Derma Flashcards

(160 cards)

1
Q

Woods lamp

A
Coral pink- erythrasma by corynebacterium minutissimun 
Pale blue- pseudomonas
Yellow fluorescence - tinea caputis 
Freckles- lesions are accentuated 
PIH - lesions fade under woods light 
Vitiligo - white 
Ash leaf spots- tuberous sclerosis
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2
Q

Multinucleated epithelial giant cells

A

HSV or VSV

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3
Q

KOH preparation

A

Hyphae- dermatophyte infection
Pseudohyphae with budding - candida
Spaghetti and meatball- tinea versicolor

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4
Q

Tzank smear-

A

herpesvirus infections, varicella zoster virus

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5
Q

Patch testing

A

Back
After 48 hourse
Detect delayed hypersensitivity

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6
Q

Eczema

A

Final common expression of some disorders
Common histology: spongiosis (intercellular edema of the epidermis)
Varied clinical findings

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7
Q

Most common location of seb derm

A

Scalp

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8
Q

Location of seb derm in the face

A

Eyebrows
Eyelids
Glabella
Nasolabial folds

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9
Q

Treatment seb derm

A

Low potency topical steroids plus anifungal agent (ketoconazole cream)
Antidandruff shampoo
High potency steroids for severe scalp involvement

Do not use topical steroids on the face! —> steroid induced rosacea or atrophy

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10
Q

Koebner phenomenon

A

Traumatized lesions develop lesions of psoriasis

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11
Q

Most common variety of psoriasis

A

Plaque type

Stable slowly enlarging plaques, remain unchanged for long periods of time

Most commonly involved areas: elbows knees gluteal cleft scalp

Symmetric involvement

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12
Q

Type of psoriasis which affect intertriginous areas

Axilla groun submammary region, navel

A

Inverse psoriasis

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13
Q

Most common type of psoriasis in children

A

Guttate (eruptive) psoriasis

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14
Q

Pustular psoriasis

A

Localized to palms and soles or generalized

erythematous skin w variable scale and pustules

Treatment of choice: oral retinoids

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15
Q

Eczema and Dermatitis

A
Atopic Derm
Lichen Simplex Chronicus 
Contact Derm (Irritant and allergic derm) 
Hand eczema 
Nummular eczema 
Asteatotic eczema 
Stasis derm and ulceration 
Seb derm
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16
Q

Papulosquamous disorders

A

Psoriasis
Lichen planus
Pityriasis rosea

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17
Q

Purple polygonal papules
Severe pruritus
Lacy white markings
Assoc w mucous membrane lesions

Histo feature: interface dermatitis

A

Lichen planus

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18
Q

Acanthosis

Vascular proliferation

A

Psoriasis

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19
Q

Rash preceded by herald patch

Oval to round plaques with trailing scale

Affects trunk

Eruption lines in skin foldings “fir tree like appearance”

Spares palms and soles

A

Pityriasis rosea

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20
Q

Tx for psoriasis

A

Mid potency topical steroids
Long term use: tachyphylaxis and atrophy of the skin

Topical Vit D analogue (calcipotriene) and retinoid - limited psoriasis

UV light- widespread psoriasis
Mutagenic, increasing the risk for melanoma and nonmelanoma skin cancer
-contraindicated in patients receiving cyclosporine

STEROIDS- do not use! May develop life threatening pustular psoriasis

Methotrexate
Cyclosporine - calcineurin inhibitor
TNF inhibitors (etanercept adalimumab infliximab golimumab ustekinumab)

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21
Q

Mainstay of therapy Lichen Planus

A

Topical glucocorticoid

Most patients have spontaneous remission 6months to 2 years after onset of disease

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22
Q

Superficial bacterial infection of the skin commonly caused by S aureus, sometimes by B hemolytic strep

Pustule that forms characteristic yellow brown honey colored crust

A

Impetigo

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23
Q

Deep non bullous variant of impetigo that causes punched out ulcerative lesions

Caused by primary or secondary infection w S pyogenes

Deeper infection than impetigo that resolves w scars

A

Ecthyma

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24
Q

Boil/ furuncle
Caused by Staph aureus

Treated with beta lactam antibiotics

Warm compress
Nasal mupirocin

A

Furunculosis

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25
Fungi that infect skin, hair, nails
Dermatophytes Include members of the genera trichiophyton, microsporum and epidermophyton
26
Most common dermatophyte infection
Tinea pedis
27
Tinea cruris
Dermatophyte infection the groin Males > female Scaling erythematous eruption sparing the scrotum
28
Most common involved area in tinea pedia
Web space between 4th and 5th digit
29
Tinea unguium or onychomycosis
Occurs w tinea pedis Opacified thickened nails and subungal debris Distal lateral variant is most common Proximal subungal onychomycosis - marker for HIV infection and other immunocompromised states
30
Tinea capitis
Predominantly caused y trichophyton tonsurans Kerion- caused by T tonsurans, markedly inflammatory dermatosis with edema and nodules
31
Diagnosis of tinea
Skin scrapings NAil scrapings Hair Culture or direct microscopic examination W KOH Nail clippings may be sent for PAS stain
32
Cutaneous neoplasms caused bu papillomaviruses
Warts
33
Typical wart
Verruca vulgaris Sessile dome shaped Causative agent also cause plantar warts (verruca plana) and filiform warts
34
HPV types that are major risk factors for intraepithelial neoplasia and squamous cell carcinoma of the cervix anus vulva and penis
HPV 16 and 18
35
Most useful and convenient method for treating warts in almost any location
Cryotherapy with liquid nitrogen
36
Treatment for genital warts
Podophyllin solution - moderately effective but associated with marked local reactions Topical imiquimod - potent inducer of local cytokine release
37
Clinical hallmark of acne vulgaris
Comedone White- closed Black- open
38
Systemic medications that can produce acneiform eruptions/ exacerbate preexisting acne
``` Oral contraceptive pills Lithium Isoniazid Androgenic steroids Halogens Phenytoin Phenobarbital ```
39
Treatment for acne vulgaris
Minimal to moderate pauci-inflammatory disease : local therapy Retinoic acid benzoyl peroxide salicylic acid Adjuncts: topical azelaic acid erythromycin clindamycin or dapsone Moderate to severe acne with prominent inflammatory component : systemic therapy Tetracycline 250-500 mg bid or doxycycline 100mg bid Severe nodulocystic acne : isotretinoin (synthetic retinoid) Side effects: teratogenic, depression, extremely dry skin, cheilitis, hypertriglyceridemia
40
Inflammatory disorder predominantly affecting the central face seen almost exclusively in adults More common in women (+) erythema telangiectasia superficial pustules but not associated with comedones Assoc w tendency for facial flushing
Acne rosacea
41
Rosacea can be associated with inflammatory eye involvement Keratitis Blepharitis Iritis and recurrent chalazion May be life threatening
Okay.
42
Treatment of acne rosacea
Topical for mild disease Metronidazole, sodium sulfacetamide, azeleic acid Oral for more severe disease Tetracycline 250-500 bid Doxycyline 100 bid Minocycline 50-100 bid Telangiectasia- laser therapy Topical steroids- AVOID, may elicit rosacea
43
Meds that cause pityriasis rosea-like drug eruptions
Beta blockers ACE I Metronidazole
44
Meds that cause lichenoid eruption
``` Thiazides Antimalarials Quinidine Beta blockers ACEIs ```
45
Secondary syphilis derm lesions
Scattered red brown papules w thin scale Involves palms and soles Can resemble ptyriasis rosea Interval bet primary chancre and secondary stage: 4-8 weeks Spontaneous resolution without therapy occurs
46
When majority if skin surface is erythematous
Erythroderma
47
Major etiologies of erythroderma
Cutaneous disease (psoriasis and dermatitis) Drugs Systemic disease- most commonly CLTL Idiopathic
48
``` Erythroderma + Fever and peripheral eosinophilia Facial swelling hepatitis Myocarditis thyroiditis allergic interstitial nephritis ```
DRESS | DIHS (drug induced hypersensitivity reaction)
49
Most common malignancy associated with erythroderma
CTCL | Cutaneous t cell lymphoma
50
Major forms of alopecia
Scarring and non scarring
51
Scarring alopecia
Assoc w fibrosis inflammation and loss of hair follicles
52
Non scarring alopecia
Hair shafts minimized or absent Preserved hair follicles Reversible nature ``` Causes common Androgenic alopecia Telogen effuvium Alopecia areata Tinea capitis Early phase of traumatic alopecia ``` Uncommon causes SLE 2ndary syphilis
53
Drugs that cause alopecia
``` Warfarin Heparin PTU Carbimazole Isotretinoin Acitretin Lithium Beta blockers Interferons Colchicine Amephetamines ```
54
Alopecia in SLE
Scarring - secondary to discoid lesions Non scarring - flares of systemic disease May involve entire scalp or just the front cap
55
Alopecia in secondary syphilis
Scattered poorly circumscribed patches of alopecia with a moth east appearance
56
Firgurate skin lesion Numerous mobile concentric arcs and wavefronts that resemble the grain in wood Search for malignancy!
Erythema gyratum repens
57
Cutaneous manifestation of lyme disease
Erythema migrans
58
Pustular lesion Large areas of erythema studded with multiple sterile pustules in addition to neutrophilia
Acute generalized exanthematous pustulosis (AGEP)
59
Telangiectasia Reticulated hypo and hyperpigmentation Wrinkling secondary to epidermal atrophy Telangiectasias Seen in skin damaged by ionizing radiation and in autoimmune(dermato)
Poikiloderma
60
Telangiectasia in SSc Face, oral mucosa and hands
Mat telangiectasia
61
Periungal telangiectasias are pathognomonic of which autoimmune connective tissue diseases?
SLE Dermatomyositis Systemic sclerosis
62
AV malformations of the dermal microvasculature Eccentric punctum with radiating legs when skin is stretched over the lesion Appears during adolescence and adulthood Major symptoms of GI bleeding and epistaxis
Hereditary hemorrhagic telangiectasia (Osler Rendu Weber Disease)
63
Autoantibody mediated intraepidermal blistering diseases
Pemphigus
64
Loss of cohesion between epidermal cells
Acantholysis
65
Separation of the epidermis on manual pressure to the skin
Nikolsky’s sign
66
Mucocutaneous blistering disease that predominantly occures in patients > 40 years Typically begins on mucosal surfaces then progress to involve the skin
Penphigus vulgaris
67
Biopsy of PV
Intraepidermal vesicle formation secondary to loss of cohesion between epidermal cells Basal keratinocytes remain attached to epidermal basement membrane
68
Autoantibodies of PV
IgG autoantibodies to desmogelins (Dsgs) Early PV - IgG to Dsg3 Advanced PV- Ig autoantibodies to Dsg3 and Dsg1
69
Bad prognostic factors for PV
Advanced age Widespread involvement Requirement for high doses of steroid with or without other immunosuppresives for control of disease
70
Treatment of PV
Mainstay is systemic steroids Moderate to severe PV: prednisone 1mg/k/d Immunosuppressive Azathioprine 2-2.5 mkd MMF 20-35 mkd Cyclophosphamide 1-2 mkd Severe, treatment resistant: Plasmapheresis IV immunoglobulin Rituximab
71
Pemphigus folaceaus vs PV
More superficial blistering Mucous membranes almost always spared IgG autoantibody: IgG to Dsg1
72
Subspidermal blisters Lower abdomen groin flexor surfaces Major histocompatibility complex HLA BQB1*0301
Bullous pemphigoid
73
Antibodies of Paraneoplastic pemphigus
IgG to cytoplasmic proteins wc are members of the plakin family and cell surface proteins that are members of cadherin family
74
Neoplasms assoc with paraneoplastic pemphigus
``` NHL CLL Thymoma Spindlecell tumors Waldenstorm’s macroglobulinemia Castleman’s disease ```
75
Pemphigus blistering disease Assoc w thymoma and myasthenia gravis Drug induced pemphigus
Pemphigus foliaceus
76
Antibodies in bullous pemphigoid
Linear deposits of IgG and C3 in epidermal basement membrane
77
Treatment of bullous pemphigoid
Systemic glucocorticoids Severe, more extensive lesions: high dose steroids plus immunosuppressives Azathioprine Mycophenolate mofetil Cyclophosphamide
78
Intensely pruritic papulovesicular disease Symmetrically distributed over extensor surface Alsmost all casess associated with gluten sensitive enteropathy
Dermatitis herpetiformis
79
IF findings of dermatitis herpetiformis
Granular deposits of IgA Biopsy of small bowel: blunting of intestinal villi and lymphocytic infiltrate of lamina propria
80
Mainstay of treatment of DH
Dapsone 50-200 mg/d Response: withing 24-48 hiurs Wof: hemolysis and methemoglobinemia in doses > 100mg/d
81
Similar to dermatitis herpetiformis But no assoc enteropathy
Linear IgA disease
82
Treatment of linear IgA disease
Dapsone Not responsive to gluten free diet
83
Cutaneous signs of dermatomyositis precede or follow myositis by weeks to years
Ok
84
Most common manifestation of DM
Purple red discoloration of eyelids | Heliotrope rash
85
Violaceous flat topped papules over the doral interphalangeal joints Pathognomonic of dermatomyositis Occurs in 1/3 of dermatomyositis patients
Gottron’s papules
86
Thin violaceous papules and plaques on the elbows and knees of patients with dermatomyositis
Gottron’s sign
87
In long standing dermatomyositis Areas of hypopigmentaion, hyperpigmentation mild atrophy and telangiectasia
Poikiloderma Rare in sle and scleroderma- may distinguish DM
88
SLE cutaneous manifestation
Acute Subacute Chronic discoid types
89
Butterfly rash Sudden in onset Associated w exacerbation of SLE
Acute cutaneous LE
90
IF findings in acute cutaneous LE
Deposits of immunoglobulins and complement of epidermal basement membrane zone
91
Treatment acute cutaneous LE
Control of systemic disease | Photoprotection
92
Widespread photosensitive nonscarring eruption Resembles psoriasis Papulosquamous form and annular form + anti Ro antibodies
Subacute lupus erythematosus
93
Treatment of SCLE
Aminoquinoline antimalarial drugs Photoprotective measures
94
Chronic cutaneous LE Discrete lesions in the face scalp and/or external ears Erythematous papules pr plaques with thick adherent scale that occludes hair follicles Perists for years and expand slowly Carpet tracking when scales are removed - relatively specific finding
Discoid lupus erythematosus
95
Progression of skin lesions of scleroderma
Commences distally on the fingbers and spreads proximally accompanied by resorption of bone of the fingertips
96
Clinical features of scleroderma
Contractures Calcinosis cutis Smooth unwrinkled brotaut skin over the nose Shrinkage of tissue around the mouth Perioral radial furrowing Matlike telangiectasia
97
Cold induced blanching cyanosis and reactive hyperemia White blue red
Raynaud’s phenomenon
98
Localized thickening and sclerosis of skin Predominantly on the trunk Begins as erythematous or flesh colored plaques that become sclerotic w centrl hypopigmentation
Morphea May be localized or generalized Skin biopsy indistinguishable from scleroderma
99
Treatment of morphea
Physical therapy to prevent contractions Phototherapy Methotrexate +- glucocorticoids
100
Most frequent cutaneous drug reactions
Morbilliform rash | Urticaria
101
Immediate drug reactions
Release of mediators of inflammation by tissue mast cells or circulating basophils ``` Histamine Leukotrienes Prostaglandins Braykinins Platelet activating factor Enzymes proteiglycans ``` IgE mediated
102
Meds/drus that cause direct mast cell degranulation or anaphylactoid reactions
NSAIDs | Radiocontrast media
103
Mot frequent cause of IgE dependent reactions to drugs Require prior sensitization
Penicillins | Muscle relaxants in general anesthesia
104
Tissue deposition of circulating immune complexes w consumption of complement Characterized by fever, arthritis, nephritis, neuritis, edema, urticarial, papular or purpuric rash
Serum sickness
105
Drugs that can cause serum sickness
``` Cephalosporins Monoclonal antibodies (infliximab, rituximab, omalizumab) ``` Develop 6 days or more after exposure to a drug
106
Classsification of adverse drug reactions
Type I IgE, urticaria angioedema anaphylaxis Type II IgG mediated Drug induced hemolysis, thrombocytopenia Type III Immune complex IgG+ antigen Vasculitis, serum sickness, drug induced lupus
107
Classification of adverse drug reactions
IVa T lymphocyte- mediated macrophage inflammation Tuberculin skin test, contact dermatitis IVb T lymphocyte-mediated Eosinophil inflammation Drug induced hypersensitivity syndrome (DIHS) , morbilliform reaction IVc T lymphocyte-mediated Cytotoxic T lymphocyte inflammation SJS/TEN, morbilliform eruption IVd T lymphocyte mediated neutrophil inflammation Acute generalized exanthematous pustulosis (AGEP)
108
Drugs that exacerbate plaque psoriasis
``` NSAIDs Lithium Beta blockers TNF Antagonists IFN ACE I ```
109
Drugs that worsen pustular psoriasis
Antimalarials | Withdrawal of systemic glucocorticoids
110
Drug that treats psoriasis but can induce psoriasis in other conditions (esp palmar-plantar)
Anti TNF
111
Associated with new onset SLE
IL2 IFN alpha Anti TNF alpha Assoc w anti histones
112
Exacerbate subacute sle
Minocycline and thiazide diuretics
113
Drug induced bullous pemphigoid
Furosemide
114
Drug assoc w linear IgA bullous dermatitis
Vancomycin
115
Can induce sweet syndrome and pyoderma gangrenosum
GCSF
116
Drug related pseudoporphyria
NSAIDs
117
Can cause melasma
Oral contraceptives
118
Drug induced lipofuscinosis with characteristic red brown discoloration
Clofazimine
119
Warfarin necrosis of the skin
Occurs during 3rd-10th day if therapy with warfarin Breast thighs and buttocks In heterozygous protein C deficiency
120
Treatment of warfarin induced necrosis
Vitamin K Heparin Surgical debridement Intensive wound care
121
Anagen vs telogen effluvium
Anagen - growth Within days of drug administration Telogen - resting 2-4 months following initiation of new medication Non scarring alopecia, reversible
122
Drugs that cause hair loss:
Anti neoplastic drugs - alkylating agents, bleomyci, vinca alkaloids, platinum compounds Anticonvulsants- carbamazepine, valproate Anihypertensive drugs- beta blockers Antidepressants Antithyroid drugs Oral contraceptives Cholesterol lowering agents
123
Inflammation of periungal skin
Paronychia
124
Transverse depression of the nail plate
Beau’s lines
125
Detachment of distal part of the nail plate
Onycholysis
126
Detachment of proximal part of nail plate Caused by temporary arrest of nail matrix mitotic activity
Onychomadesis
127
Red man syndrome Histamine related anaphylactoid reaction Flushing diffuse maculopqpular eruption hypotension
Vancomycin
128
Pruritus is a common complication of
Antimalarial therapy But is associated with almost all drug eruptions
129
Most common of all drug induced reactions
Morbilliform or maculopapular eruptions Develop within 1 week of initiation of therapy and last less than 2 weeks
130
Drugs that carry high rates of morbilliform reaction
Nevirapine and Lamotrigine
131
Second most frequent type of cutaneous drug reaction
Urticaria Pruritic red wheals lasting more than 24 hrs Most frequently with ACE I , aspirin NSAIDS penicillin and blood products
132
Mechanisms of drug induced urticaria
IgE dependent Occurs within 36 hours of drug exposure Circulating immune complexes Assoc w serum sickness like reactions 6-12 days after first exposure Non immunologic activation of effector pathways
133
Characterized by one or more sharply demarcated, dull red to brown lesions sometimes with central bulla Lesion appears in the same location upon rechallenge of the drug Lesions often involve the lips, hand, face, genitalia, and oral mucosa
Fixed Drug Eruptions
134
Drug that induces a cutaneous vasculitis accompanied by leukoplenia and splenomegaly IF: immune-complex deposition Allopurinol thiazides sulfonamides antimicrobials NSAIDs Presence of eosinophils in perivascular infiltrate
PTU
135
TEN vs AGEP
Skin biopsy: AGEP Neutrophil collection and sparse necrotic keratinocytes in the upper part of the epidermis TEN full thickness epidermal necrosis
136
Most common cause of drug induced hypersensitivity syndrome
Allopurinol With renal involvement
137
Reactivation of what viruses is seen in drug induced hypersensitivity syndrome?
Herpes virus 6 EBV Herpes viruses Associated with worse outcomes
138
Treatment of drug induced hypersensitivity syndrome
Systemic glucocorticoids 1-2 mkd Slow taper over 8-12 weeks Others: MMF
139
Other organ involvement in DIHS
Minocycline- cardiac and lung involvement Abacavir - GI involvement
140
SJS and TEN
Full thickness epidermal necrosis Without substantial dermal inflammation SJS <10% 10-30 dettachment SJS/ TEN overlap syndrome TEN >30% overlap
141
Drugs that cause SJS/ TEN
``` Sulfonamides Nevirapine Allopurinol Lamotrigine Aromatic anticonvulsants NSAIDs ```
142
Characteristic times of onset to drug reaction
Morbilliform eruptions - 4-14 days AGEP 2-4 days SJS/TEN - 5-28 days DIHS - 14-48
143
Vasculopathy plus intravascular thrombosis Associated with venous hypertension
Livedoid vasculopathy
144
Most commonly found on lower extremities Ulcerative lesion withc characteristic appearance of undermined necrotic violaceous edge and peripheral erythematous halo Most common associated conditions: ulcerative colitis and crohn’s disease
Pyoderma gangrenosum
145
Size of purpura vs petechiae
Petechiae 2 mm and below Purpura 3 mm and above
146
Classification of purpura
Palpable ``` Nonpalpable Most commonly primary cutaneous disorders Trauma Solar - extensor surfaces forearms Capillaritis - lower extremities Steroid induced- more widespread ```
147
Purpura assoc with thrombi formation within vessels
``` DIC monoclonal cryoglobinemia Thrombocytosis TTP APS Reaction to warfarin and heparin ( warfarin induced necrosis, seen more often in women, and in areas with abundant subcutaenous fat) ```
148
Waldenstrom’s hypergammaglobulinemic purpura
Chronic disorder Petechiae on lower extremitties Circulating complexes of IgG-Anti IgGmolecules Exacerbations in prolonged standing
149
Palpable purpura classification
Vasculitic and embolic
150
Vasculitis most commonly associated with palpable purpura
Leukocytoclastic vasculitis | LCV
151
Subtype of acute LCV More commonly in children and adolescents after URTI Majority are lower extremity lesions, involve thw buttocks Deposits of IgA within dermal blood vessels
Henoch schonlein purpura
152
Vasculitic vs embolic purpura
Vasculitis- circular edge/ borders Emboli- irregular border
153
Common causes of infectious emboli
``` Gram negative cocci (meningococcus, gonococcus) Gram neg rods (enterobacteriaceae) Gram positive cocci (staph) Rickettsia Aspergillus ```
154
Lesions that begina as edematous erythematous papules or plaques then develop central purpura and necrosis Classically associated with Pseudomonas aeruginosa but can be caused by Klebsiella, Eschirichia and serratia
Ecthyma gangrenosum
155
Subdivision of erythema multiforme
EM minor - due to HSV EM Major - due to HSV, mycoplasma pneumoniae, drugs - mucous membrane involvement - hemorrhagic crusts of the lips are characteristic
156
SSSS is distinguished from TEN by the following features:
younger age group (primarily infants), more superficial site of blister formation, no oral lesions, shorter course, lower morbidity and mortality rates, and an association with staphylococcal exfoliative toxin (“exfoliatin”), not drugs
157
Blistering disorders associated w staphylococcal infection
SSS | Bullous impetigo
158
Clinical manifestation of SSS
initial findings are redness and tenderness of the central face, neck, trunk, and intertriginous zones. This is followed by short-lived flaccid bullae and a slough or exfoliation of the superficial epidermis. Crusted areas then develop, characteristically around the mouth in a radial pattern
159
SSSS Vs bullous impetigo
In SSSS, the site of staphylococcal infection is usually extracutaneous (conjunctivitis, rhinorrhea, otitis media, pharyngitis, tonsillitis), and the cutaneous lesions are sterile, whereas in bullous impetigo, the skin lesions are the site of infection. Impetigo is more localized than SSSS and usually presents with honey-colored crusts
160
There are several types of porphyria, but the most common form with cutaneous findings is
porphyria cutanea tarda (PCT)