowel dysfunction.
(c) Secondary bacterial infections
(d) Herpes Zoster Opthalmicus – can result in visual impairment

Front 48

Contact Dermatitis
Essentials of Diagnosis

Back 48

Erythema and edema, with pruritis, often followed by vesicles and bullae in an area of contact with a suspected agent.
(b) Later, weeping, crusting or secondary infection.
(c) A history of previous reaction to suspected contactant.
(d) Patch test with agent positive.

Front 49

Describe Irritant Contact Dermatitis

Back 49

1) Eczematous dermatitis often caused by repeated exposure to mild irritants such as water, soaps, heat and friction. Strong irritants include acids, alkalis, and wet cement.
2) The intensity of the inflammation is usually related to the concentration of irritant and exposure time. Mild irritants cause dryness, fissuring and erythema

Front 50

Strong irritant chemicals may produce an immediate reaction characterized by burning, erythema, edema and possibly ulceration of the skin.

Back 50

True

Front 51

Approximately 80% of Contact Dermatitis cases involve exposure to irritants.
4) Background of atopy (hay fever, asthma or eczema) predisposes to an increased susceptibility to skin irritation.
5) Occupation and household chores are critical parts of the patient history.
6) Common irritants include detergents, acids, alkaline chemicals, oils, oxidants and water.

Back 51

True

Front 52

Describe Allergic dermatitis

Back 52

Allergic Contact Dermatitis
1) A delayed-type hypersensitivity reaction caused by skin contact with an allergen.
2) Sensitization is required and allergy is specific to a particular chemical.
3) Poison ivy, poison oak and poison sumac are prototypes of allergic contact dermatitis.
4) Common causes include metals (nickel, and chromate), rubber additives in gloves and shoes, preservatives or additives in skin lotions, sunscreens cosmetics and toiletries and topical medications.

Front 53

Initial exposure and primary sensitization result in clinical inflammation generally 14-21 days after exposure. Exposure to a chemical is required for allergy to develop!
6) The time required to develop clinically apparent inflammation is about 12-48 hours, but may vary from 8-120 hours. The rash is delayed somewhat from the contact and can last as long as 3 weeks after one exposure.
7

Back 53

True

Front 54

Describe the clinical findings of Allergic dermatitis

Back 54

The hands are most often affected. Both dorsal and palmar surfaces can be affected.
2) Erythema, dryness, painful cracking or fissuring and scaling are typical. Vesicles may be present.
3) Tenderness and burning are common and predominate the itching.
4) Acute irritant dermatitis may show juicy papules and/or vesicles on an erythematous patchy background with weeping and edema.

Front 55

Lab/Imaging Findings of Allergic dermatitis

Back 55

(a) KOH to exclude tinea infection
(b) Patch testing - evaluates the role of allergic contact dermatitis if history suggests it.

Front 56

Differential Diagnosis

(a) Irritant Contact Dermatitis:

Back 56

1) Allergic Contact Dermatitis
2) Atopic Dermatitis
3) Tinea infection

Front 57

Differential Diagnosis

Allergic Contact Dermatitis:

Back 57

1) Irritant Contact Dermatitis
2) Atopic dermatitis
3) Cellulitis
4) Rosacea

Front 58

Treatment of Irritant Contact Dermatitis:

Back 58

Early diagnosis, treatment and preventative measures can prevent the development of a chronic irritant dermatitis.
Avoidance of or decreased exposure to cutaneous irritants is critical for recovery of an effective skin barrier.

Medium or high-potency topical steroid ointment applied BID for several weeks can be helpful in reducing erythema, itching, swelling and tenderness.

Front 59

Allergic Contact Dermatitis:

Back 59

1) Identification and avoidance of the allergenic substance is essential to recovery.
2) Topical treatment using topical corticosteroid. Discontinue all moisturizers, lotions and topical products.
3) For severe or generalized allergic contact dermatitis, 3 week tapering course of oral corticosteroids is appropriate. Do not rely on this treatment repeatedly!
4) Antihistamines (except for their sedative effect) are ineffective in contact dermatitis.
5) Educate patient, detailing potential sources of exposure.

Front 60

Disposition of the patient with dermatitis

Back 60

Based on presentation of patient, pain level and complications. Light duty may need to be given until irritation has resolved.

Front 61

Complications

Back 61

(a) Anaphylaxis
(b) Secondary infection

Front 62

Essentials of Diagnosis Atopic dermatitis

Back 62

(a) Pruritic, exudative or lichenified eruption on the face, neck, upper trunk, wrists and hands and in the antecubital and popliteal folds.
(b) Personal and family history of allergic manifestations (asthma, allergic rhinitis, atopic dermatitis).
(c) Tendency to recur.
(d) Onset in childhood in most patients. Onset after age 30 is very uncommon.

Front 63

________is an eczematous eruption that is distressingly pruritic, recurrent, often flexural and symmetric.
Generally begins early in life and is characterized by periods of remission and exacerbation. The distribution of affected skin varies with age.

Back 63

Atopic Dermatitis

Front 64

Major Criteria (Four required for Diagnosis)

Back 64

1) Pruritis. 2) Young age at onset
3) Typical morphology and distribution
4) Flexural lichenification and linearity in adults, facial and extensor involvement in infants.
5) Chronic or chronic and relapsing course.
6) Personal or family history of asthma, allergic rhinitis or atopic dermatitis.

Front 65

This Incidence is 7-24 per 1000 and appears to be on the rise. Most common in children.
Aggravating factors include irritants and allergens, perspiration, excessive heat, rough fibers, thight clothing, cool dry air and emotional stress.

Back 65

Atopic dermatitis

Front 66

Physical Findings of atopic dermatitis

Back 66

(a) Atopic inflammation often begins abruptly with erythema and severe pruritis.
(b) Typical lesions are red pruritic papules, patches of erythema and scaling.
(c) Acute lesions may be oozing and vesicular. Sub-acute lesions are scaly and crusted. Chronic lesions are often dull red, lichenified and very pruritic.

Front 67

Distribution varies according to age.
1) Infantile Phase (2 months to 2 years):

Back 67

a) Atopic dermatitis appears on the cheeks, perioral area and scalp.
b) Extensor tops of the feet and the elbows are often involved.

c) Lesions are often exudative and weeping.

Front 68

2) Childhood Phase (2 – 12 years):

Back 68

a) Flexural involvement is typical.
b) Scratching and chronicity lead to lichenification

Front 69

3) Adult Phase (12 years to Adult):

Back 69

a) Flexural involvement is common.
b) Hand dermatitis may be the only manifestation.
(1 Dermatitis of the upper eyelid is another frequent finding.
c) Can be diffuse and patchy on the body.
d) Associated findings are dry skin, icthyosis vulgaris and keratosis pilaris.

Front 70

Lab/Imaging Findings

Back 70

(a) Not routinely indicated or performed.

Front 71

Differential Diagnosis of atopic dermatitis

Back 71

(a) Irritant or Allergic Contact Dermatitis
(b) Nummular Eczema
(c) Seborrheic Dermatitis
(d) Scabies
(e) Tinea Infections

Front 72

Treatments of Atopic dermatitis

Back 72

(a) Inflammation and infection should be controlled or eliminated.

(b) Topical steroids are applied BID to inflamed skin for 10-21 days.
(c) Oral antibiotics are administered for secondary infection.
(d) For acute lesions and severe flares, wet dressings with Burrow’s solution are applied for 20 minutes BID-TID, followed by application of a topical steroid.

Front 73

Bland emollients such as Vaseline petroleum should be used. A plain, thick, greasy moisturizer without fragrance or sensitizing preservatives is ideal and is preferred to commonly available lotions or creams.
(f) Aggravating factors must be eliminated or controlled.
(g) Pruritis must be controlled. Oral antihistamines with sedative effects are helpful, especially at night to allow for more restful sleep.
(h) Dermatologist should be consulted for management of severe, refractory disease.

Back 73

True

Front 74

Disposition

Back 74

(a) Full duty – Light duty may be indicated based on severity of condition, occupation and control of aggravating factors.

Front 75

Complications of Atopic dermatitis

Back 75

(a) Secondary infection
(b) Increase susceptibility to Viral infections
(c) Hypopigmentation or hyperpigmentation may result from previous inflammation.
(d) Emotional and/or behavioral problems.

Front 76

Essentials of Diagnosis of Seborrheic Dermatitis

Back 76

Dry scales and underlying erythema.

Scalp, central face, presternal, interscapular areas, umbilicus and body folds.

Front 77

_________is a common, chronic, inflammatory papulosquamous disease.
All ages can be affected.
(Greater severity and more difficult to treat in patients with neurologic disease or HIV infection.

Back 77

Seborrheic Dermatitis

Front 78

Physical Findings of Seborrheic Dermatitis

Back 78

(a) Papules are moist, transparent to yellow, greasy and scaling, among coalescing red patches and plaques.
(b) May be diffuse, though usually favors areas of maximal sebaceous gland concentration; the scalp margins, central face and pre-sternal areas.
(c) Characteristic locations are the eyebrows, the base of the eyelashes, nasolabial folds and paranasal skin and external ear canals.
(d) May affect flexural skin including the postauricular, inguinal and inflammatory folds as well as the anogenital area.

Front 79

Lab/Imaging Findings of Seborrheic Dermatitis

Back 79

(a) KOH and fungal culture are indicated
(b) Skin biopsy in not usually necessary.

Front 80

Differential Diagnosis of Seborrheic Dermatitis

Back 80

(a) Tinea of the face
(b) Cutaneous Lupus
(c) Rosacea
(d) Psoriasis
(e) Pemphigus Foliaceous

Front 81

Treatment of Seborrheic Dermatitis

Back 81

(a) Flares are precipitated by stress, fatigue and seasonal climate changes.
(b) Mild to moderate facial Seborrheic Dermatitis may respond well to topical antifungal creams (Ketoconazole, Ciclopirox).
(c) Daily facial washing with antidandruff shampoo or soaps diluted with water is also effective.
(d) Steroid creams or lotions applied BID for several days may be required for control

Front 82

Mild to moderate scalp involvement is best managed with frequent and extended shampooing with antidandruff shampoos.
1) Effective formulations may contain Ketoconazole (Nizoral), coal tar (Tarsum, T-Gel), selenium sulfide (Selsun) and zinc pyrithione (Head and Shoulders).
(f) Dense, thick, adherent scale is removed by applying warm mineral oil to scalp and washing several hours later.
(g) Severe cases may require oral antifungal therapy.

Back 82

True

Front 83

Disposition Seborrheic Dermatitis

Back 83

(a) Full Duty

Front 84

(9) Complications of Seborrheic Dermatitis

Back 84

(a) None

Front 85

Essentials of Diagnosis of uticaria

Back 85

(1) Eruptions of evanescent wheals or hives.
(2) Special forms of urticaria have special features (dermatographism, cholinergic urticarial, solar urticarial or cold urticaria).

Front 86

(3) Most incidents are acute and self-limited over a period of 1-2 weeks.
(4) Chronic urticaria (episodes lasting > 6 weeks) may have an autoimmune basis.

Back 86

true

Front 87

Urticaria is divided into acute and chronic forms, which is based on__________

Back 87

the duration of the hives.

Front 88

Describe Acute Urticaria

Back 88

(a) Variably pruritic, common, distinctive reaction pattern
(b) By definition, lasts for less than 6 weeks while chronic urticarial lasts more than 6 weeks.
(c) Transient, edematous, red plaques vary in size and shape. Individual lesions last less than 24 hours.
(d) May occur at any age.
(e) It is more common in atopic individuals

Front 89

Etiology is undetermined in some cases.
Histamine released by allergens (drugs, foods, pollens) is mediated by immunoglobulin E.
Histamine release is the most important cause
Hives are notoriously pruritic. The pruritus is milder in deeper forms(angioedema).

Back 89

Acute urticaria

Front 90

Describe Chronic Urticaria

Back 90

(a) Defined as urticarial or whealing of the skin for more than 6 weeks.
(b) Cause is discovered in only 5 – 20% of cases.
(c) Affects all ages, but highest incidence is in young adults.
(d) Easily diagnosed but presents a major problem in treatment and management.

Front 91

Course of this disease is unpredictable, can last months or years.
Patient should be evaluated for the five I’s:

Back 91

Chronic articuria

Front 92

five I’s of Urticaria

Back 92

1) Ingestants (common) – foods, additives and drugs such as antibiotics or other drugs that are relatively new to the patient.
2) Inhalants – dust, feather, pollen
3) Injectants – drugs, stings, bites
4) Infections – bacterial, viral, fungal, parasitic
5) Internal Diseases – chronic infections, thyroid disease, lupus erythematosus

Front 93

Physical findings of urticaria

Back 93

(a) Plaques are pink to flesh-colored, non-pitting and edematous.
(b) Lesions may be uniformly red, pink or flesh-colored or surrounded by a white or red halo.
(c) Lesions may vary in size and are round or oval; when confluent, then become polycyclic.
(d) Plaques change in size and shape by peripheral extension, migrate and regress.
(e) A dynamic process, new lesions evolve as old ones resolve.
(f) Rarely, bullae or purpuric lesions appear with intense swelling.
(g) Distribution is usually generalized and haphazard.

Front 94

Physical findings of Chronic Urticaria

Back 94

(a) Pink to red, figurate and annual, edematous, migrating wheals or plaques.
(b) Lesions vary in size from just millimeters to areas that can cover an entire hand.
(c) Plaques can be coalescing polycyclic and change in size and shape over time.

(d) Individual lesions resolve within 24 hours, while new lesions appear.

Front 95

Lab/Imaging Findings

Back 95

(1) No routine studies are required to make diagnosis.

Front 96

Differential Diagnosis
(1) Acute Urticaria:

Back 96

(a) Urticarial Vasculitis
(b) Drug eruption
(c) Viral exanthema
(d) Bites (popular urticaria)
(e) Bullous pemphigoid (elderly)
(f) Hereditary angioedema

Front 97

Chronic Urticaria:

Back 97

(a) Physical Urticaria
(b) Erythema Multiforme
(c) Urticraial Vasculitis
(d) Bullous pemphigoid

Front 98

Treatment
(1) Acute Urticaria

Back 98

(a) All suspected triggers (drugs, food and drink, inhalants) should be discontinued.
(b) Antihistamines are typically administered initially; this includes:

1) H1 blockers such as Hydroxyzine 10-25 mg q 4-6 hours.
2) Non-sedating H1 blockers do not work as well, but are useful for daytime hours. These include Loratidine (Claritin) 10 mg, Cetirizine (Zyrtec) 5-10 mg and Fexofenadine (Allegra) 60-180 mg.

Front 99

Prednisone can be given periodically and may work in people whose condition is difficult to treat with antihistamines alone.
(d) Epinephrine is administered for extensive, severe cases with intolerable itching.
(e) Generally, keeping the patient cool physically and emotionally is advisable.
(f) Cool, soothing baths can be suggested. Hot showers should be avoided as they only serve to worsen the pruritis afterwards.
(g) Topical steroids are generally not effective.

Back 99

True

Front 100

Chronic Urticaria Treatment

Back 100

(a) Should be referred to a Medical officer for complete work-up.
(b) Antihistamines are prescribed initially. Hydroxyzine 10-25 mg can be administered every 4 hours, up to 100 mg every 4 hours as needed. Can be sedating!
(c) Non-sedating antihistamine should be considered for daytime use. These include Desloratadine (Clarinex) 5 mg, Cetirizine (Zyrtec) 5-10 mg and Fexofenadine (Allegra) 60-180 mg.
(d) H1 blockers may be combined with H2 blockers such as Cimetidine 400 mg BID or Ranitidine 150 mg BID.

Front 101

Oral steroid are a second line if treatment, however, their use for Chronic Urticaria is controversial and sometimes detrimental.
(f) Empiric antibiotic therapy may be tried if an occult infection, such as a tooth abscess is suspected.
(g) Despite aggressive therapy, many cases persist indefinitely.

Back 101

True

Front 102

Disposition

Back 102

(1) Based on severity and complications. Light duty with use of antihistamines.

Front 103

Complications

Back 103

(1) Recurrence

Front 104

Dyshidrosis
Essentials of Diagnosis

Back 104

“Tapioca” vesicles of 1-2 mm on the palms, soles and sides of fingers, associated with pruritis.
(2) Vesicles may coalesce to form multiloculated blisters.
(3) Scaling and fissuring may follow drying of the blisters.
(4) Appearance in the third decade, with lifelong recurrences.

Front 105

General Considerations of Dyshidrosis

Back 105

(1) Commonly referred to as Dyshidrotic Eczema or Pompholyx.
(2) A distinctive, chronic relapsing, vesicular eczematous dermatitis of unknown etiology.
(3) Characterized by sudden eruptions of usually highly pruritic, symmetric vesicles on the palms, lateral fingers and/or plantar feet.

Front 106

Affected patients frequently have atopic background (personal or family history of asthma, hay fever, or atopiceczema). Moderate or severe itching typically precedes a flare or recurrent eruption. Hyperhidrosis (increased sweating) and performance of wet chores often aggravates or accompanies this condition. Peak incidence is in the early 20’s for women and mid-40’s for men.

Back 106

True

Front 107

General consideration of Dyshidrosis

Back 107

Vesicles are 1-5 mm in diameter, are monomorphic, deep seated, filled with clear fluid and resemble tapioca. Vesicles erupt suddenly and symmetrically on the palms or lateral fingers or on the plantar feet.
(2) Rings of scale and peeling follow the eruption as itch diminishes.
(3) Depending on the phase of the disease, the clinician may see only brown spots. When the acute process ends, the skin peels, revealing a red, cracked base with brown spots

Front 108

Vesicles resolve slowly over 1-3 weeks.
(5) Chronic eczematous changes with erythema, scaling and lichenification may follow.
(6) Waves of symmetrically distributed vesiculation can recur indefinitely.

Back 108

True

Front 109

Lab/Imaging Findings

Back 109

(1) KOH to rule out Tinea infection.

Front 110

Differential Diagnosis of Dyshidrosis

Back 110

(1) Pustular Psoriasis of the palms and soles of the feet
(2) Id reaction
(3) Inflammatory tinea
(4) Acute Allergic Contact Dermatitis
(5) Bullous Pemphigoid
(6) Cutaneous T cell lymphoma (rare)

Front 111

Treatment of Dyshidrosis

Back 111

Initial treatment consists of cold wet dressings BID with either tap water or Burow’s solution, followed by the applying a medium-potency or high-potency steroid cream.
Prednisone 0.5 – 1 mg/kg/day tapered over 1-2 weeks is prescribed.

Front 112

Fuether Treatment of Dyshidrosis

Back 112

Corticosteroids should not be relied on for repeated or chronic treatment.
Oral antihistamines can be used to alleviate pruritis.
Moderating or eliminating stressors can be helpful and is curative for some people.
Refer to a Dermatologist for chronic or severe disabling cases.

Front 113

Disposition of Dyshidrosis

Back 113

Based on severity of condition and sometimes military occupation

Front 114

Complications

Back 114

Can be incapacitating
Secondary infection

Front 115

Essentials of Diagnosis of Pityriasis Rosea

Back 115

Oval, rose or fawn-colored, scaly eruptions following cleavage lines of the trunk.
(2) Herald patch precedes eruption by 1-2 weeks.
(3) Occasional pruritis.

Front 116

General consideration of Pityriasis Rosea

Back 116

Common, self-limited, usually asymptomatic, clinically distinctive papulosquamous eruption.
(2) More than 75% of patients are between 10 and 35 years of age.
(3) Many patients report a mild prodrome or URI within a month of onset.
(4) The first lesion or “herald patch” appears, most often on the trunk.

Front 117

Lesion is an oval plaque, 1-2 cm in diameter, which develops a thin collarette of residual scale inside the border.
(5) Numerous similar but smaller lesions begin to appear 1-2 weeks later and reach a maximum number within 2 weeks.
(6) Lesions usually clear spontaneously in 4-12 weeks without scarring, although post- inflammatory pigmentary changes may take months to resolve in darker-skinned individuals.
(7) Limited outbreaks have occurred in close quarters such as fraternity houses and military barracks.

Back 117

True

Front 118

Physical findings of Pityriasis Rosea

Back 118

(1) Early lesions are broad-based papules that subsequently develop a thin collarette of scale as the center of the papule desquamates.
(2) Lesions are salmon or fawn-colored on lighter-skinned individuals and dark brown on dark-skinned individuals.
(3) Lesions are usually confined to the trunk and proximal extremities, often concentrated on the lower abdomen.
(4) The long axis of the oval lesions are oriented along skin cleavage lines reminiscent of drooping pine branches. Commonly referred to as a “Christmas Tree” pattern.

Front 119

Lab/Imaging Findings of Pityriasis Rosea

Back 119

(1) KOH to exclude tinea infection.
(2) Serologic Syphilis testing if clinically indicated.
(3) Skin biopsy for atypical cases

Front 120

Differential Diagnosis of Pityriasis Rosea

Back 120

(1) Tinea Corporis
(2) Secondary Syphilis

3) Tinea Versicolor
(4) Drug eruptions
(5) Guttate Pasoriasis

Front 121

Treatment of Pityriasis Rosea

Back 121

(1) No treatment is specific and usually no treatment in necessary.
(a) Condition is usually self-limited and usually asymptomatic.
(2) Treatment is indicated to alleviate itching.
(3) Oral Erythromycin Stearate, 250 mg QID (for adults) for 2 weeks effectively controls the eruption.
(4) Mentholated lotions or sprays can be helpful.

Front 122

Group V topical steroids and oral antihistamines provide some relief.
Prednisone, 20 mg BID, is rarely needed, but can be used to treat severe itching.
Ultraviolet-B light, either from natural sunlight or administered in metered doses by a Dermatologist hastens resolution.

Back 122

True

Front 123

Disposition

i. Complications

Back 123

(1) Full Duty

(1) Generally, self-limited

Front 124

Essential diagnosis of Psoriasis

Back 124

Silvery scales on bright red, well-demarcated plaques, usually on the knees, elbows, and scalp.
(2) Nail findings including pitting and onycholysis (separation of the nail plate from the bed).
(3) Mild itching (usually).
(4) May be associated with psoriatic arthritis.
(5) Histopathology is not often useful and can be confusing.

Front 125

General Considerations of Psoriasis

Back 125

Common, chronic, inflammatory papulosquamous disease of unknown etiology due to abnormal T lymphocyte function/communication.
(2) Skin, nail and joints are affected
(3) There are several distinct clinical forms.
(4) Common presentation is chronic scaly plaques involving the elbows, knees and scalp.
(5) Prevalence estimated at 1-3% of the population.
(6) Etiology is multifactorial and not completely understood.
(7) There are known inherited genetic factors with several documented environmental triggers.

Front 126

Physical findings of plaque Psoriasis

Back 126

Most common presentation begins as red, sharply defined, scaling papules that coalesce to form stable round to oval plaques.
(b) Typically involves the extensor extremities (elbows and knees), scalp and sacrum.
1) Usually spares the palms, soles and face.
(c) The deep rich red color is a characteristic that remains constant.
(d) Scale is adherent, silvery white and reveals bleeding points when removed (Auspitz sign).
(e) Scale may become extremely dense, especially on the scalp.

Front 127

Physical findings of Guttate Psoriasis

Back 127

(a) Unstable form, associated with the sudden appearance of innumerable monomorphic psoriasiform papules on the trunk.
(b) Often associated with group A streptococcal pharyngitis, viral infections and less often, with systemic steroid withdrawal.

Front 128

Physical findings of Localized Pustular Psoriasis

Back 128

(a) Chronic recurrent form has been associated with tobacco use.
(b) Small sterile pustules evolve from a red base on palms and soles.
(c) Pustules do not rupture but turn dark brown and scaly as they reach the surface; often quite painful.

(d) Nail involvement is common

Front 129

Physical findings of inverse (Intertriginous) Psoriasis

Back 129

(a) Uncommon form occurring in flexural or intertriginous areas; often in the groin and under the breasts.
(b) There are smooth, red and sharply defined plaques with a macerated surface.

Front 130

Physical findings of Generalized Pustular Psoriasis

Back 130

(a) Uncommon, severe form requiring immediate medical attention.
(b) May be associated with fever and tenderness.
(c) May be drug related.
1) S terile pustules are regional or generalized, often occur in waves.

Front 131

Physical findings of Erythrodermic Psoriasis

Back 131

(a) Uncommon severe form requires immediate medical attention.
(b) There may be total body redness with chills and skin pain.
(c) May be drug related.

Front 132

Physical findings of Nail Disease

Back 132

(a) Clinical findings vary and are related to the specific areas of nail matrix involvement.
(b) Pitting, onycholysis (separation of the nail from the nail bed), subungal debris , oil drop sign and nail dystrophy may occur.
(c) Nail findings offer supporting evidence of the diagnosis when skin changes are equivocal or absent.

Front 133

Physical findings of Joint Disease

Back 133

(a) Several distinct clinical patterns, which are rheumatoid factor negative.
(b) Asymmetric oligoarticular form is the most common, affecting 70% of those with arthritis.

(c) Distal interphalangeal type affects 10%, with nail changes.
(d) Symmetric polyarthritis is similar to rheumatoid arthritis.
(e) Mutilating type affects 5%, has early onset.
(f) Spinal type affects 20% and is debilitating.

Front 134

Lab/Imaging Findings of Psoriasis.

Back 134

(1) Punch biopsy shows acanthosis (thickening of the epidermis).
(2) Throat culture to confirm streptococcal pharyngitis in Guttate Psoriasis.
(3) KOH to rule out Candida is Inverse Psoriasis.
(4) Test for HIV infection in severe, recalcitrant cases.

Front 135

Differential Diagnosis of Psoriasis

Back 135

(1) Seborrheic Dermatitis (involves the face more often than Psoriasis)
(2) Eczema (Dyshidrotic hand/foot eczema; more vesicular than pustular)
(3) Tinea Capitis (Onychomycosis should be excluded with KOH exam) (4) Candidiasis (5) Pityriasis Rosea (6) Acute generalized exanthematous pustulosis

Front 136

There are three categories of treatment –

Back 136

topical therapy, phototherapy or systemic therapy – they may be combined or alternated

Front 137

Topical Tar preparations

Back 137

1) Available in lotions, ointments and shampoos.
2) Relatively inexpensive and may be compounded with topical steroids.
3) May cause irritation, odor and staining of clothing.
4) Calcipotriol (Dovonex) can be applied QD or BID as tolerated in amounts up to 100 g per week.
5) Side effects are mild/transient local irritation and erythema

Front 138

Topical Steroids (Group I-V)

Back 138

1) Topical steroids (group I-V) give fast but temporary relief.
2) Used to control irritation.
3) These are the best agents for reducing inflammation and itching.
4) Treat few, small, chronic plaques with intralesional steroid (Kenalog); use caution to avoid atrophy.
5) Become less effective with continued use.
6) Side effects include atrophy and telangiectasia with long-term use.
7) Best used in cycles, BID for 7-14 days with a break of 7-14 days.

Front 139

Topical Scalp treatment

Back 139

1) The scalp is difficult to treat. The goal is to provide symptomatic and/or cosmetic relief.
2) Scale should be removed first to facilitate penetration of the medicine.
3) Superficial scale can be removed with salicyclic acid or tar shampoos.
4) Diffuse scalp psoriasis removed with Derma Smoothe oil. This treatment removes scale and contraol inflammation.
5) Steroid gels (Lidex, Temovate, Topicort) or steroid foams penetrate through hair

Front 140

Topical Nail treatment

Back 140

1) Nails are difficult to treat so the goal is to provide symptomatic/cosmetic relief.
2) Topical Calcipotriene solution, Clobetasolsolution and Tazarotene gel may be hekpful if applied to the posterior nail fold area; may require months of treatment.
3) Intralesional Kenalog is painful to administer but often provides temporary improvement.

Front 141

Phototherapy
(a) Ultraviolet B

Back 141

1) Very effective treatment, may be used in combination with topical treatment.
2) Typically given 3-5 times per week.
3) Tar or lubricants enhance its effectiveness.
4) Steroid use diminishes the length of remission.
5) Side effects are burning, premature skin aging and skin cancer.
6) Narrow-band form is more effective than broad-band, but is less widely available.

Front 142

Psoralen plus Ultraviolet A

Back 142

1) Needs to be given three times a week until the skin is clear, then it is tapered off.
2) Patients take photosensitizing Psoralen 1.5-2 hours prior to exposure.
3) Effective method of controlling but not curing Psoriasis.
4) Indications are for symptomatic control of severe, recalcitrant, disabling plaque Psoriasis.
5) Side effects include GI intolerance of drug, sunburning, photo-damaged skin, cataracts and increased skin cancer risk.

Front 143

Systemic therapy

Back 143

(a) Patients with Psoriasis involving more than 20% of the body surface or who are very uncomfortable should consider systemic therapy. Therapy is complicated and best managed by a Dermatologist

Front 144

Rotational therapy

Back 144

A rotational approach t therapy minimizes long-term toxic effects from any one therapy and allows for effective long-term management.

Front 145

Methotrexate

Back 145

1) Effective in unstable erythrodermic, generalized pustular Psoriasis and extensive chronic plaque disease.
2) Effective for psoriatic arthritis.
3) Can be administered orally, intramuscularly or subcutaneously.
4) Work up to a dose of 12.5-22.5 mg weekly.
5) Give folic acid I mg daily, but not on the day of Methotrexate treatment.
6) Close follow-up is required; monitor CBC, LFT and liver biopsy should be performed periodically.
7) Beware of drug interactions.
8) Side effects include nausea, anorexia, fatigue, oral ulcerations, leukopenia, thrombocytopenia, hepatic fibrosis or cirrhosis. Use caution in the elderly and those with any renal insufficiency.

Front 146

Cyclosporine (Neoral)

Back 146

1) Best used for severe inflammatory Psoriasis (acute control).
2) Dosage is 2.5-5.0 mg/kg/day.
3) Taper dosage after control is achieved.
4) Close monitoring of blood pressure is needed, as well as CBC, creatinine, magnesium and cholesterol/triglyceride levels.
5) Beware of drug interactions.
6) Side effects include hypertension and nephrotoxicity

Front 147

e) Acitretin (Soraitane

Back 147

1) Highly effective for generalized pustular and erythrodermic Psoriasis.
2) Useful in combination with Psoralen plus ultraviolet A and ultraviolet B.

Front 148

Disposition

Complications

Back 148

(1) Full Duty, depending on location and severity
(2) Patients with extensive exfoliative dermatitis should be hospitalized

(1) Psoriatic arthritis often resembles rheumatoid arthritis and may be crippling
(2) Exfoliative dermatitis

Front 149

Seborrheic Keratosis
Essentials of Diagnosis

Back 149

Seborrheic Keratoses are common benign growths with multiple variants that can mimic other more worrisome skin tumors.
(2) Removal is not warranted unless lesions become inflamed and symptomatic.
(3) Some keratosis are heavily pigmented, resembling melanoma, and therefore should be biopsied.

Front 150

General consideration of Seborrheic Keratosis

Back 150

A common, benign, persistent epidermal lesions wit variable clinical appearance.

(2) It is one of the most common benign growths seen on the skin and can be confused with cutaneous malignancies.
(3) Unusual before the age of 30.
(4) Most people develop at least one Seborrheic Keratosis lesion in their lifetime.
(5) Males and female are equally affected.
(6) Lesions may be localized to the areola in both males and females.
(7) Tendency toward multiple lesions may be inherited.
(8) Condition is usually asymptomatic, but sometimes it is cosmetically bothersome.
(9) Lesion can be subject to irritation depending on its location.

Front 151

Physical Findings
(1) Skin Findings of Seborrheic Keratosis

Back 151

(a) There are usually multiple lesions, which can arise at any site except the lips, palms and soles.
(b) Size and surface appearance of the lesions vary considerably.
(c) Most are 0.2-2.0 cm (2-20 mm), although larger lesions can occur.
(d) Lesions may be flat or raised.
(e) Surface may be smooth, velvety or warty.
(f) Retained keratin cysts may be seen just under the surface within clefts.

Front 152

Color is extremely variable, including white, pink brow and black and may vary within a single lesion.
(h) Lesions tend to be sharply demarcated, oval and often oriented along skin cleavage lines.
(i) Most lesions have a ”stuck-on” appearance and waxy texture.
(j) Surface tends to crumble when picked at.

Back 152

True

Front 153

Unless disturbed, Seborrheic Keratoses tend to persist and grow slowly.
Some lesions may be removed by trauma.

Back 153

True

Front 154

Non-Skin Findings of Seborrheic Keratoses

Back 154

The sign of Leser-Trelat is the sudden explosive onset of numerous SK lesions in association with internal malignancy.

Front 155

Lab/Imaging Findings of Seborrheic Keratoses

Back 155

(1) Biopsy if there is doubt in diagnosis

Front 156

Differential Diagnosis of Seborrheic Keratoses

Back 156

(1) Pigmented Actinic Keratosis
(2) Superficial Spreading Melanoma

Front 157

Treatment of Seborrheic Keratoses

Back 157

(1) Treatment may be indicated for symptomatic lesions.
(2) Lesions in areas of friction and frequent trauma often become irritated and symptomatic.
(3) Removal is often requested for cosmetic reasons.
(4) Cryosurgery is effective for flat or minimally raised lesions.
(5) Thicker lesions are best removed by cautery and curettage under local anesthesia.
(6) Residual scarring, if any, is minimal.
(7) Hyperpigmentation or hypopigmentation are possible side effects of cryotherapy or other methods of removal.

Front 158

Disposition

Back 158

(1) Full Duty

Front 159

Complications

Back 159

(1) None

Front 160

Essentials of Diagnosis of Epidermal Cysts

Back 160

(1) Firm dermal papule or nodule
(2) Overlying black comedone or “punctum”
(3) Expressible foul-smelling cheesy material
(4) May become red and drain, mimicking an abscess

Front 161

b. General Considerations of Epidermal Cysts

Back 161

(1) An Epidermal cyst is a firm, subcutaneous, keratin-filled cyst originating from true epidermis, most often from a hair follicle.
(2) Arise spontaneously, usually after puberty.
(3) Occur most commonly on the trunk, postauricluar fold and on the posterior neck.
(4) Lesions are usually solitary.
(5) Epidermal cyst wall is fairly delicate and prone to rupture

Front 162

Physical Findings of Epidermal Cysts

Back 162

The firm, dome-shaped, pale yellowish intradermal or subcutaneous cystic nodules range from 0.5-5.0 cm in size.
(b) Cysts are somewhat mobile but are tethered to the overlying skin through a small punctum that often appears as a comedo.
1) The punctum represents the follicle from which the cyst developed.

Front 163

Non-Skin Findings of Epidermal Cysts

Back 163

Multiple epidermal cysts occurring on the face, scalp and back should raise suspicion of gardner syndrome.

Front 164

Differential Diagnosis

Back 164

(1) Lipoma
(2) Other benign and malignant tumors

Front 165

Treatment of Epidermal Cysts

Back 165

Epidermal cysts on the face may rupture and lead to scarring. The cosmesis of elective surgical excision must be weighed against scarring from rupture.

(a) Such lesions are far more difficult to remove once they have ruptured.

Front 166

Ruptured, inflamed epidermal cysts should be incised and drained under local anesthesia.
Attempts should be made to remove the cyst lining either by curettage or blunt dissection with scissors and forceps.
Very large cyst cavities may then be packed with wick to aid further drainage.

Back 166

True

Front 167

Epidermal cysts that have not previously ruptured can be excised easily and completely under local anesthesia.
Recurrent epidermal cysts that have previously ruptured and scarred are best excised along with the surrounding scar once the inflammation has subsided.

Back 167

True

Front 168

Disposition

Complications

Back 168

(1) Full Duty

(1) Epidermal cysts may rupture, creating an acute inflammatory nodule very similar to an abscess.

Front 169

Actinic Keratosis
Essentials of Diagnosis

Back 169

Small macules or papules that feel like sandpaper and are tender when the finger is drawn over them.
(2) Occur on sun-exposed parts of the body in persons of fair complexion.
(3) Considered pre-malignant, but only 1:1000 lesions per year progress to become squamous cell carcinomas.

Front 170

General consideration of Actinic Keratosis

Back 170

Actinic Keratoses are common, persistent, keratotic lesions with malignant potential.
(2) Lesions are most commonly found in the sun-exposed areas of elderly patients with fair skin types who have had significant sun exposure in their lifetime.
(3) Years of cumulative sun exposure and keratinocyte damage lead the formation of actinic keratosis.
(4) Individual lesions become progressively more common after age 40.

Front 171

Physical Findings of Actinic Keratosis

Back 171

(1) Actinic Keratoses are found along with other signs of chronic sun exposure, such as uneven pigmentation, atrophy or thinning and telangiectasias.
(2) Lesions are found predominantly on the face, head, neck and the dorsal aspect of the hands.
(3) Initially present as a poorly defined area of redness or telangiectasia.

Front 172

Lab/Imaging Findings of Actinic Keratosis

Back 172

(1) Refer for biopsy of lesions

Front 173

Differential Diagnosis of Actinic Keratosis

Back 173

(1) Squamous Cell Carcinoma
(2) Actinic Chelitis

Front 174

Treatment of Actinic Keratosis

Back 174

(1) The patient with multiple actinic keratoses requires at least annual follow-up.
(2) Visible or detectable lesions represent a fraction of the total number of atypical keratinocytes usually present.
(a) Most of the atypia is scattered within sun-damaged skin and below the level of clinical detection.
(b) These patients will almost certainly develop more clinically apparent lesions with time.

Front 175

Adequate sun avoidance with sun-protective clothing and sunscreens should be encouraged to limit further damage.
(4) Application of liquid nitrogen (cryotherapy) to solitary superficial lesions is the most common method of removal.
(5) Topical 5-fluorouracil 5% cream or solution is useful in reducing the number of atypical keratinocytes and has been the standard in topical, non-surgical treatment of actinic keratoses and the duration of treatment.
(6) 5-Fluorouracil is available as a cream of 0.5% (Carac), 1% (Fluoroplex) and 2% (Efudex) solution.
(a) Involves application of medication BID for 3-5 weeks or longer.

Back 175

True

Front 176

Imiquimod 5% cream has been shown to effectively treat multiple actinic keratoses when applied three to five times weekly for up to 4 weeks.

Back 176

True

Front 177

Disposition

Back 177

(1) Full duty
(2) All patients with Actinic Keratosis lesion(s)should be referred to a Medical Officer.
(3) Patients with multiple lesions require annual follow-up.

Front 178

Complications

Back 178

Carcinomas (SCC)

Front 179

Basal Cell Carcinoma
(1) Essentials of Diagnosis

Back 179

(a) Pearly papule, erythematous patch > 6 mm, or non-healing ulcer, in sun exposed areas (face, trunk, lower legs).
(b) History of bleeding.
(c) Fair-skinned person with history of sun exposure (often intense, intermittent).

Front 180

General Considerations of Basal Cell Carcinoma

Back 180

Basal cell carcinoma is the most common cutaneous malignancy in humans.
(b) Locally invasive and destructive and is usually slow growing. Rarely metastasizes.

May occur at any age but is more common after the age of 40.
(d) Highest incidence occurs in people with fair skin types. Less common in Asian people and rare in African-American people.

Front 181

Several clinical variants of basal cell carcinoma are recognized. Each varies in terms of clinical appearance, histology and aggressiveness: These are as follow?

Back 181

1) Nodular BCC
2) Pigmented BCC
3) Superficial BCC
4) Micronodular BCC
5) Morpheaform BCC

Front 182

Physical Findings of Nodular basal cell

Back 182

(a) Any wound on a sun exposed area that does not heal in appropriate amount of time should be referred to a Medical Officer.
(b) Nodular basal cell carcinoma is the most common variant.
(c) The lesion is a pearly-white, almost translucent, dome-shaped papule with overlying telangiectasias.
(d) The papule or nodule enlarges slowly, may become flattened in the center or may develop a raised, rolled and translucent border.
(e) Tumors frequently ulcerate, bleed and become crusted in the center.
(f) Basal cell carcinomas may contain melanin that that imparts a a brown, black or blue color through all or part of the lesions.
(g) May present as a papule or nodule on the ear that resembles squamous cell carcinoma.

Front 183

Nodular Basal Cell Carcinoma
.

Back 183

1) Lesion begins as a pearly white or pink, dome-shaped papule.
2) The center frequently ulcerates and bleeds and subsequently accumulates crust and scale.
3) Telangiectatic vessels become prominent as the lesion enlarges. The growth pattern is is irregular, forming an oval, multilobular mass

Front 184

Pigmented Basal Cell Carcinoma

Back 184

1) Equivalent to nodular basal cell carcinoma except that there is alos melanin pigment.
2) May resemble malignant melanoma and therefore must be biopsie

Front 185

Superficial Basal Cell Carcinoma

Back 185

1) Least aggressive form of basal cell carcinoma and is found more commonly on the trunk and extremities.
2) There may be multiple lesions. Lesions are flatter and not as deeply invasive as the lesions of nodular basal cell carcinoma. The borders are less distinct but have the same pearly quality.
3) Tumor spreads peripherally, sometimes for several centimeters and invades after considerable time.

Front 186

Lab/Imaging Findings

Back 186

(a) Refer for mandatory Biopsy

Front 187

Differential Diagnosis

Back 187

(a) Eczema
(b) Psoriasis
(c) Tinea Infection

Front 188

Treatment

Back 188

(a) The goal of treatment is eradication of the tumor and return to normal anatomic form and function.
(b) Treatment is determined by size and location of the tumor, by histological variant and the patient’s concerns.
(c) Clinical aggressiveness correlates with histologic patterns.

Front 189

Electro-surgery involves electrodessication and curettage of obvious tumor.
1) Usually performed for well-defined small nodularbasal cell carcinomas and superficial basal cell carcinomas.
2) 5-year cure rate can approach 92% for primary tumors but is only 60% for recurrent tumors.

Back 189

True

Front 190

Office excision is preferred for well-defined nodular basal cell carcinomas.
1) Allows for confirmation of surgical margins and may result in a more acceptable scar.
2) 5-year cure rates approach 90%for primary tumors and 83% for recurrent tumors.

Back 190

True

Front 191

Disposition

Complications

Back 191

(a) Full Duty with referral to specialty care (Dermatologist)

(a) Recurrences

Front 192

Essentials of Diagnosis of Squamous Cell Carcinoma

Back 192

(a) Non-healing ulcer or warty nodule.
(b) Skin damage due to long-term sun exposure.
(c) Common in fair-skinned organ transplant patients.

Front 193

General consideration of Squamous Cell Carcinoma

Back 193

Cutaneous squamous cell carcinoma is an invasive, primary cutaneous malignancy arising from keratinocytes of the skin or mucosal surfaces.
(b) It is most commonly found on the head, neck or hands of elderly patients.
(c) Lesions may develop from precursor actinic keratoses.
(d) Squamous cell carcinoma is the second most common form of skin cancer.

Front 194

Comprises of 20% of all primary cutaneous malignancies.
2) Lifetime risk of developing a cutaneous squamous cell carcinoma is estimated to be between 4 to 14%.
3) More than 100,000 new cases diagnosed in the United States each year. Approximately 2500 deaths occur annually from squamous cell carcinoma arising from the skin.

Back 194

True

Front 195

Primary cutaneous squamous cell carcinomas usually occur on sun-exposed skin from years of accumulated actinic change.
1) Fair complexion (skin types I and II) are at greatest risk.

Back 195

True

Front 196

Majority caused by chronic exposure to UV light, but other extrinsic factors involved.
Other forms of radiation, chemicals (hydrocarbons and arsenic), tobacco, chronic infections, chronic inflammation, burns and HPV.
Historically considered as a low–grade tumor with a metastatic rate of 1%.

Back 196

True

Front 197

Physical Findings of Squamous Cell Carcinoma

Back 197

(a) Typically occur on sun exposed areas.
(b) Tumors are found within a background of sun-damaged skin with atrophy, telangiectasias and blotchy hyperpigmentation.
(c) Early invasive squamous cell carcinomas may have the appearance of a hypertrophic actinic keratosis.
(d) Lesion has a red, poorly defines base and an adherent yellow-white scale.

Front 198

Lab/Imaging Findings of Squamous Cell Carcinoma

Back 198

Refer for skin biopsy in all suspected cases.

Front 199

Differential Diagnosis of Squamous Cell Carcinoma

Back 199

(a) Basal Cell Carcinoma

(b) Actinic Keratosis
(c) Seborrheic Keratosis

Front 200

Treatment of Squamous Cell Carcinoma

Back 200

(a) Treatment of primary squamous cell carcinoma of the skin involves wide local excision with histologic confirmation of the margins.
(b) Mohs surgery may be useful for specific sites where tissue sparing is of importance.
(c) Palpation of regional lymph nodes is mandatory for all invasive squamous cell carcinoma patients.
(d) Lymph node biopsy is indicated for suspected nodal disease.
(e) Radiation therapy may be considered when surgical resection is not feasible.

Front 201

Lymph node biopsy is indicated for suspected nodal disease.
Radiation therapy may be considered when surgical resection is not feasible.
Careful follow-up at regular intervals is recommended for all squamous cell carcinomas to include the following:

Back 201

True

Front 202

Careful follow-up at regular intervals is recommended for all squamous cell carcinomas to include the following:
1) Skin examination and biopsy of new lesions suspicious for malignancy.
2) Visual inspection and palpation of the excision scar for nodularity and other evidence of skin recurrence.
3) Careful examination of the regional lymph node with biopsy, if indicated, to detect early metastatic disease.

Back 202

True

Front 203

Sun-exposed lower lip is a common site. Palpation may reveal a deep nodular mass. Squamous cell carcinoma originating on the lip, ear and scalp tend to be more aggressive and metastasize to the regional lymph nodes and beyond

Back 203

True

Front 204

Disposition

Back 204

(a) Full Duty with referral to specialty care (Dermatologist).
(b) Limited duty based on treatment and location of treated lesions.

Front 205

Complications

Back 205

(a) Metastasis

Front 206

Essentials of Diagnosis of Malignant Melanoma

Back 206

May be flat or raised.
(b) Should be suspected in any pigmented skin lesion with recent change in appearance.
(c) Examination with good light may show varying colors, including red, white, black and bluish.
(d) Borders are typically irregular.

Front 207

General Considerations of Malignant Melanoma

Back 207

(a) Malignant Melanoma is the leading cause of death due to skin disease.
(b) Melanoma is an increasingly common malignancy of melanocytes, most often arising in the skin.
(c) It is potentially curable with early detection and treatment.
(d) Late diagnosis of melanoma carries a poor prognosis.
(e) Represents 4% of all cancers in men and 3% of all cancers in women.

Front 208

Factors that increase risk of developing melanoma include:

Back 208

1) Fair skin
2) Presence of atypical nevi in both sun-exposed and sun-protected areas.
3) Personal history of melanoma

4) Family history of atypical nevi or melanoma
5) History of blistering sunburn
6) Congenital nevi (the risk increases proportionally with increasing size)

Front 209

The most common early signs include an increase in size, change in color or shape.
(h) The most common early symptom is itching, but most are asymptomatic.
1) Later symptoms include tenderness, bleeding and ulceration.
(i) Pigmented lesions may change slowly over months to years or abruptly change.

Back 209

True

Front 210

there are clinical clues that increase the index of suspicion and warrant biopsy
1) Use ABCDE Pneumonic when evaluating suspected lesions.

Back 210

a) A - Asymmetrical
b) B – Irregular borders
c) C – Color changes
d) D – Diameter > 6mm
e) E - Evolving

Front 211

Lesion will be the “Ugly Duckling”, looks notably different than the rest of the patients’ moles.
(c) 30% of melanomas develop within a pre-existing nevus while the remaining 70% develop de novo.
(d) When melanoma develops in a pre-existing lesion, there is usually a focal area of color change.

Back 211

True

Front 212

Not one specific color is by itself diagnostic but should raise one’s index of suspicion.

Slate gray, to black or deep blue may indicate melanin pigment deep within the dermis.
2) Pink or red may indicate localized inflammation.
3) White may indicate regression or scarring.

Back 212

True

Front 213

There are 4 major clinical subtypes of melanomas, defined by clinical appearance, progression, anatomic site and histologic appearance.

Back 213

Superficial Spreading Melanoma

Nodular Melanoma
Lentigo-Maligna Melanoma

Acral Lentiginous Melanoma

Front 214

Superficial Spreading Melanoma

Back 214

a) Most common subtype, accounting for 70-80% of all melanomas.
b) Most melanomas arising from a pre-existing lesion are superficial spreading.
c) Slightly more common in females than males, usually affecting Caucasian people.
d) Affects any cutaneous site but most often on the trunk or extremities.
e) Lesions tend to be greater than 6 mm in diameter, flat and asymmetric with varying coloration.
f) Lesions appear and tend to spread laterally within the skin over a few years, before nodules develop within the lesion.

Front 215

Nodular Melanoma

Back 215

a) These account for 10-15% of all melanomas.
b) Equally common in males and females.
c) They affect any cutaneous site, but are more often found on the extremities.
d) Lesions tend to be raised, brown to black, rapidly appearing and rapidly growing papules.

Front 216

Lentigo-Maligna Melanoma

Back 216

a) Account for 5-10% of all melanomas.
b) Lentigo maligna represents in situ (intraepidermal) melanoma.
c) Progression to invade lentigo maligna melanoma occurs in 5% of patients.
d) Equally common in males and females, usually in older people.
e) Develop over years or decades on sun-exposed Caucasian skin, most often affecting the face, neck or dorsal arms.

Front 217

Acral Lentiginous Melanoma

Back 217

a) Accounts for 7% of all melanomas.
b) More common in males than females, usually occurs in older people.
c) Occurs primarily on the hands and feet, including nails of people with darker skin types.
d) Similar lesions also occur on the modified skin around the mouth, anus and genitals.

Front 218

Most common form of melanoma in the skin of Asian and Black people, accounting for more than half of melanomas in these groups.
(1 Least common form of melanoma in Caucasian people.
f) Other than location, the lesion is similar in appearance to lentigo maligna melanoma – a flat, slowly expanding macule with a fairly uniform, mottled coloration.
g) It appears and evolves over years.

Back 218

Acral Lentiginous Melanoma

Front 219

Lab/Imaging Findings

Back 219

(a) Refer for biopsy

Front 220

Differential Diagnosis

(a) Superficial Spreading Melanoma

Back 220

1) Benign nevi (moles)
2) Atypical nevus
3) Seborrheic Keratoses
4) Solar lentigo

Front 221

Differential diagnosis of Nodular Melanoma

Back 221

1) Pigmented Basal Cell Carcinoma
2) Angiokeratoma
3) Hemangioma
4) Traumatized nevus or acrochordon
5) Pyogenic Granuloma

Front 222

Differential diagnosis of Lentigo maligna

Back 222

1) Spreading pigmented Actinic Keratosis
2) Bowen’s disease
3) Solar lentigo

Front 223

Treatment

Back 223

(a) No treatment in the scope of care for IDC’s!!!
(b) All suspect lesions should be referred to a Medical Officer and warrant biopsy.
(c) Palpate the regional lymph nodes prior to biopsy and document findings.
(d) The only “perfect” biopsy technique is complete excision of the entire lesion into the subcutaneous fat.
1) Allows for accurate measurement of Breslow depth of invasion in melanoma and avoid sampling error.

Front 224

Disposition

Back 224

(a) Full Duty with immediate referral to Medical Officer and specialty care (Dermatologist).
(b) Limited duty based on severity and metastasis

Front 225

Complications

Back 225

Metastasis

Front 226

Essentials of Diagnosis of Lipomas

Back 226

Lipomas are benign tumors composed of adipose tissue.

It is the most common form of soft tissue tumor.
Lipomas are soft to the touch, usually movable, and are generally painless.

Front 227

General Considerations

Back 227

(1) Lipomas are soft, movable, subcutaneous nodules with normal overlying skin.
(2) A patient may have one or many lipomas.
(3) Occur more often in women than men and appear most commonly on the trunk, nape, and forearms.
(4) Rapidly growing lesions should be biopsied, although lipomas rarely become malignant.

Front 228

Physical Findings of lipoma

Back 228

(1) Lipomas are rarely symptomatic, but pain may occur.
(2) Diagnosis is usually made clinically.
(3) Usually easily moveable within the subcutis.
(4) While generally soft, some become firmer.
(5) Superficial dimpling may occur, but frank inflammation is not normal

Front 229

Lab/Imaging Findings

Back 229

Biopsy for rapidly growing lesions

Front 230

Differential Diagnosis

Back 230

(1) Epidermal Inclusion Cysts – more superficial and have overlying punctum.

Front 231

Treatment

Back 231

Treatment is not usually required, but bothersome lipomas may be excised or removed by liposuction.

Front 232

Disposition

Complications

Back 232

Full Duty

(1) Lipomas rarely become malignant
(2) Cosmetic concerns

Front 233

Essentials of Diagnosis

Back 233

Generalized very severe itching
1) Pruritic burrows, vesicles and pustules, especially on finger webs and wrist creases.
2) Mites, ova, and brown dots of feces visible microscopically.
3) Red papules or nodules on the scrotum and on the penile glans and shaft are pathognomic.

Front 234

General Considerations

Back 234

(a) Scabies is an intensely pruritic contagious infestation caused by the mite Sarcoptes Scabiei.
1) Itching that is worse at night is a cardinal feature.
2) Historically, Scabies is the most likely cause of the “seven-year itch”.
(b) Patients infested with Scabies complain of unremitting itching and cannot stop scratching, even while being examined.

Front 235

Physical Findings

Back 235

Itching is almost always present and can be quite severe.
(b) A burrow is the classic lesion of Scabies; it is a linear, curved or S-shaped slightly elevated vesicle or papule up to 1-2 mm wide..
1) Burrows are most likely to be found in the finger webs, wrists, sides of the hands and feet, the penis, buttocks and scrotum and the palms and soles of infants.
2) Burrows may be difficult to find because they become obscured by scratching and secondary lesions.

Front 236

Scabies rash appears 2-6 weeks after exposure.
(e) Typical locations are the wrists, web space of the hands, sides of the hands and feet, the genital area, warm intertriginous regions and the abdomen.
1) In infants, the scalp, palms and soles of the feet are affected more often
(f) Eczema and Impetigo may appear as secondary lesions.

Back 236

True

Front 237

Lab/Imaging Findings

Back 237

Mites, eggs or feces can be identified in a Scabies preparation (scrapings from burrows mixed with mineral oil, KOH or even water) and examined microscopically.
KOH and heat will make mites easier to identify but will destroy mite feces.

Front 238

Differential Diagnosis

Back 238

(a) Insect bites
(b) Eczema
(c) Impetigo
(d) Folliculitis

Front 239

Treatment

Back 239

Permethrin 5% or Lindane 1% is applied to the entire surface of the skin from the neck down, including under the fingernails and toenails an in the umbilicus. The patient should bathe after about 12 hours. Treatment regimen should be repeated in 1 week.

Front 240

Disposition

Back 240

Full Duty, take consideration for laundering clothing, bedding and those in close quarters with other persons.

Front 241

Complications

Back 241

(a) Secondary infections
(b) Recurrence

Front 242

Essentials of Diagnosis of Pediculosis

Back 242

(a) Pruritis with excoriation.
(b) Nits in hair shafts, lice on skin or clothes.
(c) Occasionally, sky-blue macules (maculae ceruleae) on the inner thighs or lower abdomen in pubic louse infestation.

Front 243

General consideration of Pediculosis

Back 243

Pediculosis (Lice) is a parasitic infestation of the scalp, trunk or pubic areas.
1) Lice are flattened, wingless insects. Each has three pairs of legs located on the anterior part of the body directly behind the head. These legs terminate in sharp claws that are adapted for feeding, permitting the louse to grasp and hold firmly on to hair or clothing.
(b) Lice attach to the skin and feed on human blood. They lay their eggs on hair shafts.
(c) Nits are white hard, oval lice eggs attached to the hair shaft.
(d) Rarely, lice can transmit disease such as epidemic typhus and relapsing fever.

Front 244

There are three different types of lice:

Back 244

1) Pediculosis Pubis – caused by Phthrius pubis (pubic louse or “crabs”)
2) Pediculosis Corporis – Pediculus humanus var corporis (body louse)
3) Pediculosis Capitis – Pediculus humanus var capitis (head louse)

Front 245

a) Heb) Direct contact is the primary source of transmission.
c) Lice are obligate human parasites, so they cannot survive on other animals or furniture.
d) Head louse does not carry any known human disease.
e) Lice feed or suck blood 3-6 hours.
f) They live for about 1 month, female can lay 7-10 eggs per day.
g) Eggs, or nits, are firm casts cemented to the hair shaft, about 1 cm from the scalp surface.
h) Nits hatch in 8-10 days. ad lice infestation is highly contagious.

Back 245

True

Front 246

(f) Head lice is typically diagnosed by school teacher or school nurse.
(g) Girls are affected more often than boys.
(h) Transmission via, hats, brushes or ear phones is common.
(i) Infestation may cause mild itching at the nape of the neck or be asymptomatic.
(j) Posterior cervical adenopathy is occasionally noted.

Back 246

True

Front 247

Physical findings

Back 247

Nits are small white eggs firmly cemented to the hair shaft.
1) Nits are sometimes easier to see than the lice.
(b) Head lice are 3-4 mm in length. They can be seen on the hair shafts and scalp with careful observation.
(c) Diagnosis is not usually difficult, but may require repeated examinations.
(d) Head lice have an elongated body, similar to a body louse, though smaller.
(e) Honey-colored crusting or secondary Impetigo and adenopathy occur if the papules become infected.

Front 248

Differential Diagnosis

Back 248

(a) Seborrheic Dermatitis
(b) Impetigo
(c) Insect Bites – bed bugs

Front 249

Treatments

Back 249

Permethrin rinse 1% (Nix), over-the-counter preparation is often the drug of first choice.
Permethrin 5% (Elimite) is administered for treatment failures. It is left on the hair overnight under a shower cap.
b) Lindane (Kwell) shampoo is left in for 5 minutes and then washed out; treatment is then repeated in 1 week. Used if OTC treatment fails.

Front 250

Malathion lotion 0.5% (Ovicide) is rapidly pediculicidal and ovicidal. It is useful for the treatment of head lice resistant to pyrethrins and permethrin. Lotion is applied for 8-12 hours, should be re-applied 7-9 days later if necessary.
2) Combing through hair with a special nit comb is also helpful in the week following treatment.
3) Treatment of all close family members is frequently recommended.

Back 250

True

Front 251

Alternative Therapies or “Home Remedies”:

Back 251

Vaseline (Petrolatum), mayonnaise, or pomades applied to the scalp overnight and covered with a shower cap, smother the lice.
a) Copious amounts must be used to smother all lice. This treatment does not kill nits, so it should be repeated for 3-4 weeks.
2) Hair Clean 1-2-3 hairspray is an oil that kills lice in 15 minutes.
3) As a last resort, shaving of the scalp can be curative.

Front 252

Disposition

Back 252

Full Duty, considerations taken for laundering clothing, bedding and those in close quarters with other persons.

Front 253

Complications

Back 253

(a) Secondary infections
(b) Recurrence

Front 254

Essentials of Diagnosis of Stevens-Johnson syndrome

Back 254

Stevens-Johnson syndrome is a rare, serious disorder in which your skin and mucous membranes react severely to a medication or infection.
(2) Often begins with flu-like symptoms.
(3) Presents a medical emergency that usually requires hospitalization.
(4) Treatment focuses on eliminating the underlying cause, controlling symptoms and minimizing complications.

Front 255

General consideration

Back 255

Stevens-Johnson syndrome is a severe blistering mucocutaneous syndrome involving at least two mucous membranes.
(2) Occurs in all ages, but is more common in children and young adults.
(3) Syndrome is similar to Erythema Multiforme and is thought to be due to immune responses directed against keratinocytes expressing foreign infectious and drug antigens.

Front 256

Mycoplasma pneumonia has been associated with SJS.
(5) Phenytoin, Phenobarbital, Carbamezpone, Sulfonamides and Aminopenicillins are frequently implicated drugs.
(a) Medications started within 1 month of disease onset are more likely to cause Stevens-Johnson syndrome.
(6) Mortality approaches 10% for patients with extensive disease.

Back 256

True

Front 257

Physical Findings
Skin Findings

Back 257

Erythematous papules, dusky appearing vesicles, purpura and target lesions are erupt acutely. Patients frequently complain of skin tenderness and burning.
Oral, genital and perianal mucosa develop bullae and erosions. Thick, hemorrhagic crusts cover the lips. Patients develop conjunctivitis and are at risk for corneal ulceration and uveitis. SJS skin lesions are more centrally distributed on the face and trunk.
Crops of lesions erupt for 10-14 days and slowly subside for the next 3-4 weeks

Front 258

Non-Skin Findings

Back 258

(a) During the early phase, 10-30% of patients develop high fever with marked constitutional symptoms.
(b) Pulmonary pneumonitis (23%), bronchits (6%), gastrointestinal (dysphagia, abdominal pain, diarrhea), central nervous system (seizure, coma) and renal (renal failure) systems can be affected.
(c) With widespread skin breakdown, patients develop increased fluid and nutritional requirements and are at risk for sepsis.

Front 259

Lab/Imaging Findings

Back 259

(1) Skin biopsy is diagnostic, showing full-thickness epidermal necrosis with a relatively normal dermis.

Front 260

Differential Diagnosis of SJS

Back 260

(1) Anticonvulsant Hypersensitivity syndrome
(2) Paraneoplastic Pempigus
(3) Pemphigus Vulgaris
(4) Herpetic Gingivostomatitis

Front 261

Treatment of SJS

Back 261

Uncomplicated Stevens-Johnson Syndrome resolves in a month.
In the case of limited disease and adequate supportive care, the mortality rate is less than 1%.
Recurrence is not common.

Front 262

Treatment regimens focus on identifying and treating sources of infection, withdrawing suspected offending drugs, maintaining fluid and nutritional requirements, providing meticulous local wound care and halting the progression of Stevens-Johnson syndrome.
(4) Lips can be soothed with frequent mouth rinses and applications of Vaseline or Aquaphor. Viscous Xylocaine or Benadryl elixir can also be helpful.
(5) Eyes should be treated frequently with topical Erythromycin ointment to prevent ocular adhesions. An Ophthalmologist should be consulted.

Back 262

True

Front 263

Disposition of nail injury

Back 263

Depends on severity, but frequently require hospitalization for effective management of condition.

Front 264

Complications

Back 264

(1) Secondary Skin Infection (Cellulitis)
(2) Sepsis
(3) Corneal ulceration
(4) Permanent skin damage

Front 265

Essential diagnosis of Ingrown Toenail

Back 265

(1) Presents with pain, redness, welling and sometimes discharge.
(2) Great toe is virtually the only toe involved, with either the medial or lateral border of the nail may be affected.
(3) Caused by lateral pressure of poorly fitting shoes, by improper or excessive trimming of the lateral nail plate or by trauma.

Front 266

(a) The nail enters the lateral or medial nail fold and enters the dermis, where it acts as a foreign body.
(b) The area of penetration becomes purulent and edematous as granulation tissue grows alongside the penetrating nail.
(4) It is not uncommon for patients to attempt self-remedies.
(5) Cellulitis may occur and require treatment with oral antibiotics.
(6) Podiatrists treat chronic recurrent ingrown nails by destroying the lateral nail matrix with phenol.

Back 266

True

Front 267

Treatment

Back 267

(a) Treatment involves removing the penetrated nail with scissors and curetting the granulation tissue.
1) Small areas of granulation tissue can be simply treated with silver nitrate.

Front 268

Ablation of the matrix tissue can be used to_______

Back 268

prevent regrowth of the nail for recurrent episodes.

Front 269

Disposition
Complications

Back 269

(a) Full Duty, however light duty may be indicated based on severity of pain and occupation.

(a) Infections
(b) Bleeding
(c) Recurrence

Front 270

Essential Diagnosis of Subungual Hematoma

Back 270

Most common of all injuries to the upper extremities.
(b) Results from a direct blow to the fingernail or a squeezing-type injury to the distal finger.
1) Causes bleeding into the space between the nail bed and fingernail itself.
a) Bleeding may cause separation of the nail
2) Intense pain caused by pressure generated by the hematoma.

Front 271

Treatment consists of evacuation of the hematoma.

Back 271

1) Wash the affected digit as thoroughly as possible with antibiotic soap to decrease potential for subsequent infection.
2) Consider digital block as pressure on the area can be extremely painful.

Create a hole in the nail directly over the center of the hematoma to allow decompression.

Front 272

a) Paperclip method:

Back 272

(1 Partially straighten a metal paperclip
(2 Grasp with forceps
(3 Heat over alcohol lamp or lighter
(4 Place on nail, allowing it to melt the tissue for a few seconds until the nail is completely performated.

Front 273

Cautery method

Back 273

Apply cautery tip to nail and create hole in the nail bed.

Front 274

Drill method

Back 274

Twist a large-bore needle or scalpel between your fingers gently in one place to create a 1-2 mm hole over the central area of the hematoma.
2 mm disposable punch biopsy tool can also be tried.
Drill devices such as a Dremmel tool or dental burr may also be used.

Front 275

(3) Disposition

(4) Complications

Back 275

(a) Full Duty

(a) Infection
(b) Pain
(c) Nail bed laceration