Clinical Dermatology Flashcards Preview

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Flashcards in Clinical Dermatology Deck (31):

1. Describe
2. how does it begin
3. what causes it?

 1. skin eruption that bursts forth or blooms
2. w/ red macules and/or papules
3. bacteria, viruses, or drugs


 Bacterial causes of exanthems (4)

 Rocky Mountain Spotted Fever (rickettsia rickettsii)
Meningococcemia (N meningitidis)
Scarlet fever (Group A strep)
Toxic shock syndrome (s aureus)


 Rocky Mountain Spotted Fever
1. Triad of symptoms
2. characteristic feature of rash
3. transmitted by

 1. fever, headache, rash
2. erythematous macules that spread from wrists and ankles to palms and soles, then trunk (spares the face)
3. ticks


1. characteristic features of rash

 1. petechiae, pustules, bullae,and hemmorrhagic lesions; may ultimately see skin necrosis


 Scarlet Fever
1. caused by
2. what precedes the rash?
3. characteristic features of rash
4. where is rash most intense?
5. Other features (3)

 1. s pyogenes
2. fever and pharyngitis
3. sandpaper-like rash which begins on upper chest, then spreads to extremities;
4. inner aspects of arms and
5. strawberry tongue
circumoral pallor
pastia lines-linear petechia along creases- antecebital and axillary folds


 Toxic shock syndrome
1. caused by
2. characteristic of rash

 1. TSST-1; S aureus (also S pyogenes)
2. generalized macular erythematous rash and desquamation of palms and soles; skin desquamates 1-2 weeks into course


 Viruses associated with rash (5)

Erythema infectiosum


 Exanthomatous Drug Eruptions
1. How common?
2. Course
3. Types of drug reactions

 1. reported for nearly all medications; 1-5% of firsttime users of most drugs
2. most self-limiting; rarely life threatening
3. Morbilliform, Urticaria, fixed drug eruption, photosensitivity


 Morbilliform Drug Reaction
1. describe rash
2. when does it appear?
3. why kind of drugs can cause it?
4. If a pt has a sore throat and has a reaction to ampiicillin or amoxacillin, what could pt have?
5. where is rash usually more intense?

1. maculopapular eruptions; spread rapidly, may coalesce; generalized distribution, systemic, often pruritic, may have low grade fevers;
2. 4-21 days after start of causative agent; can develop after drug is stopped
3. ANY drug; ampicillin, amoxacillin are classic; (PCN, sulfonamids, antiepileptics, allopurinol)
4. pt has mono
5. on proximal limbs as opposed to distal limbs


 Morbilliform reaction Pathogenesis
1. may be
2. likely mechanism
3. What determines who gets a reaction to a drug?

 1. idiosyncratic
2. T cell mediated delayed hypersensitivity reaction: Ag presenting cells present Ag composed of drug or metabolite--> Ag specific cells proliferate, infiltrate skin, release cytokines, chemokines etc --> rash
3. largely unknown; immune status & genetic factors


 Morbilliform reaction
1. How long does rash usually last?
2. Treatment (4)
6. What if drug is indicated again?

1. 1-2 weeks; may rapidly resolve after withdrawal of drug; may fade, even if drug is continued
2. ID and prompt withdrawal of suspected drug
3. Antihistamines (relieve pruritis)
4. Topical glucocorticoids (may reduce signs/symptoms)
5. Cool compress
6. rechallenge usually doesn't result in new eruption, but should be avoided bc eruption may be more severe


 Drug Reactions
1. PCNs have a 10% cross-reactivity with which drug?
2. which drugs are frequent causes of drug eruption?
3. What mediates urticaria reactions?

 1. cephalosporins
2. sulfonamide antibiotics (unlikely cross-reactivity w/ non antimicrobe sulfa)
3. IgE, type I hypersensitivity reaction


 What are signs of a serious/severe cutaneous reaction? (4)

 Mucous membrane involvement
Temperature > 38.5
Facial edema and erythema


 Erythema multiforme
1. What is it?
2. What is it associated with
3. what does it look like?
4. Pathogenesis

 1. hypersensitivity to infections (herpes simplex, mycoplasma) or drugs
2. malignancy, collagen vascular diseases
3. target lesions: red center, pallor around that, red around the pallor; can be many different types of lesions (macules, papules, vesicles, bullae)
4. Immune mediated/T cell mediated; drug/metabolite may bind covalently to poteins (triggers immune response)


 Erythema Multiforme Syndrome
1. Course
2. resolution

 1. starts on arms; itchy
2. 7-10 days normally; self-limited; low morbidity


 Steven Johnson Syndrome
1. less severe form of what?
2. what is it?
3. symptoms
4. what does the rash look like?

 1. Toxic Epidermal Necrosis
2. drug reaction
3. fevers, epidermal detachment on <10% total body surface
4. wide macules, flat atypical target lesions; erosions of lips and oral mucosa; conjunctiva, urethra, genital, perianal areas


 Steven Johnson Syndrome
1. Treatment
2. Should you rechallenge?
3. Death rate

 1. supportive care; withdrawal of offending agent
2. no
3. 1-5%


 Toxic Epidermal Necrosis
1. Implicated Drugs
2. What % are due to drug reactions?
3. Pathogenesis

1. Allpurinol, Antibiotics, NSAIDs, Anticonvulsants
2. 80% / majority
3. drug specific cytotoxic T cells have been detected in skin lesions of TEN; blisters resulting from accumulation of interstitial fluid under the necrotic epidermis contain T lymphocytes that are able to kill autologous lymphocytes and keratinocytes in a drug-specific, HLA-restricted, and perforin/granzyme-mediated pathway


 Toxic Epidermal Necrolysis
1. Symptoms
2. Rash
3. What is Nikolsky's sign?
4. What % of body surface?
5. what is almost always involved?

 1. Fever, sore throat, burning eyes
2. Steven-Johnson-like lesions; diffuse hot erythema w/in hours
3. slight rubbing of skin results in sloughing
4. over 30%
5. mucous membranes


 Toxic Epidermal Necrolysis
1. Death rate
2. what usually causes death?
3. Treatment
4. Rechallenge?
5. What significantly improves mortality rate?

 1. 34-40%
2. infection
3. discontinue suspected drug; wound care, hydration, nutritional support
4. no
5. transfer to a regional burn center


1. Vascular Ectasia
2. Telengiectasia

 1. local dilatation of pre-existing vessels
2. congenital anomaly or acquired exaggeration of preformed vessels (capillaries, venules, arterioles)


 Cherry Angiomas
1. Describe
2. Where is it found?
3. What is important about it?

 1. 1-4 mm papules
2. commonly on the trunk of adults
3. not clinically significant


 Hereditary Hemorrhagic Telengiectasia (Osler-Weber-Rendu Disease)
1. Genetics
2. What is it?
3. What other organs/systems are involved?

 1. autosomal dominant
2. telengiectasias over skin, oral mucous membranes
3. Respiratory (epistaxis), GI (GI bleeding), urinary tracts (hematuria)


 Nevus Flammeus
1. What is it?
2. progression?

 1. most common ectasia; birthmark usually on head or neck; light pink or puple
2. most ultimately regress


 Port Wine Stain
1. What is it a kind of?
2. What happens?
3. What has happened to the skin?
4. Does it fade away?

 1. form of nevus flammeus
2. grows with the child
3. thickened
4. no


 Sturge Weber Syndrome (encephalotrigeminal angiomatosis)
1. What is it?
2. What characterizes it?
3. Symptoms
4. What nerve does it involve?

 1. Rare sporadic congenital disorder
2. facial port-wine stain, venous angiomatous masses in cortical leptomeninges, abnormal blood vessels of the eye
3. Seizures, mental retardation, glaucoma
4. ophthalmic branch of the trigeminal nerve, usually on upper eyelid and supraorbital region


1. how common?
2. malignant?
3. What is it?
4. Two types

 1. common
2. benign
3. increased numbers of normal or abnormal blood vessels filled with blood
4. capillary or cavernous


 Capillary Hemangioma
1. What is it made of?
2. Where is it found?
3. Gross appearance
4. Progression

 1. aggregates of vascular channels with the caliber and structure of normal capillaries
2. skin, SQ tissue, mucous membranes (lips, mouth), and internal organs (liver, spleen, kidneys)
3. bright red to blue skin lesion, few mm to several cm
4. may enlarge with growth of child, may spontaneously regress


 Cavernous Hemangiomas
1. What is it made of?
2. where is it found?
3. Progression

 1. larger, dilated vascular channels
2. skin, mucosal surfaces, visceral organs, brain
3. do not regress spontaneously


 Von Hippel Lindau (Multiple Hemangiomatous Syndrome)
1. Genetics
2. What does it cause?

 1. Autosomal dominant; deletion of tumor suppressor gene (VHL 3p)
2. Cavernous hemangiomas in cerebellum, brainstem, retina; hemangioblastomas, renal cell carcinoma, pheochromocytoma


 What rashes characteristically affect the palms and soles?

 Rocky Mountain Spotted Fever
Secondary and congenital Syphilis
Hand-Foot-Mouth Disease (Coxsackie A virus)