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Step 2 CK > Dermatology > Flashcards

Dermatology Flashcards

1
Q

Long term use of immunomodulator meds increases the risk of developing?

A

Lymphoma

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2
Q

Atopic dermatitis (eczema)

A

chronic inflammatory skin condition that starts in infancy and persists into adulthood. characterized by puritis leading to lichenification.

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3
Q

Atopic triad

A

asthma, eczema, allergic rhinitis

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4
Q

Patients with eczema are at increased risk for?

A

2ndary infections with staph aureus and viral HSV or molluscum due to itch/scratch cycles

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5
Q

Triggers for eczema?

A

climate, food, stress, skin irritants, allergens

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6
Q

Manifestation of eczema in

Infants: Children: Adults:

A

Infants: red, edematous, weeping, puritic papules and plaques on face, scalp, extensor surfaces (diaper usually spared)

Children: dry, scaly, pruritic, excoriated papules/plaques in flexural areas and neck

Adults: lichenification and dry, fissured skin in flexural areas. hand or eyelids too

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7
Q

How to diagnose eczema?

A

Clinical.
KOH prep can help distinguish eczema from tinea
Eosinophilia and IgE may be seen in some patients with eczema but not used to diagnose

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8
Q

Treatment for Eczema

A

Topical corticosteroids- 1st line (use intermittently to avoid skin atrophy)

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9
Q

Other pharm therapy to treat eczema and avoid steroids?

A

Immunomodulators- Tacrolimus

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10
Q

Erythema toxicum neonatorum

A

begins 1-3 days after delivery and resembles eczema, presenting with red papules, pustules, vesicles with surrounding erythematous halos. Eosinophils present in the pustules or vesicles.

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11
Q

Treatment for erythema toxicum neonatorum?

A

Bening. usually resolves in 1-2 weeks without treatment.

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12
Q

Contact dermatitis

A

Type IV hypersensitivity reaction. results from contact with an allergen that patient has previously been exposed to (nickel, poison ivy, perfume/deodorant, neomycin)

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13
Q

Contact dermatitis description

A

“linear” “angular”

can spread over body if hands spread it or via transfer via circulating T lymphocytes.

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14
Q

Is latex a contact dermatitis reaction?

A

NO- type 1!

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15
Q

Type I hypersensitivity reaction

Mechanism

A

Antigen cross-links IgE on presented mast cell and basophils triggering release of vasoactive amines (histamine). develops rapidly due to preformed antibody.

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16
Q

What types of hypersensitivy reactions are antibody mediated

A

I, II, III

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17
Q

Asthma is what type of hypersensitivity reaction?

A

Type I

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18
Q

Type II hypersensitivity reaction

A

IgM and IgG bind to antigen on enemy cell- lead to lysis by complement or phagocytosis -> leading to MAC

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19
Q

goodpasture syndrome is a ___ hypersensitivity reaction?

A

Type II

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20
Q

Rheumatic fever is ___ hypersensitivity rxn?

A

type II

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21
Q

Autoimmune hemolytic anemia, erythroblastosis fetalis are type ____ hypersensitivity rxn?

A

II

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22
Q

Type III hypersens rxn

A

antigen/antibody complexes activate complement. complement attracts PMNs which release lysosomal enzymes.

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23
Q

What is an immune complex?

A

Antigen-antibody-complement

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24
Q

Glomerulonephritides and vasculitides are often type ____ hypersens rxn?

A

Type III

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25
Q

Arthus reaction

A

Type III: local reaction to antigen by preformed antibodies (vascular necrosis and thrombosis)

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26
Q

when might an arthus reaction occur?

A

rarely 4-12 hours post vaccination

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27
Q

hypersensitivity pnemonitis is what type of hypersensitivity reaction?

A

Type III (Arthus reaction)

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28
Q

Serum sickness

A

antibodies to foreign proteins are produced in 5 days. Immune complexes form and deposit in membranes- lead to tissue damage by fixing to complement.

Ex: drug reaction

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29
Q

type IV hypersensitivity

A

Delayed cell mediated. sensitized T lymphocytes encounter antigen, release lymphokines and lead to macrophage activation

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30
Q

TB skin test is what type hypersens rxn?

A

Type IV

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31
Q

transplant rejection is what type hypersens?

A

type IV

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32
Q

How do you diagnose contact dermatitis

A

Patch testing (after acute phase eruption is treated)

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33
Q

Treatment

A

topical corticosteroid and allergen avoidance (systemic corticosteroid in severe cases)

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34
Q

Seborrheic dermatitis

A

common. chronic inflammatory skin disease caused by hypersensitivity to (Malassezia furfur, a generally harmless yeast found in sebum and hair follicles)

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35
Q

Malassezia furfur

A

yeast found in sebum, hair follicles, around sebaceous glands- can lead to seborrheic dermatitis reaction

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36
Q

Presentation of seborrheic dermatitis
Infants:
Children/Adults:

A

Infants: severe, red diaper rash with yellow scale, erosions, blisters. scaling and crusting (cradle cap) on scalp

children/adult: red, scaly, patches seen around ears, eyebrows, nasolabial fold, midchest, scalp.

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37
Q

Who is at higher risk for severe seborrheic dermatitis?

A

HIV/AIDS and Parkinson disease patients

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38
Q

Diagnosis of seborrheic dermatitis?

A

clinical

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39
Q

Treatment of seborrheic dermatitis?

A

Selenium sulfide or Zinc Pyrithione shampoo

Topical antifungal (ketoconazole cream) or topical corticosteroid for other areas.

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40
Q

Stasis dermatitis

A

Lower extremitity dermatitis due to venous hypertension (forcing blood from deep to superficial venous system)

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41
Q

Venous htn is often a result of?

A

Venous valve incompetence or flow obstruction

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42
Q

Where does stasis dermatitis usually occur?

A

medial ankle. stasis ulcers may develop

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43
Q

treatment for stasis dermatitis?

A

leg elevation, compression stockings, emollients, topical steroid

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44
Q

Eczema herpeticum

A

medical emergency. grouped vesicles. emergency due to propensity for systemic spread- potentially to brain.

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45
Q

treatment for eczema herpeticum?

A

IV acyclovir

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46
Q

A rash involving extensor surfaces think?

A

psoriasis

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47
Q

Flexor surface rash think?

A

atopic dermatitis (unless infant- located on extensor)

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48
Q

Psoriasis

A

T-cell mediated inflammatory dermatosis characterized by erythematous plaques with silver scale (dermal inflammation and epidermal hyperplasia)

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49
Q

Koebner phenomenon

A

lesions of psoriasis can be provoked by local irritation or trauma

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50
Q

What medications may worsen psoriatic lesons?

A

B-blockers, lithium, Ace-Inh

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51
Q

finding is psoriatic arthritis

A

small joints in hands and feet affected. “sausage digits” and pencil in cup on xray

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52
Q

Diagnosis of psoriasis

A

Clinical. Biopsy if diagnosis uncertain.

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53
Q

Auspitz sign?

A

Pinpoint bleeding when scale of psoriasis is scraped

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54
Q

histology for psoriasis shows?

A

thickened epidermis, elongated rete ridges, absent granular cell layer, preservation of nuclei in stratum corneum (parakeratosis), neutrophil infiltrate in stratum corneum (munro microabscess)

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55
Q

parakeratosis

A

nuclei in stratum corneum in psoriasis

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56
Q

munro microabscess

A

neutrophil infiltrate in stratum corneum in psoriasis (sterile)

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57
Q

Treatment for psoriasis

A

Topical steroids
Calcipotriene (Vit D)
Tazarotene (Vit A)

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58
Q

If you have severe psoriasis or psoriatic arthritis treat with?

A

Methotrexate or anti-TNF biologics

UV light therapy can also be used for patients with lots of skin involvement

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59
Q

Urticaria (hives)

A

Result from release of histamine and prostaglandins from mast cells in type I hypersensitivity response

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60
Q

Dermal edema

A

urticaria/ wheals

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61
Q

Most common cause of chronic urticaria

A

idiopathic

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62
Q

Treatment for urticaria?

A

Systemic antihistamines

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63
Q

treatment for anaphylaxis?

A

epinephrine, antihistamine, IV fluid, airway maintenance

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64
Q

morbilliform rash should make you think of

A

drug reaction

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65
Q

Patients with drug reactions often have what on histology?

A

eosinophilia

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66
Q

When do drug reactions usually take place?

A

7-14 days after starting a new drug

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67
Q

IF a patient reacts within 1-2 days of starting a new drug is it likely the causative agent?

A

NO

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68
Q

Extreme complications of drug eruptions include?

A

Erythroderma, SJS, TEN

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69
Q

erythroderma

A

intense, wide spread reddening of the skin with exfoliation

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70
Q

treatment for drug reaction

A

stop drug. antihistamines for symptoms. topical steroids for itching if needed

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71
Q

Erythema multiforme

A

Cutaneous reaction with targetoid lesions that have many triggers (often recurrent)

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72
Q

Presentation of erythema multiforme

A

Lesions start as erythematous macules that become centrally clear and develop a blister. may have systemic symptoms (fever, myalgias, arthralgias, HA)

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73
Q

What characteristic part of body is often affected with erythema multiforme?

A

PALMS AND SOLES

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74
Q

Erythema multiforme major involves?

A

mucous membranes

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75
Q

Nikolsky sign

A

Push on rash and it exfoliates

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76
Q

Nikolsky (+) or (-) in EM, SJS, TEN?

A

EM: (-) SJS: (+) TEN: (+)

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77
Q

Treatment of erythema multiforme

A

symptomatic treatment (systemic corticosteroids have no benefit)

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78
Q

SJS and TEN

A

2 diff points on spectrum of life-threatening exfoliative mucocutaneous diseases often caused by drug induced immune reaction

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79
Q

Epidermal separation of SJS involve < ___ % of body surface area whereas TEN involves > _____ % of BSA.

A

SJS < 10%

TEN > 30%

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80
Q

Common drugs that may cause SJS/TEN

A

Sulfa, penicillins, seizure meds, quinolones, cephalosporins, steroid, NSAIDs

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81
Q

Diagnosis of SJS

A

Biopsy: degeneration of basal layer of epidermis

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82
Q

Diagnosis of TEN

A

Full-thickness eosinophilic epidermal necrosis

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83
Q

With (+) Nikolsky sign, what should be on differential?

A

SJS, TEN, SSSS, graft vs. host (after bone marrow transplant), radiation therapy, burns)

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84
Q

SSSS is usually seen in? etiology?

A

kids < 6 (infectious etiology)

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85
Q

SJS/TEN usually seen in? etiology?

A

adults, drugs

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86
Q

Treatment of SJS/TEN

A

early diagnosis. discontinue drug

cover skin, manage fluids and electrolytes like you would for burn victim

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87
Q

Erythema nodosum

A

panniculitis process of subcu adipose tissue caused by infection wth strep, coccidiodes, yersinia, TB, drug rxns (sulfa, abx, OCPs) and chronic inflammatory diseases (sarcoid, crohn, ulcerative colitis, behcet)

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88
Q

panniculitis

A

process of subcu adipose tissue

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89
Q

erythema nodosum presents as?

A

painful, red nodules on anterior shins. slowly spread- turning brown or gray. Present with fever and joint pain

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90
Q

Patients with erythema nodosum may have what false (+) test

A

VDRL

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91
Q

Work up for erythema nodosum?

A

ASO, PPD in high risk patients, CXR (sarcoid), IBD work up?

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92
Q

Treatment for erythema nodosum?

A

underlying disease. cool compress, NSAID, potassium iodide

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93
Q 
BULLOUS PEMPHIGOID
location of blisters: 
autoantibodies: 
blister appearance: 
nikolsky sign: 
mucosal involvement: 
patient age: 
med triggers: 
mortality: 
diagnosis: 
treatment:
A

location: basement membrane zone
autoantibodies: hemidesmosomes
appearance: firm, stable blisters, can be preceded by urticaria
Nikolsky: (-)
Mucosal involve: no rarely
Patient age: > 60
Trigger: idiopathic
Mortality: rare, and milder course
Diagnosis: clinical. skin biopsy with direct immunoflorecense is best test or ELISA
Treatment: prednisone

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94
Q 
PEMPHIGOUS VULGARIS
location of blisters: 
autoantibodies: 
blister appearance: 
nikolsky sign: 
mucosal involvement: 
patient age: 
med triggers: 
mortality: 
diagnosis: 
treatment:
A

location of blisters: intraepidermal
autoantibodies: desmoglein (keratinocye adhesion)
blister appearance: erosion more common bcz no keratinocyte adherence
nikolsky sign: +
mucosal involvement: common
patient age: 40-60
med triggers: ACE-in, penicillamine, phenobarb, penicillin
mortality: possible
diagnosis: clinical. skin biopsy with direct immunoflorecense is best test or ELISA
treatment: high dose therapy or immunomodulators

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95
Q

HSV1 vs HSV2

A

HSV1- oral-labial

HSV2- genital

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96
Q

Recurrent HSV-1 often triggered by?

A

sun and fever

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97
Q

Diagnosis

A

Clinical. Viral culture of lesion is most accurate test.

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98
Q

Positive Tzanck smear will show?

A

Multinucleated giant cells

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99
Q

If no multinucleated giant cells on Tzanck smear is it herpes?

A

NO

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100
Q

Treatment of herpes in immunocompromised patient

A

need to start antiviral (acyclovir, famciclovir, valacyclovir) within 72 hours of start of outbreak

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101
Q

Treatment for herpes if severe frequent recurrences- more than 6 outbreaks/year?

A

Daily prophylaxis with acyclovir, famciclovir, valacyclovir

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102
Q

Symptomatic HSV lasting > 1 month can be a sign of

A

AIDS defining illness

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103
Q

In adults, varicella zoster infections can be more severe and have associated systemic complications like

A

pneumonia and encephalitis

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104
Q

Treatment for varicella in kids?

A

self-limited

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105
Q

Treatment for varicella in adults?

A

acyclovir

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106
Q

pain control for adults with varicella?

A

neuropathic agents: gabapentin. TCAs

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107
Q

If immunocompromised, pregnant or newborn is exposed to varicella zoster how do you treat?

A

WIthin 10 days they should be given varicella immunoglobulin

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108
Q

Immunocompetent adults should receive a varicella vaccine within ____ days of exposure?

A

5

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109
Q

If you see giant molluscum contagiosum think:

A

HIV and decreased cellular immunity

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110
Q

Molloscum is spread by?

A

direct skin to skin contact

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111
Q

Diagnosis of molluscum

A

clinical. best test is large inclusions (molluscum bodies) seen under microscope

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112
Q

What subtypes of HPV lead to squamous malignancies?

A

16 and 18

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113
Q

Spread of HPV is by?

A

direct contact

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114
Q

Condyloma accuminatum - genital warts are caused by HPV subtypes

A

6,11

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115
Q

How do you visualize mucosal HPV lesions?

A

acetic acid

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116
Q

most accurate test to diagnose HPV?

A

PCR

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117
Q

Bullous impetigo is almost always caused by?

A

staph aureus

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118
Q

Impetigo affects what skin layers?

A

Epidermis

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119
Q

Cellulitis affects what skin layers?

A

Dermis and subcu fat

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120
Q

Erysipelas affects what skin layers

A

dermis

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121
Q

Nec fasc affeccts what skin layers

A

subcu and fascia and muscle

122
Q

Rash of salmonella typhi

A

small pink papules on trunk “rose spots” in groups of 10-20

123
Q

For chronic carrier state of salmonella typhi what operation should be considered?

A

cholecystectomy

124
Q

Treatment for impetigo
mild:
severe non-MRSA
severe MRSA likely

A

mild: mupirocin topical
severe non MRSA: cephalexin, dicloxacillin, erythromycin
severe MRSA: TMP-SMX, clinda, doxy

125
Q

Erysipelas

A

typically raised, indurated, well demarcated area confined to dermis and typically caused by strep

126
Q

Treatment for cellulitis

A

5-10 days of oral antibiotics. IV antibiotics if evidence of systemic tox, comorbid conditions, DM, extremes of age, hand or orbital involvement

127
Q

Nec Fasc

A

Mixed infection of anaerobic and aerobic bacteria that includes S. aureus, E.coli, C.perfringens

128
Q

Presentation of nec fasc

A

erythema quickly spreads over course of hours to days and skin becomes dusky or purple leading to necrosis

129
Q

physical exam signs suggesting nec fasc

A

gas production, crepitus, putrid discharge, bullae, severe pain

130
Q

Treatment

A

immediate surgery and debridement and broad spectrum antibiotics (penicillin G is drug of choice for strep)

131
Q

Why is clindamycin helpful in nec fasc

A

used to decrease toxin production by bacteria

132
Q

for anaerobic coverage for nec fasc use?

A

metronidazole or 3rd gen cephalosporin

133
Q

Ludwig angina

A

bilateral cellulitis of submental, submaxillary, sublingual spaces that results from an infected tooth.

134
Q

How does ludwig angina present?

A

dysphagia, drooling, fever, red, warm mouth and can lead to death from asphyxiation

135
Q

Does erythromycin cause photosensitivity?

A

No! Its doxy and tetra

136
Q

Treatment for superficial folliculitis?

A

mupirocin

137
Q

Treatment for more severe folliculitis?

A

cephalexin, cloxacillin and clinda if MRSA is suspected

138
Q

Most effective treatment for comedonal (black head) acne

A

Topical retinoid cream

139
Q

What kills p.acnes?

A

Topical benzoyl peroxide

140
Q

If retinoids and benzoyl peroxide are inadequate, what can you use for comedonal black head acne?

A

topical clindamycin or erythromycin

141
Q

General progression of pharmacotherapy for acne treatment?

A

topical benzoyl peroxide/retinoid/antibiotic/oral antibiotic/oral isoretinoin

142
Q

isoretinoin (oral) contraindications

A

teratogen
elevates LFTs
patients require periodic blood tests to check LFTs, cholesterol, triglycerides

143
Q

Pilonidal cysts

A

abscesses in the sacrococcygeal region. starts as folliculitis then becomes infected with perineal microbes like bacteroides (most common in 20-40 year old men)

144
Q

Pilonidal cysts can develop into?

A

perianal fistulas

145
Q

Risk factors for pilonidal cyst?

A

deep and hairy natal clefts, obesity, sedentary lifestyle

146
Q

Treatment for pilonidal cyst?

A

Incision and drainage and sterile packing of wound

147
Q

Tinea versicolor

A

Caused by malassezia furfur- yeast that is part of normal skin flora (humid conditions and oily skin can make organism pathogenic

148
Q

risk factors for tinea versicolor

A

cushing syndrome. immunosuppression

149
Q

presentation of tinea versicolor

A

small scaly patches of varying color on chest or back. patches can be hypopigmented or hyperpigmented

150
Q

Diagnosis

A

clinical. best test is KOH prep of scale revealing “spaghetti and meatball” (hyphea and spores)

151
Q

Treatment for tinea versicolor

A

ketoconazole cream or selenium sulfide cream

152
Q

Candidiasis presents in what areas?

A

moist areas like groin, skin folds, vagina, below breast

153
Q

Oral thrush is common in infancy?

What is it a sign of in adults?

A

Yes common in infants!

Sign of immunocompromise in adults

154
Q

Oral candidiasis presents as

A

painless white plaques that can be easily scraped off

155
Q

Candidiasis of the skin

A

erythematous patches with occasional erosions and satellite lesions often seen in skin folds and diapers of infants

156
Q

Diagnosis of candida?

A

clinical. KOH- candidal spores and psuedohyphea. Best test is fungal culture

157
Q

Treatment for oral candidiasis

A

oral fluconazole tablets
nystatin swish and swallow
clotrimazole

158
Q

treatment for superficial skin candidiasis

A

topical antifungal

159
Q

treatment for candidiasis diaper rash

A

topical nystatin

160
Q

Dermatophyte infections occur only in

A

cells with keratin (skin, hair, nails)

161
Q

Causative dermatophyte organisms

A

trichophyton, microsporum, epidermophyton

162
Q

Risk factors for dermatophyte infection

A

DM, decrease peripheral circulation, immune compromise, chronic maceration of skin (athletic activity)

163
Q

Types of dermatophyte infections

A

tinea corporus, tinea pedis/manuum, tinea cruris, tinea capitis

164
Q

tinea corporis

A

scaly, pruritic eruption with sharp irregular border and with central clearing (ringworm like rash)

165
Q

tinea pedis/manuum

A

chronic interdigital scaling with erosions between toes or as thickened scaly skin on soles of feet and involvement of 1 hand is typical in 1 hand/2 feet syndrome

166
Q

tinea cruris

A

jock itch. typically spares scrotum.

167
Q

tinea capitis

A

fungal scalp infection causing scaling and hair loss.

168
Q

keroin

A

large inflammatory, boggy mass caused by tinea capitis

169
Q

Diagnosis of tinea

A

clinical. Best initial test: KOH showing hyphea. Most accurate. fungal culture

170
Q

Treatment of tinea?

Exception?

A

topical antifungal. escalate to oral if infection is widespread.

Tinea capitis must be treated with oral medications to penetrate into hair follicles.

171
Q

Pubic lice bites often turn what color? why?

A

blue. contain anticoagulant in their saliva.

172
Q

Treatment of head lice:

A

topical permethrin. pyrethin. benzoyl alcohol. mechanical removal

173
Q

body lice treatment

A

wash body, clothes, bedding. rarely may need topical permethrin

174
Q

pubic lice

A

permethrin, pyrethin, benzoyl alcohol, mechanical removal

175
Q

can scabies be seen with naked eye?

A

no

176
Q

diagnosis of scabies.?

A

history of itching in several family members is suggestive

177
Q

treatment of scabies

A

5% permethrin from neck down. (head to toe in infants) and contacts should be treated as well.

Ivermectin can also be used
clothing and bedding should be thoroughly washed

178
Q

3 types of gangrene

A

Dry, wet, gas

179
Q

dry gangrene

A

due to insufficient blood flow to tissue- typically from atherosclerosis. early signs are dull ache, cold, pallor. necrosis sets in and tissue becomes blue/black
(DM, vasculopathy, smoking are risk factors)

180
Q

wet gangrene

A

bacterial infection with skin flora. tissue appears bruised, swollen, blistered with pus

181
Q

gas gangrene

A

c.perfringes infection (med emergency!)

associated with dirty wounds contaminated with dirt or fecal matter

182
Q

subcu injection of black tar heroin is a risk factor for?

A

gas gangrene

183
Q

Skin finding for paraneoplastic sign of GI adenocarcinoma

A

Acanthosis nigricans

184
Q

lichen planus 6 P’s

A

planar, purple, polygonal, pruritic, papules, plaques

185
Q

What drugs can induce lichen planus?

A

thiazide, quinolone, b-blocker

186
Q

lichen planus is associated with what infection?

A

HCV

187
Q

Wickham striae

A

lacy white lines present on lichen planus lesions

188
Q

Koebner phenom

A

lesions that appear at site of trauma (can occur in lichen planus)

189
Q

Treatment of mild lichen planus

A

topical corticosteroids

190
Q

Rosacea

A

chronic disorder of pilosebaceous units without a clear etiology

191
Q

Central facial erythema with telangiectasias is an early sign of?

A

rosacea

192
Q

rhinophyma

A

longstanding facial rosacea can lead to severe overgrowth of nasal connective tissue

193
Q

Treatment for rosacea

A

topical metronidazole

for severe or ocular disease- oral doxycycline

194
Q

How can you differentiate pityriasis rosea from 2ndary syphillus?

A

pityriasis spares palms and soles

195
Q

Pityriasis roseA

A

acute dermatitis reaction best hypothesized to result from viral infection with human herpesvirus

196
Q

herald patch

A

initial lesion of pityriasis rosea. erythematous with peripheral scale.

197
Q

differential for pityriasis

A

secondary syphilis. tinea corporis.

198
Q

Treatment of pityriasis rosea

A

heals in 6-8 weeks without treatment. skin lube, antipruritics, antihistamine for symptoms

199
Q

Vitiligo often presents on?

A

hands, face, genitals

200
Q

treat vitiligo with?

A

topical steroids, tacrolimus ointment, UV and laser therapy

201
Q

eyelid lesions types

A

xanthelasma, hordeolum, chalazion

202
Q

xanthelasma

A

soft, yellow plaques on medial aspects of eyelids associated with hyperlipidemia and primary biliary cirrhosis

203
Q

hordeolum

A

painful acute eyelid gland infection (stye) (usually staph aureus located on edge of lid)

204
Q

Chalazion

A

painless cyst due to blocked eyelid gland

205
Q

Seborrheic keratosis

A

very common skin tumor that appears in almost all people after age 40. no malignant potential.

206
Q

presentation of seborrheic keratosis

A

exophytic, waxy brown papule and plaque with superficial keratin cysts. “stuck on appearance”

207
Q

Treatment

A

cryotherapy, shave excision, currettage. Some may appear similar to melanoma so biopsy may be needed

208
Q

Actinic keratosis

A

flat areas of erythema and scale caused by exposure to sun. need to be treated to prevent transformation into squamous cell carcinoma

209
Q

Treatment actinic keratosis

A

cryosurgery, topical 5-FU, topical imiquimod

210
Q

Cutaneous squamous cell carcinoma

A

2nd most common skin cancer. sun exposure most common cause. chemical carcinogens, radiation therapy, burns or trauma (draining infection sinuses in osteomyolitis), chronic immunosuppression (transplant recipient) all dispose patients to SCC

211
Q

Presentation of SCC

A

erythematous, ulcerated, papule or nodule

212
Q

Marjolins ulcer

A

type of rare SCC that arises in sites of scars, burns, ulcers

213
Q

Arsenic exposure

A

rare cause of multiple SCC in palmoplantar distribution

214
Q

SCCs that rise from actinic keratosis are more or less likely to metastasize than those on lips and those that form ulcers?

A

less likely if from actinic keratosis

215
Q

Diagnosis

A

confirm with shave biopsy

216
Q

Treatment of SCC

A

surgical excision. Mohs surgery (very thin slices excised and examined). lesions with high metastatic potential may need radiation or chemo.

217
Q

basal cell carcinoma

A

most common malignant skin cancer. slow growing and locally destructive but has VIRTUALLY NO METASTATIC POTENTIAL.

218
Q

inherited basal cell nevus syndrome

A

multiple BCCs appearing early in life and on non-sun exposed areas

219
Q

Melanoma

A

most common life threatening derm disease.

220
Q

Risk factors for melanoma

A

fair skin, tendency to burn, intense burst of sun exposure (especially in childhood and with intermittent exposure), presence of large congenital melanocytic nevi, increased number of nevi or dysplastic nevi. Immunosuppression increases risk.

221
Q

FAM-M syndrome

A

familial atypical mole and melanoma syndrome (inherited predisposition to melanoma)

222
Q

ABCDEs of melanoma

A

asymmetric, irregular border, color variation, diameter >6, evolution (change)

223
Q

Diagnosis

A

excisional biopsy on any suspiciuos lesionq

224
Q

itching in a changing skin lesion is suspicious for?

A

malignancy

225
Q

Staging of malignant melanomas?

A

Breslow thickness (depth of invasion in millimeters) and by tumor-node-metastasis (TNM)

226
Q

poor prognostic sign for melanoma?

A

ulceration

227
Q

Name the 5 types of melanoma

A
  1. superficial spreading
  2. nodular
  3. acral lentiginous
  4. lentigo maligna
  5. amelonotic
228
Q

superficial spreading melanoma

A

60% of all. Can occur at any age. most common in young adults. presents on trunk in men. legs in women. Prolonged horizontal growth allows for early diagnosis when still confined to epidermis

229
Q

Nodular

A

Lesions have rapid vertical growth phase and appear as fast growing red-brown nodules with ulcerations

230
Q

acral lentiginous

A

begins on palms, soles, nail beds as slowly spreading pigmented patch. most common in asian and black

231
Q

lentigo meligna

A

arises in a solar lentigo. common on sun damaged areas of face

232
Q

amelanotic

A

lesion without clinical pigmentation. difficult to identify. can be further classified into any above type

233
Q

Patients with early melanoma are at high or low risk of recurrence? high or low risk of subsequent melanomas?

A

low risk of recurrence.

high risk of subsequent melanomas.

234
Q

What bacterial infection can mimic kaposi sarcoma?

A

bacillary angiomatosis caused by bartonella henselae.

235
Q

how do you treat bacillary angiomatosis?

A

erythromycin

236
Q

Treatment for Kaposi’s?

A

HAART therapy if HIV. small local lesions can be treated with radiation or cryotherapy. Systemic spread to GI tract or lung requires systemic chemo.

237
Q

Mycosis fungoides

A

slow progressive neoplastic proliferation of T cells. More common in men.

238
Q

Presentation of mycosis fungoides?

A

non-specific psoriatic appearing plaques or patches that are itchy and on trunk and butt. later lesions are skin tumors with palpable lymph nodes.

239
Q

Sezary syndrome

A

Leukemic phase of cutaneous T-cell lymphoma characterized by circulating sezary cells in peripheral blood- erythroderma and lymphadenopathy

240
Q

Diagnosis of mucosis fungoides

A

clinical features, histology, sezary cells on microscopy (ceribriform lymphocytes)

241
Q

treatment for mycosis fungoides

A

phototherapy. electron beam radiation.

242
Q

cherry angiomas (hemangiomas)

A

small, vascular, red papule that appear anywhere on body. most common benign vascular tumor. no treatment needed.

243
Q

Immediately after a burn injury, what organisms predominate?

A

Gram positive

S.aureus

244
Q

After more than 5 days, which organisms predominate in wound infections?

A

gram negative or Fungi

Pseudomonas, Candida

245
Q

Who is at highest risk of a wound infection after a burn?

A

patients with >20% surface area burns

246
Q

What is the first sign of burn wound infection?

A

change in appearance- partial thickness burns turn into full thickness injury or wound loses loss of viable skin graft

247
Q

Burn wound sepsis findings for vital signs

A

temp <36.5 (97.7), >39 (102.2)
Progressive tachy >90
Progressive tachypnea >30
Refractory hypotension <90 systolic

248
Q

In burn patients oliguria, unexplained hyperglycemia, thrombocytopenia, mental status changes are concern for?

A

wound infection

249
Q

how do you diagnose wound infection in burn patients

A

quantitative wound culture and biopsy for histopathology

250
Q

Treatment for burn infections?

A

empiric broad spectrum antibiotics IV (Pip/tazo, carbapenem) with possible Vanc for MRSA coverage or an aminoglycoside for multidrug resistant pseudomonas

251
Q

delayed neuropsychiatric syndrome

A

carbon monoxide poisoning due to fire exposure can lead to mental status change

252
Q

why does metabolic rate increase after large surface area burns?

A

release of inflammatory mediators

253
Q

signs of increased metabolic rate with surface area burns?

A

increased temp to 38.5 (101.3), tachycardia, tachypnea, hyperglycemia

254
Q

Signs of deliberate burn injury and child abuse?

A

Linear demarcation with no splash marks, extensive burns to back and butt with sparing of flexural creases (due to dipping in boiling water)

255
Q

Compare erysipelas vs cellulitis

A

erysipelas: superficial dermis, raised and sharply demarcated edges, rapid spread, fever early in course
cellulitis: deep dermis and subcu fat, flat edges poor demarcation, slow spreading, fever later in course

256
Q 
Tinea corporis (ringworm)
risk factors, presentation, treatment
A

Risk factors: athletes who have skin-to-skin contact, humid environment, contact with infected animals (rodents)

Presentation: scaly, red, itchy patch with centrifugal spread and later central clearing with a raised annular border

treatment: topical antifungal (clotrimazole, terbinafine) 
oral antifungals (terbinafine, griseofulvin)
257
Q

nummular eczema
presentation
treatment

A

red, itchy patch with some scale. can be confused with tinea corporis

treatment- topical corticosteroid and moisture

258
Q

Porphyria cutanea tarda presentation

A

blisters, bullae, scarring, hypo/hyperpigmentation on sun-exposed skin (back of hands, forearms, face)
scarring and calcifications like with scleroderma

259
Q

Conditions associated with porphyria cutanea tarda

A 
Hep C 
HIV
Excessive alcohol
Estrogen use
Smoking
260
Q

Testing for porphyria cutanea tarda diagnosis

A

elevated liver enzymes and iron overload

elevated plasma or urine porphyrin

261
Q

porphyria cutanea tarda leads to photosensitivity due to accumulation of?

A

porphyrinogens that react with oxygen by UV light

262
Q

porphyria cutanea tarda is due to deficiency of

A

uroporphyrinogen decarboxylase

263
Q

Treatment for porphyria cutanea tarda

A

Phlebotomy or hydroxychloroquine

264
Q

Allergen induced delayed type hypersensitivity

A

contact dermatitis

265
Q

bacterial invasion of superficial skin infection

A

impetigo

266
Q

subepidermal anti-transglutaminase IgA autoantibody?

A

Dermatitis herpetiformis (autoimmune reaction triggered by dietary gluten)

267
Q

vasculitis due to cryoglobulin immune complexes

A

mixed cryoglobulinemia
(associated with hep C)
palpable purpura, arthralgias, glomerulonephritis

268
Q

cherry angiomas (hemangiomas) are also known as

A

senile hemangiomas

269
Q

cavernous hemangiomas

A

dilated vascular spaces with thin-walled endothelial cells. present as soft, blue, compressible masses growing up to a few cm. appear on skin, mucosa, deep tissues, viscera

270
Q

cavernous hemangiomas of brain and viscera are associated with?

A

Von Hippel-Lindau disease

271
Q

spider angiomas

A

bright red arterioles surrounding by outwardly radiating vessels. they blanch with pressure. blanch with pressure. estrogen dependent and seen in preg, OCP use, and cirrhosis related hyperestrogenemia

272
Q

strawberry (infantile) hemangiomas

A

appear during first weeks of life. grow rapidy and then regress spontaneously by 5-8

273
Q

SCC typically present as

A

enlarging nodule in sun exposed areas with thick rough skin surface or ulceration

274
Q

Is it typical for SCC to cause numbness and paresthesias

A

Yes- can invade perineural area early

275
Q

Seborrheic dermatitis

A

common inflammatory disease that affects the scalp (dandruff), face (eyebrow, nasolabial folds, external ear, chest and intertriginous areas.

276
Q

What disorders can seborrheic dermatitis be associated with?

A

Parkinson disease

HIV

277
Q

itchy red plaques with fine, loose, yellow greasy looking scale?

A

seborrheic dermatitis!

278
Q

Treatment for seborrheic dermatitis?

A

topical antifungals

279
Q

dermatofibroma

A

fibroblast proliferation causes isolated or multiple lesions- most commonly on lower extremities.

lesions are non-tender and can be triggered by trauma in area or insect bite.

280
Q

“dimple or buttonhole” sign

A

dermatofibroma with a firm fibrous component that may cause dimpling in the center when its pinched

281
Q

Treatment of dermatofibroma

A

cryosurgery or shave excision

282
Q

pyogenic granuloma

A

benign vascular skin tumor that presents as small red papule and grows rapidly over weeks-months to a pedunculated or sessile shiny mass. most commonly occur on lip or oral mucosa and can bleed with minor trauma

283
Q

skin infection caused by poxvirus?

A

molluscum contagiosum

284
Q

treatment for molluscum

A

its self limited and lesions usually resolve in 6-12 months

285
Q

SSSS

A

caused by exfoliative toxin-producing strains of S.aureus

286
Q

why are cultures from bullae in SSSS usually sterile?

A

because its a toxin mediated process

287
Q

HSV is the most common infectious agent associated with what acute-self limited skin eruption?

A

erythema multiforme

288
Q

what adults can be affected by SSSS?

A

kidney disease or immunocompromised

289
Q

if you biopsy erythema toxicum neonatorum- you will find

A

eosinophils and sterile pustule

290
Q

initial management of comedonal acne ?

A

topical retinoid with organic acid preparations (salicylic, azelaic, glycolic acid)

291
Q

when should you use benzoyl peroxide for acne?

A

inflammatory pustular acne

292
Q

histopathology “tombstone cells”

A

pemphigous vulgaris

293
Q

netlike itercellular IgG and C3 on immunoflourescence?

A

pemphigous vulgaris

294
Q

autoantibodies against desmogleins 1+3

A

pemphigous vulgaris

295
Q

acantholysis

A

detached keratinocytes

296
Q

linear IgG deposits at basement membrane and tense bullae?

A

bullous pemphigoid

297
Q

Flaccid bullae and mucocutaneous blisters with biopsy showing intraepidermal cleavage

A

pemphigous vulgaris

298
Q

Two types of contact dermatitis

A

allergic (type IV hypersensitivity)

irritant (physical or chemical contact)

299
Q

A rash typically beginning as small papules that become confluent and evolve into vesicles or bullae and eventually crust in 7-10 days. Rash is limited to single dermatome but may involve adjacent dermatomes

A

Herpes Zoster

300
Q

Widely scattered, red, scaly papules and plaques that often follow strep infection or can occur in patients with RA (on TNF-a)

A

Guttate Psoriasis

301
Q

Treatment for guttate psoriasis

A

UV phototherapy
Topical glucocorticoids
Vitamin D

Step 2 CK (26 decks)

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