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Dermatology > 3) Drug Eruptions > Flashcards

3) Drug Eruptions Flashcards

1
Q

Exanthematous (morbilliform) drug reactions

A
  • 2% of individuals exposed to drugs
  • Accounts for 95% of cutaneous reactions
  • Highest rates associated with antibiotics
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2
Q

Exanthematous (morbilliform) drug reactions mechanism

A
  • Possibly a delayed type T-cell mediated immune reaction

- Genetic predisposition, underlying viral disease, and administration of multiple medications

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3
Q

Exanthematous (morbilliform) drug reactions characteristics

A
  • Erythematous maculopapular rash in trunk and proximal extremities
  • Developing within 5-14 days
  • May occur as early as 2-3 days in previously sensitized patients
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4
Q

Exanthematous (morbilliform) drug reactions symptoms

A
  • Pruritis (usually in legs or area of dependence)
  • Low grade fever
  • Mild eosinophilia
  • Mucosal involvement is absent
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5
Q

Exanthematous (morbilliform) drug reaction diagnosis

A
  • Resolution in 7-14 days or with discontinuation of offending drug
  • DDx includes viral & bacterial exanthems, systemic disease rashes, and cutaneous diseases
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6
Q

Exanthematous (morbilliform) warning signs of more serious condition

A
  • Erythroderma
  • High fever
  • Facial edema
  • Mucositis
  • Skin tenderness
  • Blistering
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7
Q

Exanthematous (morbilliform) drug reaction treatment

A
  • Removal of offending drug
  • Symptomatic relief with topical corticosteroids and oral antihistamines
  • High potency topical corticosteroid applied once or twice daily for pruritic relief (or oral histamines until subsides)
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8
Q

Exanthematous (morbilliform) drug reaction eliciting drugs

A
  • Penicillin
  • Cephalosporin
  • Macrolides
  • Quinolones
  • Tuberculostatic
  • Sulfonamides
  • Anticonvulsants
  • NSAIDs
  • Paracetamol
  • RTIs
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9
Q

Acute generalized exanthematous pustulosis (AGEP)

A
  • 1-5 per million, rare
  • 90% of cases caused by drugs
  • Most often antibiotics, antifungals, calcium channel blockers, and antimalarials
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10
Q

Acute generalized exanthematous pustulosis (AGEP) mechanism

A
  • Thought to be T-cell mediated neutrophilic inflammation involving drug specific CD4/8, cytokines, and chemokines
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11
Q

Acute generalized exanthematous pustulosis (AGEP) characteristics

A
  • Dozens to hundreds of nonfollicular, sterile pustules beginning on the face and extending to trunk and limbs
  • May occur a few hours to days after drug has been introduced
  • Median time for antibiotics was one day while others were 11 days
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12
Q

Acute generalized exanthematous pustulosis (AGEP) signs/symptoms

A
  • Dozens to hundreds of pinhead-sized pustules
  • Fever > 38 ˚ C
  • Leukocytosis w > 7,000 neutrophils
  • Pustular smear negative for bacteria
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13
Q

Acute generalized exanthematous pustulosis (AGEP) diagnosis

A
  • Typical signs (one or more) presenting with an acute, febrile pustular eruption a few hours to days after starting a new drug
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14
Q

Acute generalized exanthematous pustulosis (AGEP) DDx

A
  • Generalized acute pustular psoriasis
  • Stevens-Johnson syndrome/toxic epidermal necrolysis
  • Sneddon-Wilkinson disease
  • Bullous impetigo
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15
Q

AGEP treatment

A
  • Removal of offending drug, supportive cate, and symptomatic treatment
  • Supportive care involves moist dressings and antiseptic solutions during pustular phase
  • Symptomatic relief includes medium potency topical corticosteroids and oral antihistamines
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16
Q

AGEP eliciting drugs

A
  • Aminopenicillins
  • Macrolides
  • Quinolones
  • Sulfonamides
  • Hydroxychloroquine
  • Terbinafine
  • Diltiazem
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17
Q

New onset urticaria

A
  • Common (20% of population)
  • Allergic reactions to medication, food, or insect bites/stings
  • Common viral and bacterial infections
  • Classified as acute (< 6 weeks) or chronic (> 6 weeks) –> 2/3 fall under acute classification
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18
Q

New-onset urticaria mechanism

A
  • Involves cutaneous mast cells in the superficial dermis which release histamine and vasodilatory mediators causing itching and localizing swelling
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19
Q

New-onset urticaria lesions

A
  • Intensely pruritic appearing as circumscribed, raised, erythematous plaques with central pallor
  • Shape may be round, oval, or serpinginous ranging from < 1cm to several cm
  • May enlarge and usually disappear within 24 hours
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20
Q

New-onset urticaria characteristics

A
  • Transient w/out residual affect
  • Non painful, but pruritic lesions
  • With or without angioedema
  • May affect any area of the body
  • Many associated triggers as seen in chart
  • Infections are associated with over 80% of acute urticarial reactions in pediatric population
  • Antibiotics are most frequently implicated in
  • causing IgE-mediated urticaria (beta-lactams)
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21
Q

New-onset urticaria diagnosis

A
  • Clinical one based on your H&P as well as characteristic lesions
  • Resolution of individual lesions from the eruption in about 24
    hours
  • DDx includes atopic dermatitis, contact dermatitis, insect bites, bullous pemphigoid, or erythema multiforme minor, etc.
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22
Q

New-onset urticaria must r/o anaphylaxis

A
  • Generalized, rapid onset and evolution
  • Related to an allergen which may resolve on its own or require respiratory and/or CV support along with emergency treatment
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23
Q

New-onset urticaria treatment

A
  • Initial treatment: short term relief of pruritus and angioedema if present
  • Two-thirds of cases are self limiting and will resolve spontaneously
  • Second generation H1 antihistamines are first line treatment drugs in mild cases
  • If symptoms are moderate to severe, then addition of an H2 antihistamine is recommended
  • Patients with prominent angioedema and persistent symptoms despite treatment with H1 & H2 antihistamines, then a glucocorticoid should be added in a short term dose (~5-7 days)
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24
Q

Fixed drug eruption

A
  • Seen in about 2-3% of population taking the drug
  • Accounts for 14-22 percent of
    cutaneous drug reactions
  • Most often implicated are the
    antibacterial sulfonamides, antibiotics, NSAIDs, analgesics, and hypnotics
25
Q

Fixed drug eruption mechanism

A
  • Believed to be due to intraepidermal CD8 T-
    cell with an effector-memory phenotype
  • These have been found to be established in these type of lesions and remain quiescent until re-challenged
26
Q

Fixed drug eruption characteristics

A
  • Well demarcated, round to oval, single (usually) or a small number of dusky red or violaceous macules that evolve into plaques
  • Once resolved, leave post inflammatory hyperpigmentation
27
Q

Fixed drug eruption presentation

A
  • Usually a solitary lesion
  • Present 30 minutes to 8 hours after drug
    administration
  • Resolve spontaneously in 7-10 days after discontinuation of offending drug
  • Pustular smear negative for bacteria
28
Q

Fixed drug eruption diagnosis

A
  • Clinical based on lesion morphology as well as detailed history that should include any new drugs in past hours to days
  • Spontaneous resolution within 7-10 days after discontinuation of the offending drug
  • DDx includes Stevens-Johnson Syndrome/toxic epidermal necrolysis, Erythema Multiforme, Bullous Pemphigoid, Large- Plaque Parapsoriasis, etc.
29
Q

Fixed drug eruption treatment

A
  • Removal and avoidance of offending drug
  • Symptomatic treatment for relief of pruritis includes medium to high potency topical corticosteroids and oral antihistamines
  • Systemic or topical provocation test are helpful when identifying culprit drug when unclear or if multiple are suspected
30
Q

Fixed drug eruption eliciting drugs

A
  • Penicillins
  • Tetracyclines
  • Quinolones
  • Sulfonamides
  • Dapsone
  • NSAIDs/acetaminophen
  • Barbiturates
  • Antimalarials
31
Q

Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS)

A
  • Rare condition that is drug induced and potentially life threatening
  • Characterized by a long latency period (2-8 wks)
  • Most often antiepileptics and allopurinol, followed by
    sulfonomides and vancomycin
32
Q

Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS)
presentation

A
  • Potentially life-threatening, drug-induced hypersensitivity reaction that includes skin eruption, hematologic abnormalities lymphadenopathy, and internal organ involvement
  • Morbilliform eruption progressing into a diffuse, confluent, and infiltrated erythema with follicular accentuation
  • Usually > 50% of body surface area and/or two or more of facial edema, infiltrative lesions, scaling, and purpura
33
Q

DRESS mechanism

A
  • Likely involves a strong, drug specific immune response carried out by CD4/8
34
Q

DRESS presentation

A
  • Begins usually in face and upper trunk
  • Involves 50% or more of BSA
  • Facial edema in 50% of cases
  • Leukocytosis with eosinophils >
    700/microL
  • Increased ALT
  • Reactivation of HHV-6 and other viruses
  • Patients have a > 90% of having at least one organ involved, while 50-60% will have two or more organs involved
  • Exfoliative dermatitis in 20-30% of patients when BSA is > 90%
35
Q

DRESS diagnosis

A
  • Suspected when a new drug was started 2-6 weeks and presents with a skin eruption as described, fever (38 to 40˚ C), facial edema, and enlarged lymph nodes
  • Laboratory testing, skin biopsy, herpesvirus screening/testing, and imaging studies may aid in diagnosis
  • DDx includes acute generalized exanthematous pustulosis, Stevens-Johnson Syndrome/toxic epidermal necrolysis, hypereosinophilic syndromes, acute cutaneous lupus erythematosus, etc.
36
Q

DRESS treatment

A
  • ID/withdrawal of offending drug with supportive care
  • Avoidance of new medication
  • Most recover weeks to months after drug withdrawal
  • Supportive care for severe cutaneous reactions may require hospitalization as well as fluids, electrolytes, and nutritional support for those with exfoliative dermatitis
  • Absence of severe organ involvement: high potency topical corticosteroids
  • Severe lung/kidney involvement: systemic corticosteroids
37
Q

DRESS prevention

A
  • Strict avoidance of offending drug

- Increased risk w/ cross-reacting drugs that are chemically related (such as antiepileptics)

38
Q

DRESS eliciting drugs

A
  • Antiepileptics
  • Allopurinol
  • Febuxostat
  • Olanzapine
  • Sulfonamides
  • Dapsone
  • Minocycline
  • Vancomycin
39
Q

Drug induced pigmentation

A
  • Diffuse cutaneous hyperpigmentation with a increased production of melanin and/or the deposition of drug complexes or metals in the dermis are responsible for the skin discoloration
  • Usually resolves with discontinuation of offending agent (but may be prolonged months to years)
40
Q

Drug induced pigmentation variations

A
  • Linear
  • Reticulate
  • Non patterns
41
Q

Pseudoporphyria

A
  • Unknown incidence
  • Most often caused by medications including NSAIDs, antibiotics, diuretics, and antineoplastic agents
  • Protracted course
42
Q

Pseudoporphyria incidence

A
  • Unknown

- Study reported 10% of children taking naproxen for juvenile idiopathic arthritis developed this condition

43
Q

Pseudoporphyria mechanism

A
  • Unknown
  • Considered photodynamic phototoxic drug reaction
  • May occur a few hours to months after exposure to causative agent, but characteristically will persist for months to years
44
Q

Pseudoporphyria presentation

A
  • Skin fragility, bullae, and vesicles in sun-exposed areas of the body
  • Typically dorsum of hands, forearms, face, as well as lower legs and feet
  • Normal porphyrin levels
45
Q

Pseudoporphyria histology

A
  • Subepidermal blister with scant perivascular lymphocytic infiltrate
  • IgG, IgM, C3, and fibrinogen at dermal-epidermal junction and in vessel walls on direct immunofluorescence
46
Q

Pseudoporphyria diagnosis

A
  • Cutaneous manifestations as described above along with histological findings, normal porphyrin levels, potentially phototoxic medication use, or UVA exposure
  • Resolution may take months to years after discontinuation of the drug
  • One study of 16 patients resulted in six month resolution of five patients but persited an average of 2.5 years for the remaining 11
  • DDx includes Porphyria cutanea tarda, Epidermolyisis bullous acquisita, Bullous pemphigoid, Pemphigus, etc.
47
Q

Pseudoporphyria treatment

A
  • Removal of offending drug if any, and photoreception (including avoidance of tanning beds)
  • Education and discuss expectations with regards to the protracted course of the condition
  • Medications known to induce condition
48
Q

Erythema multiforme (EM)

A
  • Uncommon, likely less than one percent
  • Most frequent in young adults, 20-40 years of age, slight male predominance
  • Most common cause is infection, usually herpes simplex virus (HSV)
  • EM Minor refers to without mucosal disease, EM Major is with mucosal involvement
49
Q

Erythema multiforme incidence

A
  • Unknown
  • Available data is based on HSV-associated EM which thought to involve a cell-mediated immune response directed against viral antigens deposited in lesional skin
50
Q

Erythema multiforme hallmark

A
  • Target lesions
  • Begins as round erythematous papules evolving into classic target lesion which consists of a dusky central area or blister, a dark red inflammatory zone surrounded by pale ring of edema, and an erythematous halo at extreme periphery
51
Q

Erythema multiforme presentation

A
  • Symmetric distribution of target lesions to the face, neck, palms, soles, and extensor surfaces of acral extremities
  • Mucus membrane involvement with cutaneous lesions in
    EM major
  • Severe cases may have elevated ESR, WBC, and liver enzymes
52
Q

Erythema multiforme diagnosis

A
  • Based on the history of the eruption and clinical findings of the hallmark target lesions
  • Skin biopsy may helpful to establish the diagnosis
  • History of HSV infection should be questioned in all patients
  • Less than 10% are associated with medication so HSV infection should be considered in all patients
  • Appears over 3-5 days and resolves in about 2 weeks
  • DDx includes Urticaria, Stevens-Johnson Syndrome, Fixed Drug Eruption, Pemphigoid, Rowell Syndrome, Cutaneous Small Vessel Vasculitis, etc.
53
Q

Erythema multiforme treatment

A
  • Normally self limiting where treatment varies with severity and is targeted to reduce pain or pruritis if present
  • Symptomatic relief includes medium potency topical corticosteroids and oral antihistamines with anesthetic mouthwash, while painful oral manifestations usually necessitate systemic glucocorticoids
  • In the severe recurrent variant of EM associated with
    HSV, continuous antiviral therapy is recommended
54
Q

Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN)

A
  • Seen in about 2-7 cases per million, rare
  • Leading trigger are
    medications
  • Most often implicated are allopurinol, aromatic anticonvulsants, antibacterial
    sulfonamides, and “oxicam”
    NSAIDs
55
Q

SJS and TEN mechanism

A
  • Incompletely understood
  • Studies suggest that drug-specific CD8+ cytotoxic T cells, along with natural killer (NK) cells are thought to be the major inducers of keratinocyte apoptosis
56
Q

SJS and TEN presentation

A
  • Fever exceeding 39˚C, and influenza-like symptoms precede by 1-3 days
  • Exanthematous eruption is some, skin tenderness and/or blistering
  • Cutaneous and mucosal lesions are usually ill-defined, coalescing erythematous macules with pruritic centers
  • As progresses, lesions become vesicles and bullae and in a few days the skin begins to slough
57
Q

SJS and TEN signs and symptoms

A
  • Prodrome with fever exceeding 39˚C
  • Cutaneous and mucosal lesions (> 90%)
  • Cases with < 10% of skin detachement are considered SJS, while those with 30% or more are considered TEN; 10-30% are overlap SJS/TEN
  • Nikolsky sign
  • Abnormal labs include anemia and lymphopenia
58
Q

SJS and TEN diagnosis

A
  • There is no accepted universal diagnosis criteria
  • Dx based on aforementioned clinical features as well as recent drug exposure
  • Skin biopsy is useful for confirming the diagnosis
  • Clinical course lasts 8-12 days while re-epithelialization may
    begin after several days and typically requires 2-4 weeks
  • DDx includes generalized acute pustular psoriasis, generalized bullous fixed drug eruption, erythema multiforme, Staphylococcal scalded skin syndrome, etc.
59
Q

SJS and TEN treatment

A
  • Mainstay of treatment of removal of offending drug, supportive care, wound care, pain control, and fluids and nutrition
  • Supportive care is along the
    main principles of burn injuries
  • Monitoring for superinfections because sepsis is a major cause of death

Dermatology (5 decks)

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