Rash Flashcards
Differential diagnosis for macular papular rash
Drug eruption (morbilliform (measels looking), Drug induced hypersensitivity syndrome (DRESS), Stevens johnson/toxic epidermal necrolysis)
Viral exanthem
Graft v Host disease
Secondary syphilis
Irritant or allergic contact dermatitis
exanthematous drug eruption AKA Morbilliform drug eruption
- Most common type of drug-induced eruption
- Mechanism likely immunologic, often thought to be delayed (type 4) hypersensitivity reaction
- Occurs 7-14 days after drug started
- Low grade fever may be present
- spontaneously resolves in 1-2 weeks
Penicillins, cephalosporins, sulfonamides
(macrolides, vancomycin (red man syndrome), tetracyclins, quinolones, metronidazole and erythromycins)
Drug - albutorol, antiepileptics, antipsycotics, NSAIDs
stevens johnson syndrome Toxic epidermal necrolysis
- Onset between 1-3 weeks of drug initiation
- typical lesions are tender, dusky red or pupuric macules that progress to flaccid bullae and erosions
- Involvement of the buccal, ocular and genital mucosae in >90%
- Respiratory tract involved in 25%
- Often fever, LAD, hepatitis, cytopenias
- Most commonly caused by allopurinol, anticonvulsants, antibiotics, NSAIDS
SJS- SJSTEN– TEN
nikolsky +
Pink lichenified papules and plaques with scale and excoriations in bilateral antecubital and popliteal fossae
Inflammatory (atopic dermatitis, seborrheic dermatitis, Allergic contact dermatitis, psoriasis)
Infectious- Scabies, tinea corporis
Drug exanthem
Nutritional deficiency (Zinc deficiency)
Immunodeficiency (Wiskott Aldrich)
Atopic Dermatitis
Chronic disease with period of worsening and remission
US prevalence (10-12% in kids, .9% adults)
Infantile stage- more acute, involves face, scalp, extensor surfaces of the extremities, diaper area spared, secondary impetiginization common
Childhood stage- more chronic, involves flexural fold and extremities, more lichenification
Adult stage - variable course, hand dermatitis common
Immunopathophysiology of atopic dermatitis
- Considered a prototypic type 2 Helper T cell disease
- Increased IL4, IL5 IL13, Decreased IL2, IFN-y
- Defects in epidermal skin barrier, Decreased essential fatty acids, fillagrin mutations, increased susceptibility to allergens, increased water loss
- defects in cell mediated immunity (increased susceptibility to viral, bacterial and fungal infections of the skin), Majority of pts colonized with S, aureus
Molluscum contagiosum
- Most common in kids, increased risk with atopic dermatitis
- appear 7 weaks after exposure to the virus
- Firm, small pink or flesh colored dome-shaped papules with central umbilibation
- Spread by contact with infected skin or clothing
- Most have complete clearing in 2-4 months
- Lesions persist an are more numerous in those with weakend immune systems
- Very large ds DNA virus- pox virus family
- Replicates exclusively in the cytoplasm of infected cell-a unique feature for a DNA virus
- A single life cycle lytic replication
- Histology of lesions includes molluscum bodies- large eosinophilic inclusions in the cytoplasm (viral factories)
Eczema herpeticum (Kaposi varicelliform eruption)
- Refers to viral infection of a pre existing dermatosis
- sudden eruption of painful, edematous, cursted vesciles, pustules and erosion
- may be associated with high temperature, malaise, LAD
- Most commonly caused by disseminated HSV infection in patients with atopic dermatitis and referred to as eczema herpeticum
HSV iv drug
acyclovir
Famciclovir and valacyclovir
Acyclovir MOA
prodrug
only gets activated where the virus is
Phosphorylated form is produced 40-100x facter in infected cells, inhibits cells, inhibits herpes DNA polymerase 10-30x more effectively than host cell DNA polymerase
Competes with deoxy-GTP for DNA polymerase
Terminates DNA chain elongation
Fam and Val have better oral bioavailability
Acyclovir can be given IV with more frequent dosing
Mutations in HSV that make resistane
HSV tyrosine Kinase mutations
drug- Foscarnet (directly inhibits DNA polymerase without being phosphorylated)
Eczema herpeticum other chronic conditions
allergies- environmental, food allergies, allergic rhinitis
asthma
allergic contact dermatitis- Latex, nickel
Topical emollients, topical corticsteroid, calcineurin inhibitors
Antihistamines, phototherapy, immunosuppressives
cyclosporine moa
its binding to cyclophilin inhibits the phosphatase of calcineurin, thereby blocking activation of the NFAT transcription factor
Blocking NFAT suppresses IL2 production (T helper cells in particular need IL2
Azathioprinte methotrexate and mycophenolate MOA
They all block DNA sythesis in different ways
MTX- inhibits DHFR, blocks thymidine sythesis
AZA- converted to 6MP, which is misincorporated into DNA and RNA
Mycophenolate- reversibly inhibits IMP dehydrogenase, blocking purine (GMP) synthesis
Bone marrow suppression
AZA- thiprine phase 2 ennzyme
Mycophenolate- lymphocytes are dependent on denovo synthesis
basal cell carcinoma
- Most common human cancer
- Secondary to chronic sun exposure
- can be locally destructive
- Slow growing tumor that rarely metastasizes
- When it metastasizes the patient is often immunocompromised
