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Clinical Medicine I > Dermatology > Flashcards

Dermatology Flashcards

1
Q

What does annular mean?

A

ring shaped

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2
Q

What is a cyst?

A

a soft, raised, encapsulated lesion filled with semisolid or liquid contents

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3
Q

What does herpetiform mean?

A

in a grouped configuration

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4
Q

What is a lichenoid eruption?

A

Violaceous to purple, polygonal lesions that resemble those seen in lichen planus

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5
Q

What are milia?

A

small, firm, white papules filled with keratin

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6
Q

What is a morbilliform rash?

A

Generalized, small erthematous macules and/or papules that resemble lesions seen in measles

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7
Q

What does nummular mean?

A

coin-shaped

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8
Q

What is poikiloderma?

A

skin that displays variegated pigmentation, atrophy, and telangiectases

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9
Q

What are polycyclic lesions?

A

a configuration of skin lesions formed from coalescing rings or incomplete rings

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10
Q

What is pruritis?

A

itching

Predominant symptom of inflammatory skin diseases

Commonly associated with xerosis and aged skin

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11
Q

What is a macule?

A

a flat, colored lesion, <2cm in diameter, nonpalpable

Not raised above the surface of the surrounding skin

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12
Q

What is a patch?

A

Large, flat lesions with a color different from the surrounding skin

nonpalpable, > 2cm

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13
Q

What is a papule?

A

a small, solid lesion, <0.5cm in diameter

Raised above the surface of the surrounding skin and thus palpable

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14
Q

What is a nodule?

A

a larger, firm lesion raised above the surface of the surrounding skin and thus palpable

> 0.5 cm to 5.0cm

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15
Q

What is a placque?

A

a large ( > 1cm ), flat-topped, raised lesion

Edges can be distinct or blend in with surrounding skin

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16
Q

What is a vesicle?

A

a small, fluid filled lesion, < 0.5cm in diameter

Raised above the plane of surrounding skin

Fluid is often visible and the lesions are translucent

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17
Q

What is a pustule?

A

a vesicle filled with leukocytes

pus filled

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18
Q

What is a bulla?

A

A fluid-filled, raised, often translucent lesions > 0.5cm in diameter

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19
Q

What is a wheal?

A

A raised, erythematous, edematous papule or placque

Usually represents a short lived vasodilation and vasopermeability

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20
Q

What is telangiectasia?

A

A dilated, superficial blood vessel

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21
Q

What is lichenification?

A

A distinctive thickening of the skin that is characterized by accentuated skin-fold markings

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22
Q

What is a scale?

A

excessive accumulation of stratum corneum

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23
Q

What is a crust?

A

dried exudate of body fluids that may be either yellow or red

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24
Q

What is erosion?

A

Loss of epidermis without an associated loss of dermis

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25
Q

What is an ulcer?

A

loss of epidermis and at least a portion of the underlying dermis

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26
Q

What is excoriation?

A

linear, angular erosions that may be covered by crust and are caused by scratching

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27
Q

What is atrophy?

A

an acquired loss of substance

may appear as a depression with intact epidermis or as sites of shiny, delicate, wrinkled lesions

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28
Q

What clinical manifestations are different between Cellulitis, Erysipelas, and an Abscess?

A

Cellulitis occurs in the deeper dermis and SQ fat whereas Erysipelas occurs in the upper dermis and superficial lymphatics and an Abscess will occur in the upper and deeper dermis

Cellulitis develops over a period of days whereas Erysipelas occurs acutely

Cellulitis can be purulent or nonpurulent whereas Erysipelas is always nonpurulent

Cellulitis has less distinct borders whereas Erysipelas is clearly marked

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29
Q

What epidemiology is different between Cellulitis and Erysipelas?

A

Cellulitis typically occurs in middle aged and older adults whereas Erysipelas typically occurs in young children and older adults

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30
Q

What are the clinical manifestations of Cellulitis and Erysipelas?

A 
Erythema
Edema
Warmth
Bacterial breach in skin
UNILATERAL
Lower extremities involved
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31
Q

What are the risk factors for Cellulitis, Erysipelas, and an abscess?

A 
Pressure ulcers
Trauma
Eczema
Impetigo
Tinea
Radiation Therapy
Edema due lymphatic drainage or venous insufficiency 
Obesity
Immunosuppression
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32
Q

What bacteria causes cellulitis?

A

Strep and Staph aureus including MRSA

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33
Q

What bacteria causes Erysipelas?

A

Strep and S. pyogenes

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34
Q

What are the complications associated with Cellulitis, Erysipelas, and an Abscess?

A

Necrotizing fascitis
Bacteremia and sepsis
Osteomyelitis
Septic Joint

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35
Q

What is Cellulitis and Erysipelas hard to distinguish from?

A

Gout
DVT
Venus stasis dermatitis

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36
Q

What is your first line treatment for Cellulitis?

A

Nonpurulent: IV Cefazolin or Ceftriaxone
PO Penicillin or Amoxicillin or Bactrim
Purulent: IV Vanco plus Ceftriaxone plus Metronidazole or Vanco plus Unasyn
PO Doxycycline plus amoxicillin or Clindamycin

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37
Q

If the patients Cellulitis is caused by MRSA, what would you treat it with?

A

IV Vanco if Nonpurulent

PO Bactrim if purulent

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38
Q

How long should you treat Cellulitis with Antibiotics for?

A

7-10 days

Improvement should be seen within 24-48 hours

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39
Q

What do you use to treat Erysipelas?

A

IV Cefazolin or Ceftriaxone
PO Penicillin or Amoxicillin or Bactrim
IV Vanco if caused by MRSA

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40
Q

What bacteria causes an Abscess?

A

Staph aureus including MRSA

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41
Q

What are the clinical manifestations of an Abscess?

A 
Edema
Warmth
Erythema
Bacterial breach in skin
PAINFUL
Fluctuant/soft/movable
Red/Erythematous nodule
Can occur with or without cellulitis
Has a hard surrounding
Regional adenopathy
Systemic toxicity such as fever and chills
Often occurs on neck, face, or buttocks
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42
Q

What is furuncle?

A

infection of the hair follicle that causes an abscess

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43
Q

What is a carbuncle?

A

multiple hair follicles are infected

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44
Q

How would you treat an abscess?

A

IV Vanco plus Ceftraxone plus Metronidazole or Vanco plus Unasyn
PO Doxycycline plus Amoxicillin or Clindamycin
PO Bactrim for MRSA

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45
Q

What is Impetigo?

A

contagious superficial bacterial infection

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46
Q

What is the difference between primary and secondary impetigo?

A

Primary is a direct bacterial invasion of normal skin and secondary occurs at sites of skin trauma

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47
Q

What is the most common form of impetigo?

A

Nonbullous

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48
Q

What is nonbullous impetigo?

A

Papules form vesicles surrounded by erythema that then form pustules the enlarge, breakdown, and form thick adherent golden crusts

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49
Q

What is bullous impetigo?

A

Vesicles enlarge to form bulla with clear fluid that then become darker and rupture to leave thin brown crusts

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50
Q

What is bullous impetigo caused by?

A

S. aureus

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51
Q

Who and where does bullous impetigo effect?

A

Children and on the trunk

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52
Q

If you see what looks like bullous impetigo on an adult, what should you check them for?

A

HIV infection

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53
Q

What is ecthyma impetigo?

A

the ulcerative form of impetigo

Appear as punched out ulcers covered by yellow crusts

Lesions extend through epidermis and deep dermis

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54
Q

What is ecthyma impetigo caused by?

A

Strep pyogenes

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55
Q

What is sequelae impetigo?

A

Impetigo that occurs after 1-2 weeks of a strep infection

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56
Q

What are the clinical manifestations of sequelae impetigo?

A

Edema
HTN
Hematuria
Rheumatic fever

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57
Q

Who is impetigo most commonly seen in?

A

children ages 2-5

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58
Q

When is impetigo most commonly seen?

A

Summer and fall

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59
Q

Where is impetigo most commonly found?

A

Southeast US

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60
Q

How would you diagnose IMpetigo?

A

Honey colored, brown, or punched out crusty ulcers

Gram stain and culture

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61
Q

How would you treat mild impetigo?

A

Topical Mupirocin or Retapamulin

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62
Q

How would you treat severe and ecthyma impetigo?

A

PO Dicloxacillin or Cephalexin

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63
Q

What is Urticaria?

A

Hives
Welts
Wheals

Circumsized, raised, erythematous placques with central pallor

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64
Q

What are the clinical manifestations of Urticaria?

A

Intense itch
Can effect any area of the body
Lesions can be transient in nature
Lesions vary in size and shape

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65
Q

What is the severe form of urticaria?

A

Angioedema of lips, extremities, and genitals

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66
Q

What causes urticaria?

A

Caused by histamine and vasodilators being released by mast cells in the superficial epidermis

This is in response usually to something the patient is allergic to

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67
Q

What is the difference between acute and chronic urticaria?

A

Acute occurs for less than six weeks

Chronic is recurrent most days of the week for more than 6 weeks

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68
Q

If you suspect that an allergy is the cause for a patients urticaria, what test could you do do diagnose this?

A

Serum test for allergen specific IgE anitbodies

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69
Q

What is the treatment plan for patients with urticaria?

A

Relieve the pruritis and angioedema because the lesions will resolve on their own typically

Use first or second Gen. antihistamines:
Diphenhydramine or Ranitidine

A steroid may be used if the patients symptoms are longer than 2-3 days or are severe

Angioedema requires immediate treatment with PO or IV prednisone

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70
Q

What is a lipoma?

A

Benign soft-tissue neoplasm

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71
Q

What are the clinical manifestations of a lipoma?

A

Contains mature fat cells enclosed in thin fibrous capsule

Superficial

Soft and painless SQ nodule

Round, oval, multilobulated

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72
Q

Where does a lipoma typically occur?

A

upper extremities and trunk

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73
Q

How large is a lipoma?

A

1 to > 10 cm

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74
Q

Where do 50% of lipomas develop?

A

SQ tissue

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75
Q

What is the treatment for a lipoma?

A

None if stable and asymptomatic

Surgical excision can be done if necessary

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76
Q

What is tetanus?

A

Nervous system disorder characterized by muscle spasms

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77
Q

What is tetanus caused by?

A

C. Tetani

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78
Q

What are the clinical manifestations of Tetanus?

A

Trismus (lockjaw)
Masseter muscle reflex pasms
Tonic contractions of skeletal muscles
No consciousness impairment

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79
Q

What is the incubation period for Tetanus?

A

8 days but depends on how far from the CNS the inoculation site is

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80
Q

What is the pathophysiology behind Tetanus?

A

C. tetani turns into vegetative rod-shaped bacterium–>
Produces metalloprotease tetanospasmin (tetanus toxin)–>
Toxin blockes neurotransmission that modulates muscle contraction

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81
Q

What is the treatment for tetanus?

A 
IV Metronidazole
     Pen G
    Diazepam - for muscle contractions
    Midazolam - paralyze patient if severe
Pancuronium or Vecuronium
IM Human tetanus immune globulin
Wound debridement
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82
Q

What are the clinical manifestations of an epidermal inclusion cyst?

A 
Skin colored dermal nodule
Visible central punctum
Size can vary but usually smal
Lesions may be stable or get bigger
Spontaneous rupture can occur
Cheesy material comes out of it
Firm nodule
Asymptomatic
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83
Q

What disease are Epidermal Inclusion cysts associated with?

A

Gardener syndrome

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84
Q

Where do epidermal inclusions cysts most commonly occur and who do they occur in?

A

Face, neck, scalp, and trunk
Twice as common in men
Near hair follicle

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85
Q

What causes an epidermal inclusion cyst?

A

Result of trauma that causes implantation and proliferation of epithelial elements in the dermis

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86
Q

What is the treatment for Epidermal inclusion cysts?

A

Excision if symptomatic
None if asymptomatic
Intralesional injections with triamcinolone

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87
Q

What do you use to distinguish Necrotizine fascitis from cellulitis or an abscess?

A

LRINEC score

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88
Q

What score is associated with necrotizing fascitis?

A

> 6

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89
Q

What is acne?

A

Most common cutaneous disorder effecting adolescents and young adults
Inflammatory disease of pilosebaceous follicles
NO cure

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90
Q

What type of acne are women most prone to?

A

post-adolescent acne

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91
Q

What type of acne are men most prone to?

A

Adolescent acne

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92
Q

What are the four factors that cause acne?

A

1) Follicular hyperkeratinization
2) Increased Sebum Production
3) Cutibacterium acnes within follicle
4) Inflammation

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93
Q

What causes growth and secretory functions of sebaceous glands?

A

Androgens

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94
Q

What are some differential diagnoses of hyperandrogenism?

A

PCOS
Congenital adrenal hyperplasia
Adrenal or ovarian tumors

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95
Q

What is the onset of acne associated with?

A

Increase in DHEA-S levels as puberty hits

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96
Q

What are the four types of acne?

A

1) Inflammatory/Comedonal acne
2) Inflammatory lesions
3) Infant acne
4) Nodular acne

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97
Q

What are the causes of acne?

A 
External factors
Medications
Diet
Family History
Stress
Insulin Resistance
BMI
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98
Q

What is the treatment for follicular hyperproliferation?

A 
Topical Retinoids:  Retin A
Oral Retinoid:  Accutane
Azelaic acid
Salicylic acid
Hormonal therapies
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99
Q

What is the treatment for Increased sebum production?

A

Oral isotretinoin

Hormonal therapies

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100
Q

What is the treatment for C. acnes proliferation?

A

Benzoyl peroxide
Topical or oral Doxycycline
Azelaic acid

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101
Q

What is the treatment for inflammation caused by acne?

A

Oral isotretinoin
Topical retinoids
Azelaic acid

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102
Q

Patients with what disease are prone to getting cellulitis?

A

Rosacea

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103
Q

What is Erythematotelangiectatic Rosacea?

A 
Persistent central erythema
Flushing
Enlarged cutaneous blood vessels
Roughness and scaling
Skin sensitivity 
Erythema congestivum
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104
Q

What is papulopustular rosacea?

A

Papules and pustules on central face
Mistaken for acne but this doesn’t have comedomes
Inflammation extends beyond follicle

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105
Q

What is phymatous rosacea?

A

Thickened skin with irregular contours from tisue hypertrophy
Occurs most often on nose
Adult men

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106
Q

What is ocular rosacea?

A 
Occurs in > 50% of pts. with disease
Can precede, follow, or occur simultaneously with other types of rosacea
Conjunctival hyperemia
Blepharitis
Keratitis
Lid margin telangiectasias
Abnormal tearing
chalazion
Hordeolum
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107
Q

Who does rosacea commonly occur in?

A

fair skinned individuals and adults over 30

Mostly women

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108
Q

What causes rosacea?

A

Abnormalities in innate immunity
Inflammatory reactions to cutaneous microorganisms
UV damage
Vascular dysfunction

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109
Q

What are exacerbating factors of rosacea?

A 
Exposure to extreme temps.
Sun
Hot beverages
Spicy food
Alcohol
Exercise
irritation from topical products
Emotions
Drugs
Skin barrier disruption
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110
Q

What is the treatment for Erythematotelangiectatic rosacea?

A

AVOID triggers

Laser/light therapy

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111
Q

What is the treatment for Papulopustular rosacea?

A

Topical:
Metornidazole
Azelaic acid
Ivermectin

Oral:
Tetracycline, Doxycycline, or Minocycline
Isotretinoin

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112
Q

What is the treatment for ocular rosacea?

A

Lid scrubs
Warm compresses
Topical antibiotics like ilotycin
Refer to ophthalmologist

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113
Q

What is the treatment for phymatous rosacea?

A

Laser ablation and surgery

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114
Q

What is psoriasis?

A

inflammatory skin disease

Well-demarcated, erythematous placques with silver scales

Associated with psoriatic arthritis

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115
Q

What are the risk factors for psoriasis?

A 
Genetics
Smoking
Obesity
Drugs
Infections
Alcohol
Vit. D deficiency 
Stress
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116
Q

What is psoriasis caused by?

A

Immune mediated

Caused by hyperproliferation and abnomral differentiation of the epidermis, as well as, inflammatory cell infiltrates and vascular dilatation

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117
Q

What is chronic placque psoriasis?

A

Symetrically distributed
Found on scalp and extensor areas (elbows, knees, and gluteal cleft)
Itchy

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118
Q

What is the common type of psoriasis?

A

Chronic placque

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119
Q

What is Guttate placque psoriasis?

A 
Abrupt
Multiple, small papules and placques
<1cm
Found on trunk and proximal extremities
Associated with recent strep infection
Children and young adult
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120
Q

What is Pustular Psoriasis?

A 
LIFE THREATENING
SEVERE
acute onset
wide spread erythema, scaling, and sheets of superficial pustules
Malaise
Fevere
Diarrhea
Leukocytosis
Hypocalcemia
Can be caused by pregnancy, infection, and withdrawal of steroids
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121
Q

What is Erythrodermic psoriasis?

A

NON-LIFE THREATENING
uncommon
acute or chronic
Generalized erythema and scaling from head to tow
Caused by loss of adequate barrier electrolyte abnormalities

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122
Q

What is inverse psoriasis?

A

Found in intertriginous areas (inguinal, perineal, genital, axillary, etc. )
Can be misdiagnosed as a fungal or bacterial infection

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123
Q

What is nail psoriasis?

A

Seen after cutaneous type of psoriasis is diagnosed
Common in pts. with psoriatic arthritis
Nail pitting

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124
Q

How do you treat mild to moderate psoriasis?

A 
Emollients
Topical Corticosteroids:  hydrocortisone
Vitamin D analogs
Tar-T/Gel shampoo
Topical Retinoids
Anthralin
Tacrolimus or Pimecrolimus
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125
Q

How do you treat moderate to severe psoriasis?

A

Phototherapy in 25 treatments - usually UVB
Excimer laster in 10 treatments
Systemic therapies: Methotrexate
Biologics: Entanercept

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126
Q

What is alopecia?

A

Immune mediated disorder that targets active hair follicles (anagen) causing nonscarring hair loss

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127
Q

What are the clinical manifestations of Alopecia?

A

Smooth, circular, discrete patches of complete hair loss
Develops over a period of 2-3 weeks
Occasional itching or burning
Can spread into bizarre patterns
Can involve any and all body hair but typically occurs on scalp
Onychorrhexis

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128
Q

What is alopecia areata?

A

discrete patches

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129
Q

What is alopecia totalis?

A

entire scalp

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130
Q

What is alopecia universalis?

A

Entire body

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131
Q

What causes alopecia?

A

T-cells cause inflammation which disrupts the normal hair cycle

Hair follicle is then prematurely inactivated

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132
Q

What are the risk factors for alopecia?

A 
Genetic
Severe stress
Drugs and vaccines
Infections
Vitamin D deficiency
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133
Q

What diseases are associated with alopecia?

A 
Lupus
Vitiligo
Atopic dermatitis
THYROID DISEASE
Allergic rhinitis
Psoriasis
Down Syndrome
Polyglandular autoimmune syndrome type 1
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134
Q

What are characteristic signs to look for to diagnose alopecia?

A

Exclamation point hair at margins

Swarm of Bees pathology

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135
Q

How do you treat limited hair loss?

A

Topical or intralesional corticosteroids

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136
Q

How do you treat extensive alopecia?

A

Topical immunotherapy
Minoxidil
Systemic therapies

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137
Q

What are the clinical manifestations of Hidradenitis Suppurativa?

A

Axillae is most common site but occurs in other intertriginous areas also
Primary lesions is solitary, painful, and deep-seated inflammed nodule
Chronic disease causes sinus tracts and scarring

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138
Q

Who does Hidradenitis Suppurative most commonly effect?

A

Women from puberty to age 40

Usually african american women

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139
Q

What causes Hidradenitis Suppurativa?

A

Caused by follicular occlusion, follicular rupture, and the associated immune response

Ductal keratinocyte proliferation –> ductal pluggin –> expansion –> Rupture and release of contents –> immune response stimulated –> sinus tracts

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140
Q

What are the risk factors for Hidradenitis Suppurativa?

A 
Genetics = 40% with first degree relative
Mechanical stress
Obesity
Smoking
Hormones
Bacteria
Drugs
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141
Q

What do we use to diagnose the clinical stages of Hidradenitis Suppurativa?

A

Hurley Clinical Staging

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142
Q

What is Hurley Stage 1?

A

Abscess formation

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143
Q

What is Hurley Stage 2?

A

Recurrent abscess formation with sinus tract formation and scarring

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144
Q

What is Hurley Stage 3?

A

Diffuse involvement of multiple interconnected sinus tracts

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145
Q

How do we treat Hidradenitis Suppurativa?

A 
Prevent it:
Avoid skin trauma
Stop smoking
Weight management
Antiseptics
Emollients
Manage comorbidities
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146
Q

How do we treat Hurley Stage 1 HIdradenitis Suppurativa?

A

Topical Clindamycin
Intralesional corticosteroid
Punch debridement
Chemical peel

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147
Q

How do we treat Hurley Stage 2 Hidradenitis Suppurativa?

A 
Oral tetracyclines for several months
Clindamycin or Rifampin
Oral retinoids
Antiadrenergic therapies
Punch biopsy of fresh lesions
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148
Q

How do we treat Hurley Stage 3 Hidradenitis Suppurativa?

A

TNF alpha inhibitors
Systemic glucocoritcoids: Prednisone
Cyclosporine
Surgery

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149
Q

What causes Molluscum Contagiosum?

A

Poxvirus, MCV 1-4

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150
Q

Who does Molluscum Contagiosum commonly affect?

A

CHILDREN
Sexually active adults
Immunosuppressed

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151
Q

How is Molluscum Contagiosum transmitted?

A

Direct skin to skin contact
Pools
Gym equipment
Spread by autoinoculation

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152
Q

What does Molluscum Contagiosum look like?

A

Non-pruritic flesh colored, dome shaped papules
3-6 mm
Curd like material inside

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153
Q

Where can Molluscum Contagiosum appear?

A

Anywhere but usually face, trunk, extremities, and groin

Anyplace that kids like to put their hands

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154
Q

What are the differential diagnoses for Molluscum contagiosum?

A

Warts

Milia

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155
Q

How would you diagnose Molluscum Contagiosum?

A

Clinical exam and history

Punch biopsy

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156
Q

What is the treatment plan for Molluscum Contagiosum?

A

None; it is self-limited and will resolve after a few months to a few years

Tell patient to avoid autoinoculation

Topical Cantharadin or Cryotherapy have been used to speed up the healing process by mildly irritating the papules

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157
Q

What causes warts (Verruca)?

A

HPV

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158
Q

What is Verruca Vulgaris?

A

Common wart

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159
Q

What is Verruca PLana?

A

flat wart

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160
Q

What is Verruca Plantaris?

A

plantar wart

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161
Q

What increased the risk of getting Verruca vulgaris?

A

frequent water exposure

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162
Q

Who are most likely to get Verruca Vulgaris?

A

Patients ages 5-20

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163
Q

Where are Verruca Vulgaris typically found?

A

Hands
Palms
Periungual
Nail folds

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164
Q

What does Verruca Vulgaris look like?

A

Papules with a rough grayish surface and skin like projections

Pinpoint size to > 1 cm

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165
Q

Who are Verruca Plana most common in?

A

Children and young adults

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166
Q

Where do Verruca Plana typically occur?

A

Groups on face, neck, wrists, and hands

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167
Q

What do Verruca Plana look like?

A

2-4mm flat topped, flesh colored papules

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168
Q

Where are Verruca PLantaris found?

A

anywhere on the sole of the foot where there are usually pressure points

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169
Q

How do you diagnose Verruca?

A

Clinical exam or punch biopsy

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170
Q

How are Verruca treated?

A

65% will regress spontaneously within 2 years so they aren’t typically treated

If they are extensive, causing issues, or not gone in 2 years they can be treated with:
Cryotherapy
Salicyclic Acid/Cantharadin
Occlusive Dressing

Intralesional injection of Bleomycin is only used in severe cases

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171
Q

What causes Tinea Versicolor?

A

Malassezia Furfur = a yeast

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172
Q

What does Tinea Versicolor look like?

A

Hypo or hyperpigmented macules that do not tan

Well defined, round macules with scaling on trunk, arms, or face

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173
Q

What is a differential diagnosis of Tinea Versicolor?

A

Vitiligo

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174
Q

How do you diagnose Tinea Versicolor?

A

KOH scraping –> spaghetti and meatballs (hyphae and spores) seen under microscopy

Wood’s lamp –> Flourescent and orange or mustard colored

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175
Q

How do we treat Tinea Versicolor?

A

Daily Selenium sulfide shampoo for 15 min. for 7 days

Topical Ketoconazole cream daily for 3 weeks

Oral ketaconazole 200 mg daily for 2 weeks = severe cases and risk of elevated LFTs

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176
Q

What is Tinea Corporis caused by?

A

Dermatophytes

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177
Q

How does patient get Tinea Corporis?

A

comes in direct contact with organism

Often seen in wrestlers due to close contact

178
Q

What does Tinea Corporis look like?

A

Annular with peripheral enlargement and central clearing

Scaly “active border”

Assymmetric disribution on face, trunk, and extremities

Pruritic

Papular, NOT flat

179
Q

What is a differential diagnosis of Tinea Corporis?

A

Acute Lyme Disease –> this isn’t scaly though and looks more like a target

180
Q

How do we diagnose Tinea Corporis?

A

Positive KOH

Fungal cultures

181
Q

How do we treat Tinea Corporis?

A

Topical Antifungals:

Naftin or Ketoconazole cream twice a day for 2 weeks

182
Q

What does Tinea Pedis look like?

A

Scale and maceration on toe web spaces

Moccasin type distribution on plantar surfaces

Distinct borders

Pruritic feet

Inflammation and fissures can occur

183
Q

How do we diagnose Tinea pedis?

A

Positive KOH

Fungal culture

184
Q

What is the treatment for Tinea pedis?

A

Keep feet dry

Zeasorb-AF (Miconazole) powder

Topical antifungal creams twice a day:
Naftin
Ketoconazole
Lotrimine

Lostrisone cream once a week if severe (steroid + antifungal)

185
Q

What is causes Vitiligo?

A

Auto-immune destruction of melanocytes

Idiopathic

186
Q

What are the signs/symptoms of Vitiligo?

A

Hypopigmentation macules

Focal or generalized pattern

Hair in vitiliginous areas can also become white

Seen in areas with microscopic trauma

187
Q

How do you diagnose Vitiligo?

A

Clinical exam

Punch biopsy

Woods lamp –> Milky white appearance

188
Q

How do you treat Vitiligo?

A

Sunscreen/avoiding sun exposure

Cosmetic coverups

Non-steroidal anti-inflammatory medications:
tacrolimus ( Protopic)
Pimecrolimus (Elidel)

Phototherapy:
UVB
Exciser laser

189
Q

What causes Varicella (chickenpox)?

A

Varicella Zoster Virus

190
Q

Who does Varicella most commonly occur in?

A

Children < 10

In tropical areas = teenagers

191
Q

What is the incubation period for Varicella?

A

10-21 days

192
Q

How is Varicella transmitted?

A

Direct contact with lesion

Respiratory route

193
Q

How long is the patient infectious for with Varicella?

A

4 days before and 5 days after lesions appear

Once lesions are crusted over, they are no longer infectious

194
Q

What are the clinical manifestations of Varicella?

A

Rash

Malaise

Low grade temp.

Faint macules that change to Teardrop vesicles on a erythematous base

Appears on extremities

Vesicles are first pruritic, then pustular, then crusted; all phases can appear

195
Q

What complications can occur from Varicella?

A

Staph or strep infection from opening the lesions

196
Q

What are adults who get Varicella at risk for?

A

Pneumonia

197
Q

How do we diagnose Varicella?

A

Clinical exam

TZANK SMEAR from vesicle –> multinucleated giant cells

198
Q

How do we treat Varicella?

A

In healthy children < 13:
Supportive care like oatmeal baths, calamine lotion and antihistamines

AVOID ASPIRIN in any age group that has this disease

Immunocompetent adult > 13:
Oral Acyclovir within 24 hrs. for 5 days

Immunocompromised:
IV Acyclovir

Immunization

199
Q

What is Herpes Zoster?

A

shingles

Reactivation of Varicella Zoster Virus

200
Q

Where does Varicella Zoster Virus like to hide in the body?

A

Sensory dorsal root ganglion

201
Q

What does the rash in Herpes Zoster correspond to?

A

Dermatomes

202
Q

Who most commonly get Herpes Zoster?

A

patients older than 50

203
Q

How do patients spread the virus?

A

Through direct contact only

204
Q

What are the clinical manifestations of Herpes Zoster?

A

Prodrome of pain followed by rash along affected Dermatome

Pain feels like burning, electrical, or throbbing

UNILATERAL lesions

Papules and placques of erythema develop into vesicles which can become hemorrhagic or bullous

205
Q

When do lesions typically appear in Herpes Zoster?

A

1-5 days after reactivation

206
Q

How long do lesions usually last in Herpes Zoster?

A

2-3 weeks

Up to 6 weeks in the elderly

207
Q

What sign is a red flag in Herpes Zoster patients?

A

Hutchinson’s Sign:
Lesions on the side and tip of the nose

GET OPTHALMIC CONSULT immediately

208
Q

What are the differential diagnoses of Herpes Zoster?

A

There are many if lesions have not appeared and patient only comes in with a chief complaint of pain

209
Q

How do we diagnose Herpes Zoster?

A

Clinical exam is fine once lesions appear

TZANK SMEAR if not

210
Q

How do we treat Herpes Zoster?

A

Antiviral Therapy within 3-4 days:
Valacyclovir or Famiciclovir for 7 days

Prednisone

Domboro solution

Pain management:
Aceteminophen or NSAIDS –> NO ASPIRIN
Narcotics
Lidoderm patch

211
Q

How do we prevent Herpes Zoster?

A

Zostervax vaccine in patients over 60

212
Q

What is a complication of Herpes Zoster?

A

Post herpetic neuralgia

213
Q

How is herpetic neuralgia treated?

A

Nertontin
Tricyclic antidepressants
Gabapentin

214
Q

Where does HSV-1 reside and what type of herpes simplex is it associated with?

A

Trigeminal ganglia

Oro-labial herpes

215
Q

Where does HSV-2 reside and what type of herpes simplex is it associated with?

A

Presacral ganglia

Genital herpes

216
Q

How is Herpes Simplex transmitted?

A

By direct contact with infected secretions:
Sexual intercourse
Autoinoculation –> Herpetic Whitlow
Vertical from mother to baby

217
Q

What is the incubation period for Herpes Simplex?

A

2-20 days after exposure

218
Q

How long is a patient with Herpes Simplex infectious for?

A

Lifelong infection that can come back again and again

219
Q

What are the triggers for latent infections of Herpes Simplex?

A 
Stress
Menses
Fever
Infection
Sunlight
220
Q

Who is at an increased risk of getting Herpes Simplex?

A

Those with increased number of sexual partners

Those whose first intercourse was at a young age

221
Q

What are the clinical manifestations of Herpes Simplex?

A

Primary infections are asymptomatic usually

Fever
Myalgias
Malaise

222
Q

What does Oro-labial herpes Simplex present as?

A

Tender grouped vesicles/blisters on erythematous base
ULcerative
“cold sore”
Last 1-2 weeks
Reoccurence present with tingling/itching before breakout

223
Q

What does Genital Herpes Simplex present as?

A

Grouped blisters and erosions on vagina, rectum, or penis

1-2 weeks

224
Q

What does Herpetic Whitlow Herpes Simplex present as?

A

Occurs on fingers and periungually

Tenderness and erythema with deep seated blisters

225
Q

How do you diagnose Herpes Simplex?

A

TZANK SMEAR –> Giant nucleated cells seen

Fluroescent anitbody test/Western blot –> HSV-1 vs. HSV-2

226
Q

What is the treatment for Herpes Simplex?

A

No cure; decrease duration of symptoms, viral shedding, and time to health

227
Q

What is the primary treatment for Herpes Simplex?

A

Acyclovir 200mg five times a day for 10 days

Valacyclovir (Valtrex) 1 gm twice a day for 10 days***

228
Q

What is the Suppressive treatment for Herpes Simplex?

A

Acyclovir 400 mg twice a day

Valtrex 1 gr. daily

229
Q

What is the Recurrent treatment for Herpes Simplex?

A

Acyclovir 400mg three times a day for 5 days

Valtrex 2gm. twice a day for 1 day

230
Q

What is Paronychia?

A

Inflammatory reaction involving the folds of the skin around the fingernail

Can be acute or chronic

231
Q

What causes Paronychia?

A

A break in the skin associated with trauma to the eponychium or nail fold maceration of the proximal nail fold

232
Q

What causes Acute Paronychia?

A

Agressive manicure

Nail biting

Staph aureus/Gram +

233
Q

What causes Chronic Paronychia?

A

Frequent handwashing

Nail biting

Pseudomonas aeuginosa or Candida albicans

234
Q

What are the clinical manifestations of Acute Paronychia?

A

Erythema
Swelling
Pain extending to the proximal and lateral nail fold

Starts red, warm, and painful swelling of skin around nail and then progresses to formation of pus that may separate the skin from the nail

235
Q

What are the clinical manifestations of Chronic Paronychia?

A

Swollen
Erythematous
Tender without fluctuance
Nail can become thickened with transverse ridges

Occurs for > 6 weeks

236
Q

What is the differential diagnosis of Paronychia?

A

Herpetic Whitlow

237
Q

How do we diagnose Paronychia?

A

Fluctuant is usually bacterial so Culture and gram stain

KOH wet mount –> hyphae if acute and yeast if chronic

Clinical history and exam

238
Q

What is the treatment for Acute Paronychia?

A

Warm water soaks 3-4 times a day

PO antibiotic for Gram + staph aureus:
Augmentin 2gr. per day for 5 days

Topical steroid cream

Incision and drainage if it becomes abscessed

239
Q

What is the treatment for Chronic Paronychia?

A

Avoid inciting factors like moisture and manicuring

Warm soaks

Topical steroid cream

Antifungal:
Spectazole

240
Q

What is onychomycosis?

A

Infection of finger or toe nails by yeast or fungi

241
Q

Who is onychomycosis most common in?

A

Patients with other nail problems like nail trauma, immunocompromised, vascular insufficiency and Down syndrome

242
Q

What agent causes onychomycosis of the hands?

A

T. Mentagrophytes

243
Q

What agent causes onychomycosis of the feet?

A

C. albicans

244
Q

What are the clinical manifestations of onychomycosis?

A

Nail thickening

Subungual hyperkeratosis = scale build up

Nail dystrophy

Onycholysis = nail plate elevation from nail bed

Asymptomatic

245
Q

How do we diagnose Onychomycosis?

A

Positive KOH

Fungal/yeast culture

246
Q

How do we treat Onychomycosis?

A

Very difficult to treat and there aren’t a lot of options that are effective

Topical Agents:
Penlac Lacquer (Ciclopirox) solution
Jublia (Efinaconazole) solution

Lamisil 250 for 6-12 weeks is a PO med but the cure rate is <40% and you must check LFTs before, during, and after use

White vinegar soaks

247
Q

What are Eczematous Eruptions?

A

Dermatitis and Eczema

Family of superficial, pruritic, erythematous skin lesions that can be red, blistering, oozing, or thickened skin

248
Q

What is the most common type of Eczema?

A

Atopic Dermatitis

5-10% of the population has it

249
Q

What type of reaction is Atopic Dermatitis?

A

Type 1 IgE mediated hypersenstivity reaction

250
Q

What other diseases do patients with Atopic Dermatitis usually also have?

A

Asthma or allergic rhinitis

251
Q

What are the Clinical Manifestations of Atopic Dermatitis?

A

“the itch that rashes”

Occurs on FLEXOR surfaces:
Neck
Eyelids
Face
Dorsum of hands and feet

Papules or plaques

Edema

Erosion

With or without scales or crusting

Persistent dry skin

Dennie Morgan lines

Hyperlinear palmar creases

252
Q

What is Atopic Dermatitis characterized by?

A

Pruritis

Flexural lichenification

Occurs in infancy on face and extensor surfaces

Personal or family history of allergic rhinitis, asthma, or atopic dermatitis

Skin is inflamed, not dry

253
Q

What can exacerbate Atopic Dermatitis?

A

Foods
Alcohol
Cold/hot/humid weather
Mites

254
Q

What histology is seen in Atopic Dermatitis?

A

varies with stage of lesion

Older lesions:
Hyperkeratosis
Acanthosis = epidermal thickening
Excoriation

Staph colonization

Eosinophil deposition

255
Q

What is infantile atopic dermatitis?

A

presents in first year of life

Appears on cheeks, chest, neck, and extensor/flexor extremities

Eruption can be generalized

Scaly, red, occassionally oozing lesions

Symmetric

256
Q

What is adult/adolescent atopic dermatitis?

A 
Will be seen more on flexor surfaces than extensors:
Hands
Wrist
Ankle
Feet
Nape of Neck
Eyelids
Vulva
Scrotum

Lichenified plaques are not as marked

Typically blends into surrounding skin

Post-inflammatory hyper/hypo pigmented changes occur

257
Q

What are the differential diagnoses of Atopic Dermatitis?

A

Contact Dermatitis
Scabies
Psoriasis

258
Q

How do we treat Atopic Dermatitis?

A

Topical Steroids for shorter period

High potency:
Betamethasone dipropionate
Clobetasol

Low potency:
Desonide
Dexamethasone

Antihistamines for itch:
Atarax (Hydroxasine)
Zyrtec (Cetrizine)

Topical Immunomodulators:
Tacrolimus (protopic)
Pimecrolimus (elidel)

Nonsteroidal:
Crisaborole (Eucrisa)

Biologic:
Dupilumab (Dupixent) –> SQ injection every 2 weeks

PO antibiotics:
Keflex (cephalexin) 500mg every day for 10 days –> secondary staph infection

259
Q

What are the clinical manifestations of Nummular Eczema?

A

Coin shaped pruritic plaques and patches

Occur in clusters

Atopic pts.

Clear central space

Healing lesions display post-inflammatory hyperpigmentation

260
Q

Where does Nummular Eczema usually occur?

A

Lesions on legs

261
Q

How is Nummular Eczema diagnosed?

A

Clinical appearance

Negative KOH

262
Q

What are the differential diagnoses of Nummular Eczema?

A

Tinea corporis

Positive KOH or fungal culture

263
Q

How do we treat Nummular Eczema?

A

Acute:
Intermediate strength topical steroid –> Triamcinolone cream 0.1%
Severe –> high potency Clobetasol ointment with or without occlusion

Long-term:
Less potent topical steroid

264
Q

What is Dyshydrosis?

A

Wet eczema

265
Q

What causes Dyshydrosis?

A

Lesions occur from inflammation and foci of intercellular edema which becomes loculated in the skin of the palm and soles

266
Q

What are the clinical manifestations of Dyshydrosis?

A

Small vesicles

Appear on hands and feet

Pruritis

267
Q

How do we treat Dyshydrosis?

A

Cetaphil –> mild cleanser

Emollient barrier creams, protective gloves, and avoidance of irritants

Burrow’s solution as an antibacterial astringent

Topical corticosteroids:
High –> Clobetasol Ointment for acute flare
Moderate –> Triamcinolone 0.1% or Fluocinoide 0.05% with or without occlusion

Protopic and Elidel for long-term management

268
Q

What is contact dermatitis?

A

Applies to acute or chronic inflammatory reactions to substances that come in contact with the skin

269
Q

What is Irritant Contact Dermatitis caused by?

A

Direct toxic reaction to rubbing, friction, maceration, or exposure to a chemical or thermal agent

270
Q

What types of irritants can cause irritant contact dermatitis?

A

Alkalis
Acids
Soaps
Detergents

Diaper Rash

271
Q

What are the clinical manifestations of Irritant Contact Dermatitis?

A

Erythematous

Scaly

Eczematous Eruption

272
Q

How do we treat Irritant Contact Dermatitis?

A

avoid offending agent

273
Q

What causes Allergic Contact Dermatitis?

A

Type IV Delayed Hypersensitivity reaction after an exposure to an allergic substance such as poison ivy, nickel, or chemicals

274
Q

How long does it take before symptoms of allergic contact dermatitis appear?

A

a few days

275
Q

What are the clinical manifestations of allergic contact dermatitis?

A

Well demarcated, linear, pruritic rash at site of contact

Itching/burning

Poison Ivy –> linear streaks of Juicy papules and vesicles

276
Q

What is the differential diagnosis of Allergic Contact dermatitis?

A

Herpes Zoster

277
Q

How do we treat Allergic Contact Dermatitis?

A

Remove the offending agent

Cool showers

Burrow’s solution

Potent or super potent topical steroids

Severe cases may warrant a systemic steroid

278
Q

What are the clinical manifestations of diaper dermatitis?

A

Erythema

Scaley papules and plaques

Neglecting the rash causes erosion and ulceration

279
Q

What is diaper dermatitis caused by?

A

Overhydration of the skin

Skin is then irritated by chafing, soaps, and prolonged contact with urine and feces

280
Q

What does diaper dermatitis spare?

A

The creases where the diaper doesn’t make contact with the skin

281
Q

What is the differential diagnosis for Diaper Dermatitis?

A

Candida albicans infection –> This is more beefy red

282
Q

How do we treat Diaper Dermatitis?

A

Zinc oxide ointment

Frequent diaper changes

OTC hydrocortisone cream

Air it out

283
Q

Who does Perioral Dermatitis typically occur in?

A

Young women and children

284
Q

Where does Perioral Dermatitis typically occur?

A

Around the mouth

285
Q

What does Perioral Dermatitis look like?

A

Clustered papulopustules on erythematous bases

May have scales

286
Q

How do we treat Perioral Dermatitis?

A

Topical Antibiotics:
Metronidazole
Erythromycin

If severe use PO:
Minocyclin or Doxycycline

Avoid topical steroids

287
Q

What causes Stasis Dermatitis?

A

Venous insufficiency

Incompetent valves –> decreased venous return –> increased hydrostatic pressure –> edema –> tissue hypoxia

288
Q

Where is Stasis Dermatitis usually seen?

A

lower legs

289
Q

Who is Stasis Dermatitis usually seen in?

A

women with genetic predisposition to varicosities

290
Q

What are the clinical manifestations of Stasis Dermatitis?

A

Erythematous scale develops into erythema, edema, erosions, crusts, and secondary infections

Erythema will change to hyperpigmented skin that is thick with a WOODY appearance

Can develop ulcers

291
Q

How do we treat Stasis Dermatitis?

A

Elastic compression stockings

Burrow’s solution

Moderate Topical Steroid –> Desonide ro Triamcinolone cream

Use Keflex to treat secondary infection

292
Q

What is Seborrheic Dermatitis caused by?

A

Yeast, P. ovale

293
Q

Where is Seborrheic Dermatitis distributed?

A

Scalp
Face
Body folds

Areas where there are a lot of sebaceous glands

294
Q

What are the clinical manifestations of Seborrheic Dermatitis?

A

Pruritic

Yellowish Gray

Scaly macules

Greasy look on body folds, face, and scalp

Cradle cap in infants

Dandruff in adults

295
Q

How do we treat Seborrheic Dermatitis?

A

Scalp:
Zinc shampoo
Ketoconazole shampoo

Face and Intertriginous areas:
Low potency topical steroids –> Desonide or Valisone Cream

296
Q

What are the clinical manifestations of Lichen Simplex Chronicus?

A

Chronic

Solitary

Pruritic

Eczematous Eruption

Caused by repetitive rubbing and scratching

Focal lichenification placque or multiple plaques

Hemosiderin staining

297
Q

Where is Lichen Simplex Chronicus usually distributed?

A

Nape of Neck

Vulvae

Scrotum

Wrists

Extensor forearms

Ankles - pretibial area

Groin

298
Q

What are the differential diagnoses of Lichen Simplex Chronicus?

A

Tinea Cruruls
Candidiasis
Inverse Psoriasis

299
Q

How do we treat Lichen Simplex Chronicus?

A

Intermediate strength topical steroid –> Triamcinolone cream 0.1% PRN

Occlusion when able

Oral antihistamines

Protopic or Elidel 1%

300
Q

What areas does Lichen Planus effect?

A

Skin
Mucous Membranes
Hair follicles
Flexor aspects of wrists, lumbar area, eyelids, shins, and scalp

301
Q

What are the 4 P’s of Lichen Planus?

A

Purple
Polygonal
Pruritic
Papule

Lesions

302
Q

What are the clinical manifestations of Lichen Planus?

A

The 4 P’s
Lesions are groups together
Reticular white lesions on buccal mucosa
Variations can be ulcerative

303
Q

How do we treat Lichen Planus?

A

Potent topical steroids with occlusion

Intralesional steroid injections

304
Q

What else is Seborrheic Keratosis called?

A

Senile Wart

Basal Cell Papilloma

305
Q

Who does Seborrheic Keratosis usually occur in?

A

adults over the age of 60

306
Q

What are the clinical manifestations of Seborrheic Keratosis?

A

“stuck on”, flat or raised papule or plaque 1 to several cm in diameter

White, flesh-colored to tan, brown, warty, or smooth

May look like a barnacle on lower extremities

They start flat and then become raised

307
Q

What is the treatment for Seborrheic Keratosis?

A

Nothing

308
Q

What causes Kaposi Sarcoma?

A

Genetic factors

Hormonal factors

Immunodeficiency

Infection with HHV-8

309
Q

What are the types of Kaposi Sarcoma?

A

Classic

HIV-associated

Endemic/African

Iatrogenic Immune Suppressed

310
Q

Which type of Kaposi Sarcoma is aggresive and patient usually dies within 2 years?

A

Endemic/African type

311
Q

What are the clinical manifestations of Kaposi Sarcoma?

A

Lesions start as red to purplish macules that then become infiltrative plaques and nodules or tumors

Lesions occur on mucous membranes or skin

Lesions are often found on lower extremities first and then on hands and arms much later

Lymphedema

Lesions start out painless and small but then become large and ulcerative

312
Q

What would you see histologically in the early stage of Kaposi Sarcoma?

A

Endothelial cells of capillaries are large and protrude into the lumen like buds

Capillaries will become blocked and dilated

313
Q

What would you see histologically in the late stage of Kaposi Sarcoma?

A

Proliferation of vessels around preexisting vesicles and adnexal structures

Capillaries become very large and protrude into the skin

314
Q

What is the treatment for Kaposi Sarcoma?

A 
HIV antiretroviral treatment
Radiation therapy
Cryotherapy
Surgical excision of individual nodules
Topical Alitretinoin (panretin) gel
Pulsed dye laser
315
Q

What is actinic keratosis?

A

In situ dysplasia resulting from UV radiation that may progress to squamous cell carcinoma

316
Q

What is the most common UV radiation to cause actinic keratosis?

A

UVA because it penetrates deeper and longer

317
Q

Who is most effected by actinic keratosis?

A

White skinned

Men more than women

> 50

Those who lead an outdoor lifestyle

318
Q

What does the epidermis look like in patients with actinic keratosis?

A

Cellular atypia

Hyperkeratosis

Inflammatory infiltrate

319
Q

What are the clinical manifestations of actinic keratosis?

A

Rough, “sandpaper” texture of lesions when felt

Lesions found in areas chronically exposed to the skin:
Face
Ears
Scalp
Dorsal hands
Forearms
Anterior legs

Multiple, discreet, flat or elevated verrucuous or keratotic, red, pigmented or skin colored lesions

Lesions may have a scale or can be smooth and shiny

3mm-2cm

320
Q

What are the differential diagnoses for actinic keratosis?

A

Basal cell carcinoma

Seborrheic keratosis

Squamous cell carcinoma

Lupus Erythematosus

321
Q

What is the treatment for actinic keratosis?

A

Cryotherapy–> be careful of bleaching of skin

Topical Medications:

Imiquimod 5%, 3X a week for one month or 3.75% daily for 2 weeks on and 2 weeks off for 2 months–> extenisve and broad lesions; causes erythema and crusting of skin

Ingenol Mebutate (Picato) –> Daily for 3 days to face or 2 days to body

5-FU –> twice a day for four weeks; extremely irritating to the skin; insurance typically covers this

322
Q

When should an actinic keratosis be biopsied?

A

If it is not responding to treatment

There is a possibility it might be SCC

323
Q

What is the prognosis for actinic keratosis?

A

Good if patient listens to patient education, covers up in the sun, and continues to treat lesions

Should follow up every 2-6 months

324
Q

What two skin cancers are subtypes of Nonmelanoma SKin cancers?

A

Basal Cell carcinoma and Squamous cell carcinoma

325
Q

What is the most common form of all cancers?

A

Nonmelanoma Skin cancers

326
Q

When do nonmelanoma skin cancers usually occur?

A

In patients over the age of 55

327
Q

Which type of skin cancer makes up the majority of Nonmelanoma skin cancers?

A

Basal Cell Carcinoma

328
Q

What is basal cell carcinoma?

A

An epithelial tumor of basal keratinocytes

329
Q

Which type of nonmelanoma skin cancer has the lowest risk of metastasis?

A

basal cell carcinoma

330
Q

What are the risk factors for basal cell carcinoma?

A

Having white skin
Living close to the equator
Patients > 40
Outdoor lifestyle

331
Q

What increases a patients risk of getting basal cell carcinoma 10 fold?

A

Immunosuppression for organ transplant

332
Q

What are the clinical manifestations of Basal cell carcinoma?

A

Patient will report a slowly enlarging lesion that doesn’t heal and bleeds easily

May have a “rolled edge”

Pearly and translucent

Occurs mostly on face, hands, and neck

Flat, firm, pale area that is small, raised, pink, or red, translucent, pearly, and waxy and the area may bleed following minor injury

Runs a slow course and becomes ulcerative –> Rodent ulcer

333
Q

What are the types of Basal Cell Carcinoma?

A

Nodular
Superficial
Morpheaform (sclerosing)
Pigmented

334
Q

What is the most common type of basal cell carcinoma?

A

Nodular

335
Q

What does nodule BCC look like?

A

waxy, pearly, semi-translucent nodules or papules with “rolled edge” forming around a central depression that may or may not be ulcerated, crusted, and bleeding

336
Q

What does Superficial BCC look like?

A

Dry, scaly lesions, superfical flat growths

may be misdiagnosed as eczema or psoriasis

Edge shows a threadlike, raised border

337
Q

What does morphaeform (sclerosing) BCC look like?

A

White, sclerotic plaque with telangiectasia

Scar like in appearance

338
Q

What does pigmented BCC look like?

A

Similar to nodular but has brown or black pigmentation

339
Q

What are the differential diagnoses of BCC?

A 
SCC
Sebaceous hyperplasia
Actinic keratosis 
Eczema
Psoriasis
340
Q

How do we diagnose BCC?

A

biopsy which will show large, round or oval tumor islands within the dermis, often with an epidermal attachment

341
Q

What is the treatment for BCC?

A 
Surgical:
Electrodessication and Curettage
Cryosurgery
Excision with margins
Mohs Micrographic Surgery

Topical:
5% Imiquimod
5-FU

Radiation

342
Q

What types of BCC is Electrodessication and Curettage used for?

A

superficial lesions on non-hair bearing areas

343
Q

What is the gold standard treatment for BCC tumors greater than 2cm and on facial areas?

A

Mohs Micrographic Surgery

344
Q

What types of BCC is Imiquimod and 5-FU used to treat?

A

superficial BCC

345
Q

What are the risk factors for having squamous cell carcinoma?

A

> 50

Male

Light skinned

Tobacco and alcohol use

Living close to the equator

History of previous NMSC

Immunosuppression

HPV

Cehmical carcinogens like arsenic, tar, and polyaromatic hydrocarbons

346
Q

What are the types of squamous cell carcinoma?

A

SCC in sity = Bowen’s disease –> full thickness of epidermis

Invasive –> Penetrates in dermis

347
Q

What are the clinical manifestations of Squamous cell carcinoma?

A

Begins at site of actinic keratosis

Superficial papules, plaques or nodules, discrete and hard arising form an indurated, round elevated base

Lesions become large and ulcerated over months

Lesions are initially covered by crust

Invades underlying tissues

348
Q

What does lower lip SCC look like?

A

starts as actinic cheilitis then progresses to local thickening of keratosis, then firm nodule that may grow outward as sizable tumor

occurs in patients with a history of smoking

349
Q

What does Periungal SCC look like?

A

Presents with signs of swelling, erythema, and localized pain

commonly on nail folds of hands, resembling a wart

likely related to HPV

350
Q

What are the differential diagnoses of SCC?

A

Actinic keratosis

Eczematous rash/atopic dermatitis

351
Q

How do we diagnose SCC?

A

Biopsy –> Presence of Keratin or “keratin pearls”

352
Q

What is the treatment for SCC?

A

Excision

Mohs

Radiation

353
Q

Once a patient is diagnosed with SCC, what is their follow up plan?

A

Annual skin checks

354
Q

What is the most deadly cancer?

A

Melanoma

355
Q

What is melanoma?

A

Skin cancer of the melanocyte

356
Q

What are the risk factors for Melanoma?

A

MMRISK

M --> atypical moles
M -->  > 50 common moles
R -->  Red hair and freckles
I --> Inability to tan
S -->  Sunburn; sever and blistering
K --> Kindred/family history; usually in first degree relative
357
Q

What is the greatest risk factor for metastasis of Melanoma?

A

depth of invasion

358
Q

What are the clinical manifestations of melanoma?

A

Macular or nodular

Color varies from white to non-pigmented to dark black, blue, or red

Lesions borders tend to be irregular

Growth is quick or slow

Distribution can be on non-sun exposed areas also

359
Q

What method do we use to check pre-existing nevi for melanoma?

A

ABCD method

A –> Asymmetry
B –> Border is irregular
C –> Color is varied and nonsymmetric
D –> Diameter is greater than 6 mm

360
Q

What are the types of Melanoma?

A

Superficial spreading
Lentigo maligna
Nodular
Acral-lentiginous

361
Q

What is Superficial spreading melanoma?

A

Does not have tendency for sun damaged skin

Tendency to have multidiscoloartion including black, red, brown, blue, and white

Borders tend to be more sharply defined

362
Q

What is Lentigo Maligna Melanoma?

A

Start as macular and flat then become nodular

Most common on sun-damaged skin

Insidious slow growth

363
Q

What is nodular melanoma?

A

Arise without apparent radial growth phase

Primarily in sun exposed areas of head, neck, and trunk

Smooth and dome shaped

Friable and ulcerated and bleeding

Quickly invades deeply and has a higher rate of metastasis

364
Q

What is acral-lentiginous melanoma?

A

Most common in darker skin types

Light brown uniform pigmentation initially

On palms, soles, or nail beds

Lesions become darker, nodular, and may ulcerate

Many times, there is a delay in diagnosis

Should be concerned for this if you see lesion is spilling through proximal nail fold

365
Q

What is the staging system used for melanoma?

A

TNM system:

T –> tumor; 1-4 based on Breslow thickness
N –> Lymph nodes; 0-3 based on spread
M –> Metastasize

366
Q

When does melanoma automatically become Stage III?

A

When there is any lymph node involvement

367
Q

When does melanoma automatically become Stage IV?

A

When there is metastasis

368
Q

What is Breslow thickness?

A

The total vertical height of the melanoma, from the very top granular layer to the area of deepest penetration in to the skin

Ocular micrometer used to measure the thickness of the excised tumor

369
Q

How do we diagnose melanoma?

A

Excisional biopsy

Palpate lymph nodes

LDH

For stage IIIa –> chest xray

For Stage IIIB/C –> fine needle aspiration of lymph involvement

For Stage IV –> Consider abdominal or pelvic imaging or PET scan

370
Q

What is the treatment for melanoma?

A

Surgery –> simple excision for early stage or wide local excision for primary melanoma

Radiation –> used after surgery

Chemotherapy –> advanced malignant melanoma; Dacarbazine and Temozolomide

Adjunct therapy:
Cytokines (Intergeron Alpha and IL-2)

371
Q

What is the follow up plan for patients who survive melanoma?

A

Full skin check by dermatologist every 6 months for 2 years

Self-skin checks once a month

Sun protection

372
Q

How is measles transmitted?

A

Respiratory droplets

373
Q

What is the incubation period for measles?

A

9-12 days

374
Q

How long does it take for measles to clear?

A

4-7 days

375
Q

What are the prodrome symptoms?

A

3 C’s:

COugh

Coryza

Conjunctivitis

376
Q

What are the clinical manifestations of Measles?

A

Fever and then rash will appear

Rash starts as macular or morbilliform rash on anterior scalp and behind ears

By day 2-3, the rash spreads down the trunk to the extremities

Erythematous papules will coalesce

Includes palms and soles of hands and feet

Lesions will fade chronologically

Descending rash that takes days

377
Q

What is the diagnosis for Measles?

A

KOPLICK spots

378
Q

What are Koplick spots?

A

pathognomonic white papules 1mm on buccal mucosa and pharynx

379
Q

What is the treatment for Measles?

A

Supprotive care

Prevention through vaccination

380
Q

What is Rubella caused by?

A

Toga virus

381
Q

How is Rubella spread?

A

Respiratory secretions

382
Q

What is the incubation period for Rubella?

A

12-23 days

383
Q

Is there prodrome with Rubella?

A

No

384
Q

What are the clinical manifestations of Rubella?

A

1-5 days of fever, malaise, sore throat, and headache

Pain with lateral upward eye movement

Posterior cervical, suboccipital, and postauricular Lymphadenopathy

Lesions are pale, pink morbilliform macules smaller than rubeola

Rash will begin on face and spread inferiorly covering the entire body within 24 hours

Forschemier’s Sign

385
Q

How long does it take for the rash to resolve?

A

Day 3

386
Q

What is the Forschemier’s Sign?

A

Petechiae on soft palate and uvula

387
Q

What is the treatment for Rubella?

A

Supportive Care

Prevention with MMR vaccine

388
Q

What is Fifth Disease (Erythema Infectiosum) caused by?

A

parovirus

389
Q

How is Fifth Disease spread?

A

Respiratory droplets

390
Q

When does Fifth disease usually occur?

A

late winter and early spring

391
Q

When does viral shedding stop in Fifths disease?

A

by the time the rash appears

392
Q

What is the incubation period for Fifth Disease?

A

4-14 days

393
Q

What are the clinical manifestations of the 1st phase of Fifth Disease?

A

Abrupt asymptomatic erythema of cheeks that is diffuse and macular

SLAPPED CHEEK

394
Q

What are the clinical manifestations of the 2nd phase of Fifth Disease?

A

By day 4, discrete erythematous macules and papules on proximal extremities and later the trunk

These will evolve into lacey reticular pattern by day 9

395
Q

What are the clinical manifestations of the 3rd phase of Fifth Disease?

A

Eruption is reduced or invisible but will reoccur with exposure to heat or sunlight

396
Q

What is the treatment for Fifth Disease?

A

Supportive Care

397
Q

What is Pityriasis Rosea?

A

Acute, benign, self-limiting eruption

398
Q

When is Pityriasis Rosea most common?

A

Spring/fall

399
Q

What are the Clinical Manifestations of Pityriasis Rosea?

A

Herald patch

Over a period of 2 weeks, oval or elliptic erythematous patches with fine scale develop

Macular or papular lesions will develop on trunk, neck, extremities, and skin folds

Lesions will follow a christmas tree pattern

May be pruritic

May have prodrome of viral symptoms prior to rash

400
Q

How long does Pityriasis Rosea last?

A

3-8 weeks

401
Q

What is the treatment for Pityriasis Rosea?

A

Nothing, it resolves on its own

May prescribe antihistamines for the itching

402
Q

What type of drug eruption is the most common?

A

Morbilliform

403
Q

What drugs may cause morbilliform reactions?

A

Ampicillin

Amoxicillin

Bactrim

404
Q

What is the pathogenesis behind morbilliform drugs reactions?

A

Type IV allergic reaction mediated by T-helper cells

405
Q

What are the clinical manifestations of morbilliform drug reactions?

A

Erythema with macules and papules initially on trunk then generalizing within 2 days

Can present within first 2 weeks of exposure and up to 10 days after stopping

406
Q

How do we treat morbilliform drug reactions?

A

Stop medication and it will clear within 2 weeks

Symptomatic relief like antihistamines or low potency topical steroids may be needed

407
Q

What drugs cause fixed drug reactions?

A

Anything taken intermittently:

NSAIDS
Sulfonamides
Barbituates

408
Q

What are the clinical manifestations of Fixed drug reactions?

A

Round/oval erythematous plaques that may be pruritic/burning or asymptomatic

Reoccur at same site with each exposure

Usually 6 or fewer lesions but often just 1

Can appear anywhere: commonly occurs on genitals or oral mucosa

Localized

409
Q

What is the treatment for fixed drug reactions?

A

Antihistamines or topical steroids if symptomatic

410
Q

What is Erythema Multiforme?

A

Self-limited eruption brought on by drug exposure, viral infections, or topical steroids

411
Q

What are the clinical manifestations of Erythema Multiforme?

A

Lesions begin as macules and become papular, then vesicles and bullae form in the center of the papules

Localized to hands and feet or can become generalized

Mucosal lesions are painful and will erode

Fever and malaise may occur

Target like appearance

412
Q

What is the treatment for Erythema Multiforme?

A

Avoid target substances

Severe reactions may require systemic steroids

413
Q

What is SJS and TEN?

A

immune mediated, mucocutaneous, blistering drug reactions

414
Q

What are the clinical manifestations of SJS and TEN?

A

Fever

Mucosal inflammation

Lesions begin on trunk and may be painful

TEN will exhibit a higher fever and more epidermal separation than SJS

415
Q

What is the treatment for SJS and TEN?

A

Withdrawal of offending agent

Treatment at burn center for fluid and electrolyte imbalance

Wound care

Corticosteroid treatment

416
Q

What type of disease is Bullous Pemphigoid?

A

autoimmune disease that causes separation of epidermis from dermis

417
Q

What are the clinical manifestations of Bullous Pemphigoid?

A

Occurs in sixth decade of life

Prodrome of urticarial lesions

Bullae are large and may contain serous or hemorrhagic fluid

Occurs on axillae, thighs, groin, and abdomen

Usually self-limiting

Takes 5-6 years to resolve

418
Q

How do we diagnose Bullous Pemphigoid?

A

Biopsy and Immunofluorescence

C3 will all be lined up on the epidermal-dermal junction

419
Q

What are the Differential diagnoses of Bullous Pemphigoid?

A

Blistering Disease epidermolysis Bullosa acquista (EBA)

Bullous Scabies eruption

420
Q

What is the treatment for Bullous Pemphigoid?

A

Localized/LImited:
Potent topical corticosteroid –> Clobetasol ointment twice day with occlusion

Moderate/Severe:
Either Clobetasol or
Prednisone 0.5 to 0.75 mg/kg/day which should be tapered cautiously once remission is achieved

Immunosuppressive medications for patients who cannot tolerate steroids:
Azathioprine (Imuran)
MMF (CellCept)
Antibiotics
Tetracycline and Niacinamide combo
TCN or Doxy or Minocycline
Dapsone
Recalcitrant, IVIg, and plasmapheresis
421
Q

What are the clinical manifestations of Pediculus Humanus Capitis?

A

LIce on scalp

Female louse can survive for more than 3 days off the human head

Presents with intense pruritis of the scalp with posterior cervical lymphadenopathy, excoriations, and small specks of louse dung on the scalp

Lice and nits may be present on hair shaft

422
Q

What are the clinical manifestations of Pediculus Humanus corporis?

A

Lice feeds on body but infests clothing

Prefers cooler temps and will lay their eggs on fibers of clothing usually close to the seams

The adult female louse can survive as long as 10 days away from the human body without a blood meal

Associated with poor hygeine

Initially, small pruritic papules that progress due to scratching to crusted and infected papules

SPARES HANDS AND FEET

423
Q

What are the clinical manifestations of Phthirus pubis?

A

Pubic lice/crabs

Less mobile and rest while attached to human hairs

They cannot survive off the human host for more than 1 day

Spread by close contact

Intense pruritis in affected area

Small blue macules can be present

424
Q

What are the differential diagnoses of Pediculosis?

A

Scabies –> This won’t spare hands and feet

Eczema

Delusions of parasitosis

425
Q

What is the treatment for Pediculosis?

A

Topicals:
OTC Nix cream Rinse, RID action –> permethrin active ingredient; kills adult lice but not nits; repeat treatment in one week

Ovid lotion –> Most effective; kills both lice and nits; not for children < 6 months; apply to dry hair, sit for 8-12 hours then rinse

Elimite cream –> 5% permethrin; left on overnight; repeat in one weeks; not to be used in pregnant women

Bactrim
vaseline

426
Q

What is the environmental eradication for Pediculosis?

A

Fomites should be washed in hot water and dried –> temps greater than 50-55C for at least 5 minutes

Seal potential fomites in plastic bags for at least 2 weeks so taht all the nits hatch and die without a blood meal

427
Q

Who else should be treated for lice besides the patient infested?

A

Anyone in close contact with the patient like parents, siblings, etc.

428
Q

What is Scabies caused by?

A

Infestation of Sarcoptes scabeie

429
Q

What are the clinical manifestations of Scabies?

A

Pruritic lesions taht vary considerably from vesicles or papules, nodules located between web spaces of fingers, flexor aspects of wrists, axilla, antecubital area, abdomen, umbilicus, genital and gluteal areas and feet

Spares the face

BURROW is the pathognomonic of scabies

Likes warm areas

430
Q

What does the Burrow in scabies look like?

A

Thin, short, gray brown, wavy channel on the skin

431
Q

What is Crusted/Norwegian Scabies?

A

Seen in immunocompromised or debilitated patients

Crusts and scales teem with mites

Psoriasis like scaling around nails with crusting

Often misdiagnosed as psoriasis

Not very common

432
Q

How do we diagnose Scabies?

A

History
Scraping
Biopsy

433
Q

What are the differential diagnoses of Scabies?

A

Bite reaction
Atopic dermatitis
Delusions of parasitosis

434
Q

How do we treat Scabies?

A

Topical Medications:
Permethrin 5% cream (Elimite) –> apply to all skin below the neck for 8-12 hours; repeat in one week

Lindane 1% lotion or cream (Kwell) –> More toxic and not for pregnant women or kids <2

Precipitated Sulfur ointment 6% –> Best for pregnancy or breastfeeding women; applied to all areas from the neck down and is washed off in 8-12 hours

Oral Medication:
Ivermectin (Stromectol) –> 200micrograms/kg/day for 2 days

After treatment –> bedding, clothing, and towels should be washed in hot water or removed for 72 hours; treat affected family members

435
Q

What is the most common cause of necrotic arachnidism in the US?

A

Brown Recluse Spider Bite (Loxoscelism)

436
Q

What are the clinical manifestations of Brown Recluse Spider Bite (Loxoscelism)?

A

Localized

Bite site becomes painful after 3 hours

Necrotic cutaneous loxoscelism, extensive necrosis develops with edema within 8 hours with bulla and surrounding erythema and ischemia that can extend to muscle

IN one week, central portion becomes gangrenous and dark

437
Q

What is the treatment for Loxoscelism?

A

Rest, ice, and elevate site of bite

Analgesics

Tetanus prophylaxis

Surgical debridement

438
Q

What are the characteristics of the Loxosceles Reclusa spider?

A

Most common in Midwest and southwest

Found in woodpiles, grass, and rocky bluffs and barns

Stings in self-defense

Identified by violin markings over cephalothorax and 3 sets of eyes

Light brown, 1 cm in length

439
Q

What is the major toxin in Brown Recluse spider venom?

A

Sphingomyelinase

440
Q

What are the characteristics of the Latrodectus mactans spider?

A

Found in continental US as well as Caribbean

Found in wood piles and outhouse seats

13mm long, shiny, black, with red hourglass shaped markings on abdomen

Long legs spread up to 4cm

Bites only when disturbed

441
Q

What are the clinical manifestations of a Black Widow Spider bite (latrodectism)?

A

Locally limited to a small circle of redness around the immediate bite site

A central reddened fang puncture site surrounded by an area of blanching and an outer halo of redness is described as a target appearance

Systemically, pain/cramping within an hour that will spread to extremities and trunk

Tachycardia

Hypertension

Pulmonary edema

Fever

Chills

Vomiting

Violent cramps

Delirium or partial paralysis

Abdominal pain is most severe

442
Q

How do we treat Latrodectism?

A

ACLS

Antivenom administered in the ER but there is a risk of allergic reaction

Analgesics like morphine

Antihistamine like benadryl

Tetanus

Clinical Medicine I (15 decks)

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