derm Flashcards
Psoriasis
- Immune-mediated disease characterized by inflammation caused by dysfunction of the immune system
- Overactive immune system speeds up skin cell growth
- Normal cells shed in about 28 days; psoriatic cells shed in about 4 days
- Plaques build up, causing burning and itching
- Most commonly found on the elbows, knees, scalp, and nails
- 1 in 3 people with psoriasis will also have Psoriatic Arthritis
Psoriasis: A Papulosquamous Disease
*Raised, pink, scaly, silvery plaques
Extensor surfaces of elbows, knees, and scalp but can appear anywhere
Genetic predisposition
Can occur in an area of previous trauma or in children with strep pharyngitis
Variants: Vulgaris*, Pustular, Guttate (spares the palms and soles)
Clinical Diagnosis: Biopsy if unsure
psoriasis tx
Mild: Topical steroids
Moderate: Add UVB, PUVA, de-scalers such as Retin A, Calcipotriene
Severe: Methotrexate, Biologics
Important: Look for signs of Psoriatic Arthritis and refer to a rheumatologist accordingly
Lyme Disease - Tick Bites; MC clinical marker?, systemic effects?
Vector: Ixodes tick (aka deer tick), primary vector for Borrelia burgdorferi
Ixodes nymphs: Active in spring, cause most Lyme cases due to their small size/undetectable
Geography: Most cases on the East Coast
Erythema Migrans: Most common clinical marker
- Targetoid rash usually occurs 7-10 days post-bite but can happen earlier
- Rash alone does not confirm Lyme Disease; it’s a hypersensitivity reaction
Systemic Effects: Dermatologic, Rheumatic, Neurologic, and Cardiac manifestations
Signs and Symptoms lyme
Headaches
Erythema migrans on other parts of the body
Facial palsy
Arthritis
Joint, muscle, tendon, nerve, and bone pain
Inflammation of the brain and spinal cord
Numbness/tingling in hands and feet
Laboratory Testing
lyme
2-Step Process:
- Step 1: EIA (enzyme immunoassay) or immunofluorescence assay
- Step 2: If positive, confirm with Western immunoblot assay
- Timing: Antibodies take weeks to develop, so do not test too early!
Treatment:
- In endemic areas, tick bites are often treated immediately with Doxycycline 200 mg QD
- Late-stage Lyme Disease: Treated with longer courses of Doxycycline or other antibiotics
lyme prevention
Avoid exposure (stay on trails, avoid high grass)
Use insect repellents (DEET, permethrin)
Perform body checks after outdoor activities
Dry clothing in a hot dryer
Bullous Pemphigoid
Autoimmune blistering eruption
Affects the elderly (mean age 64-80)
Associated with neurological diseases (dementia, Parkinson’s, epilepsy)
Cause: Autoantibodies target the basement membrane zone (BMZ)
BMZ is important in attaching the epidermis to the dermis
Antibodies create a space, leading to tense blisters
Early Signs: Can present with pruritic urticarial rash before bullae form
Clinical Features bullous pemphigoid
Blisters: Bilateral, symmetric, on the trunk and proximal flexural extremities
Biopsy Site: Edge of an intact bullae
Direct Immunofluorescence (DIF): Normal skin + edge of blister shows IgG deposits along BMZ
Differential: Other conditions can mimic it, requiring histopathology and DIF
Management bullous pemphigoid
Chronic, relapsing disease (can resolve spontaneously)
Tense bullae can be drained with a sterile needle
Treatment:
- Mild: Topical steroids, oral tetracyclines
- Moderate-Severe: Oral steroids, methotrexate
remember: TENSE Blisters… YOU SEE THEM!
Elderly
Associated Conditions-Parkinson’s, Dementia, Epilepsy
Look for words… Auto antibodies… Basement membrane zone (BMZ)
Pemphigus Vulgaris
Rare blistering disease affecting skin and mucous membranes
Age: Older patients (38-72 years)
Associated with: Autoimmune diseases (Thyroid Disease, Myasthenia Gravis, Sjögren’s, RA)
Blisters: Often present as crusted erosions or flaccid blisters
Oral involvement: Some cases only affect oral mucosa
Common sites: Head, upper trunk, intertriginous zones
Positive Nikolsky Sign: Skin shears off when rubbed
“Pemphi-gus + Nikolsky = bad breath” (oral involvement, positive Nikolsky sign)
dx and tx Pemphigus Vulgaris
Diagnosis:
- 2 Biopsies: Edge of blister + DIF (normal skin + blister edge)
Treatment:
- Mild: Topical steroids (gel-based for mucosal lesions)
- Moderate-Severe: Oral steroids (short or long-term), Rituximab, methotrexate
- Watch for infection!
Pityriasis Rosea: summary, features, dx, tx
Usually asymptomatic
Preceding illness possible
Guttate erythematous papules with trailing scale
Hallmark Features:
Herald Patch: Large oval plaque with collarette scale
“Christmas tree” distribution on back
Diagnosis: Clinical (take a thorough history!)
Treatment:
- Self-limiting (weeks to months); pt reassurance
- Topical steroids for itching
- UVB phototherapy for persistent cases
Acanthosis Nigricans: summary, types, risk groups, appearance, workup,
Common manifestation of insulin resistance (secondary to diabetes, obesity)
Types: Benign, obesity-associated, malignant, drug-induced
Risk Groups: Native American, African, Hispanic populations
Appearance: Thick, VELVETY brown/black plaques (neck, axilla, groin)
Workup:
- Blood tests (A1C, lipid panels, fasting glucose)
- BMI and blood pressure
- bx if unclear diagnosis
Molluscum Contagiosum: summary, causative agent, tx
Benign poxvirus infection
Highly contagious!
Appearance: White, pink, or flesh-colored lesions with central umbilication
- Itchy, red sore and swollen
- lesions appear anywhere on the body
Treatment:
- Cryotherapy, Cantharone, Podophyllin, acids, Retin A, Imiquimod
Herpes Zoster (Shingles): definition, triggers, distribution, hutchinson’s sign and ramsey hunt syndrome
Reactivation of varicella-zoster virus (chickenpox virus)
Triggers: Stress, illness, immunocompromise
Distribution: Follows dermatomes, rarely crosses midline
Hutchinson’s Sign: Vesicles on tip or side of nose (indicates eye involvement)
Ramsay Hunt Syndrome: Facial palsy with ear/TM involvement, possibly with tinnitus, vertigo, deafness
Diagnosis & Treatment herpes zoster
Diagnosis: Usually clinical, but PCR preferred if confirmation needed
- Tzank Smear- not diagnostic can’t diff between herpes
- Culture, and PCR testing more specific for Zoster (PCR Preferred)
Treatment:
- Famcyclovir 500mg po q8 hrs x 7 days
- Acyclovir 800mg q4h x 7-10 days
- Valacyclovir 1g TID x 7 days
- Pain management
- watch for Post herpetic neuralgia
- Shingrix vaccine for prevention
Atopic Dermatitis (Eczema)
- Chronic, pruritic, inflammatory skin condition
- Triad: Often associated with asthma and allergic rhinitis
- Genetic, environmental, and immunologic factors contribute
- Key Protein Mutation: Filaggrin mutation increases risk
- Immune Dysregulation: Plays a role in pathogenesis
atopic dermatitic presentation, distribution, and dx
Features:
* Ill-defined plaques with scale
* Yellow crusting
* Sparing of the nasal tip is common
* Distribution varies- Babies- extensor surfaces. Children and adults- flexoral
Diagnosis:
- Clinical, but biopsy may be needed
- Biopsy Findings: Spongiosis, inflammatory cell infiltration in the dermis
Treatment atopic dermatitis
- First-Line: Topicals that repair the skin barrier
- Steroids: Key treatment but avoid overuse, avoid oral
- Topical Calcineurin Inhibitors: Tacrolimus, Pimecrolimus (used when steroids are insufficient)
- Managing Infection: Bleach baths to reduce bacterial colonization
- Severe Cases: Monoclonal antibody therapy (Dupilumab/Dupixent)
- Avoid Oral Steroids: Due to risk of rebound flares
- Phototherapy: Narrowband UVB for refractory cases
Contact Dermatitis allergic vs irritant
Allergic Contact Dermatitis (ACD): Delayed hypersensitivity reaction (Type IV), requires sensitization
Irritant Contact Dermatitis (ICD): Non-immunologic; direct chemical damage to skin
allergic contact dermatitis: examples, sign, presentation dx, tx
Examples: Poison ivy, nickel allergy
Hallmark Sign: Linear rash (e.g., poison ivy)
Presentation: Pruritic vesicles, scaly plaques
Diagnosis: Clinical; confirmed with patch testing
Treatment:
Mild: Topical steroids
Severe/Widespread: Short course of systemic steroids
irritant contact dermatitis: examples, patho, tx
- Most common type
- Causes: Chemicals, detergents, prolonged exposure to water
- Pathophysiology: Direct damage to keratinocytes
- Management: STOP the offending irritant, skin barrier repair (moisturizers, emollients)
Normal Nevi vs. Melanoma
Normal Nevi (Moles):
* Benign melanocytic growths
* Usually <6mm
* Homogenous color
* Symmetrical shape
* between 10-40 on a person’s body
* Well-defined borders
* Growth: Typically grows with the individual!
* MC in light skinned ppl and sun exposure
* Suspicion for malignancy? Biopsy!
Melanoma:
* Most deadly skin cancer
* 30% arise from existing nevi
* some pts will complain of change in normal moles; most are found on routine skin exams
* Risk Factors: Sun exposure, fair skin, family history
* MC location: trunk and legs
melanoma types
- Superficial melanomas are mostly found on sun exposed areas-
- Types: Superficial spreading, nodular, lentigo maligna, acral lentiginous
stages of melanoma
melanoma dx and managment
- Biopsy: Punch biopsy preferred
- Prognosis: Depth is key (>0.8mm → Sentinel Node Biopsy indicated)
- Regular Monitoring: High risk of recurrence
Types of Allergic Reactions
Type I and IV - T helper cells *
Type I or anaphylactic reactions
Type II or cytotoxic reactions
Type III or immunocomplex reactions
Type IV or cell-mediated reactions
Type I allergic rxn
Type I (Anaphylactic) – IgE Mediated
- Most severe – can be life-threatening
- Examples: mediated by proteins called IgE antibodies produced by the immune system. They are produced in response to the allergens such as pollen, animal dander, dust mites, or even certain foods. This causes the release of histamine and other chemicals causing inflammation and swelling.
- bronchialasthma, allergic rhinitis, allergicdermatitis,food allergies,allergic conjunctivitis(eye inflammation) and
anaphylaxis(allergicshock).
allergic rhinitis
allergicdermatitis,
food allergies,
allergic conjunctivitis(eye inflammation) and
anaphylaxis(allergicshock).
- Treatment: Epinephrine (IM), antihistamines, steroids
Type II allergic rxn
Type II (Cytotoxic) – IgG/IgM Mediated
- Mechanism: Antibodies attack own cells (complement activation)
- mediated by proteins called IgG and IgM antibodies. The antibodies damage cells by activating a component of immunity called the complement system. Can be seen in certain conditions like
- Examples: autoimmune hemolytic anemia, immune thrombocytopenia, autoimmune neutropenia
Type III allergic rxn
Type III (Immune Complex-Mediated)
- Formation of antigen-antibody COMPLEXES
- Also mediated by proteins i.e. IgM and IgG antibodies. Antibodies react with the allergen to form immunocomplexes (antigen-antibody complexes). These complexes are responsible for the reaction
- Examples: Lupus, serum sickness, drug reactions
Type IV allergic rxn
Type IV (Delayed Hypersensitivity)
- T-cell mediated, takes 24-72 hrs
- occur after at least 24 hours of exposure to the allergen. These reactions typically take 48-72 hours or longer to appear after contact with the allergen. Certain skin sensitivity reactions (esp. to metals) may also belong to this type.
- Examples: Tuberculin skin test, contact dermatitis (poison ivy), chronic inflammation
