Symptom To Diagnosis - Rash Flashcards
12 morphologies of rash:
- Macule.
- Patch.
- Papule.
- Plaque.
- Nodule.
- Tumor.
- Cyst.
- Vesicle.
- Bulla.
- Pustule.
- Wheal.
- Comedone.
Macule:
Lesion without elevation or depression, <1cm.
Patch:
Lesion without elevation or depression, >1cm.
Papule:
Any solid, elevated “bump” <1cm.
Plaque:
Raised plateau-like lesion of variable size, no depth, often a confluence of papules.
Nodule:
Solid lesion with palpable elevation, 1-5cm.
Tumor:
Solid growth, >5cm.
Cyst:
Encapsulated lesion, filled with soft material.
Vesicle:
Elevated, fluid-filled blister <1cm.
Bulla:
Elevated, fluid-filled blister >1cm.
Pustule:
Elevated, pus-filled blister, any size.
Wheal:
Inflamed papule or plaque formed by transient and superficial local edema.
Comedone:
A plug of keratinous material and skin oils retained in a follicle, open is black, closed is white.
Acne vulgaris - Textbook presentation:
Presents in adolescence with chronic, waxing and waning lesions. A variety of lesions are present, including inflammatory papules, pustules, comedones, and nodulocysts over the face, chest, and back.
What is the main cause of acne?
Obstruction of sebaceous follicles on the face and trunk.
3 factors are involved in the development of acne lesions:
- Increased sebum production (androgen dependent) –> Obstructs the follicles.
- Excessive desquamation of epithelial cells and keratin into follicles –> Obstructs the follicles.
- Inflammation 2o to proliferation of the anaerobe Propionibacterium acnes.
Besides the main 3 factors - 4 other factors that may contribute to the disease?
- Hyperandrogen states –> PCOS or androgenic progestins in OCPs.
- Exposure to topical comedogens (cocoa butter, mineral oil, lanolin, fatty acids).
- Numerous factors that lead to follicular obstruction.
- Medications known to trigger or exacerbate acne –> Steroids, INH, Li, androgens.
EBD of acne:
Diagnosis is typically clinical.
EBD of acne - Histopathology:
Will vary depending on the lesion. Comedones have a distinctive histologic appearance.
EBD of acne - Work-up:
Work-up for hyperandrogenism is appropriate when there are signs of PCOS, virilization, or an atypical presentation (such as later in life).
Rosacea - Textbook presentation:
- Adults - Facial rash.
- Gradual development of telangiectasia and persistent centrofacial erythema occasionally with inflammatory red papules and papulopustules.
- Comedones are ABSENT.
- History of easy flushing.
- Rash may worsen with sun exposure, ingestion of spicy food and hot liquids, emotional stress, and exercise.
Rosacea - Description of lesion:
- Centrofacial persistent erythema.
- Telangiectasias.
- Inflammatory papules and papulopustules.
Rosacea - Epidemiology:
- MC in fair-skinned individuals of northern European descent.
- Can be seen in people with darker skin as well.
- Women > Men.
Rosacea epidemiology - Complicated disease with sebaceous gland hyperplasia and rhinophyma (sebaceous overgrowth causing deformity of the nose) develops more common in men or women?
Men.
Rosacea epidemiology - When does it begin?
Typically begins later than acne and reaches a peak in middle age - Possible overlapping.
EBD of rosacea:
Diagnosis is by clinical presentation.
EBD of rosacea - Histopath:
Varies according to the stage and variant of the disease and is often non specific.
VZV textbook presentation:
A rash over a single, unilateral dermatome.
- -> Lesion begin as closely grouped vesicles on an erythematous base.
- -> Over 2-3 days, the lesions become pustular and then crust over after 7-10days.
- -> Pain and paresthesias along the involved dermatome often precede the rash by a few days.
VZV description of the lesion:
Small, tightly grouped vesicles on an erythematous base, occurring in one dermatome.
–> Very early –> Lesions are large papules and then become vesicular, then pustular, and ultimately crusted.
VZV - Rash tends to occur where?
In the region of the primary VZV infection (chickenpox) was most severe.
VZV - MC dermatomes are:
- Trigeminal.
- T3-L2.
- -> Not uncommon to have a few vesicles in contiguous dermatomes.
VZV - New lesions may appear for?
Several days, occasionally for up to 7 days.
Shingles is caused by?
Reactivation of VZV in a dorsal root ganglion.
VZV complications - Herpes zoster ophthalmicus:
- Can occur when there is involvement of the V1.
2. HIGH RISK of corneal damage.
VZV complications - Ramsay-Hunt syndrome:
- Reactivation of VZV within the geniculate ganglion.
- Bell’s palsy (facial paralysis) + ear pain.
- Vesicles can often be seen in the ear canal.
- Vestibular and hearing disturbances (vertigo and hearing loss or tinnitus) are frequently reported.
EBD of shingles:
Clinically, without additional tests.
EBD of shingles - Detection of virus:
- Rapid by immunofluorescence.
2. Bedside Tzanck smear of material scraped from a fresh vesicle –> Cannot distinguish between VZV/HSV.
EBD of shingles - Gold standard:
Viral cultures.
Bullous impetigo - Textbook presentation:
Most commonly seen in children, bullous impetigo presents as flaccid, transparent bullae in the intertriginous areas. Blisters rupture easily and leave a rim of scale and a shallow moist erosion.
Bullous impetigo - Description of the lesion:
Flaccid bullae on normal skin.
Bullous impetigo - Location of the lesion:
- On grossly INTACT skin as a result of local toxin production.
- Lesions most commonly develop on moist, intertriginous skin.
Bullous impetigo - Causative agent:
S.aureus.
Bullous impetigo - Mechanism of lesion:
Blistering is caused by the production of exfoliatin or epidermolytic toxins.
EBD of bullous impetigo:
- Clinical diagnosis.
2. Culture of blister fluid or the moist edge of a crusted plaque may be diagnostic.
Bullous arthropod bites - Textbook presentation:
This condition commonly presents as a cluster of tense blisters on exposed skin.
–> Blisters tends to be large (>1cm) and surrounding skin is normal.
Bullous arthropod bites - Description of the lesion:
Large, often tense blisters on normal skin.
Bullous arthropod bites - Character and location of the lesion:
- Lesions tend to develop in exposed areas of the skin, such as the extremities.
- Patient will otherwise appear well.
- Lesions are typically extraordinarily pruritic.
- Although the blisters arise from otherwise normal skin, surrounding inflammatory changes from rubbing and scratching are often present.
What are basically arthropod bite reactions?
Dermal HSR to antigens in the saliva of insects.
Common arthropod culprits?
Fleas and bedbugs.
EBD of bullous arthropod bites:
- Clinical diagnosis.
2. Histopath is supportive –> Edema, subepidermal blister, dermal inflammation with EOSINOPHILS.
Bullous pemphigoid - Textbook presentation:
Usually seen in elderly patients with the sudden onset of 1-2cm tense blisters and bright red, urticarial plaques.
–> Lesions often begin on the lower extremities and progress upward.
Bullous pemphigoid - Description of lesion:
Tense bullae arising on skin that may be normal, erythematous, or urticarial.
Bullous pemphigoid - Autoantibodies:
Components of the epidermal BM zone, thus triggering separation and blistering.
Bullous pemphigoid - Lesion heal?
Heal without scarring.
Bullous pemphigoid - Character and location of the lesion:
- Predilection of blisters for the extremities.
- Lesions range from asymptomatic to intensely pruritic.
- Mucosal surfaces are rarely involved.
EBD of bullous pemphigoid - Histopath:
Supportive information, demonstrating a subepidermal blister plane and accumulation of EOSINOPHILS.
EBD of bullous pemphigoid - Immunopath:
Confirms diagnosis by demonstrating linear deposits of IgG and C3 at the DERMAL-EPIDERMAL junction.
EBD of bullous pemphigoid - Circulating IgG?
In 70-80% of patients, circulating IgG that recognizes the identified antigens of the BM zone can be found.
Stevens-Johnson syndrome (SJS) - Textbook presentation:
Typically presents in a patient with fever, malaise, headache, and myalgias who is taking a potentially causative medication.
- -> After 1 week of symptoms –> MACULAR RASH develops on the CHEST + FACE.
- -> Lesions subsequently blister and then rapidly erode.
- -> Skin is excruciatingly tender!
SJS - Description of the lesion:
- Flaccid bullae and vesicles that develop centrally within pre-existing target lesion.
- Bullae rapidly erode, leaving red and raw skin.