Rosacea & Insects Flashcards
Driving Factors of Acne Vulgaris
Follicular hyperkeratinization (occurs when the cells of the follicle become cohesive and do not shed normally onto the skin’s surface)
Increased sebum production
Cutibacterium acne within the follicle
Inflammation
Microcomedo
Considered the precursor for the clinical lesions of acne vulgaris (First stage of acne)
Increased sebum production
Follicular hyperkeratinization
Closed Comedome - Whitehead
Accumulation of sebum and keratinous material converts a microcomedo into a closed comedo
Small or no opening of the follicle to the skin
Build-up of sebaceous material
Inflammation surrounding the follicle
Open Comedome - Blackhead
The follicular orifice is opened with continued distension, forming an open comedo
Opening of pore dilates
Build-up of sebaceous material
Inflammation surrounding the follicle
Inflammatory Papule (Pimple)
Follicular rupture and presence of bacteria contributes to the development of inflammatory lesions
Bacterial byproduct causes inflammation and infection in the surrounding skin
Inflammatory Pustule
Immune system sends white blood cells to fight infection and creates pus in the pore
Nodule or Cyst
Follicle wall bursts and a capsule is created via enzymes secreted by white blood cells to contain infection.
Marked inflammation is present in addition to erythema and tenderness.
Contributing Factors to Acne Vulgaris
Androgens (sex hormones) stimulate the growth and secretory function of sebaceous glands
Mechanical trauma can rupture comedos, causing inflammatory lesions
Stress seams to have an effect on severity
Topical Retinoids
Beneficial for both comedonal and inflammatory lesions
Topical Antimicrobial Therapies
Beneficial for inflammatory lesions
Oral Antibiotics
For severe inflammatory acne
Benzoyl Peroxide
Decreases the emergence of antibiotic resistant bacteria
Often used in conjunction with other therapies (topical retinoids, antimicrobial therapies, oral antibiotics)
Treatment of Comedonal (noninflammatory) Acne
Topical Retinoid - Tretinoin
Treatment of Mild Papulopustular and Mixed Acne
Benzoyl peroxide +/- topical antibiotic (erythromycin, clindamycin) and topical retinoid
Treatment of Moderate Papulopustular and Mixed Acne
Benzoyl peroxide + topical retinoid + oral antibiotic (tetracycline class)
Treatment of Severe Acne
Retinoid + oral abx (tetracycline class) + benzoyl peroxide
OR
Oral isotretinoin monotherapy
Treatment of Acne during Pregnancy
Some acne medications are teratogenic
Retinoids are super contraindicated in pregnancy
Safe regimen for pregnancy: oral erythromycin, topical clindamycin, topical azelaic acid
Acne Rosacea
Chronic skin disorder of the central face
- Most prevalent in fair-skinned individuals
- Female > Males
- Usually emerges in 30s
- Estimated 1-10% in white population
Pathogenesis of Acne Rosacea
Not well understood
- Abnormalities in immunity
- UV damage
- Vascular dysfunction
- Inflammatory reactions to cutaneous microorganisms
Presentation of Acne Rosacea
Erythema of central face, persisting for months or more
Nose, cheeks, chin, and forehead are commonly affected
Four subtypes:
- Erythematotelangiectatic
- Papulopustular
- Phymatous
- Ocular
Erythematotelangiectatic Rosacea
Chronic redness of central face
Flushing (wet or dry)
Skin sensitivity
Dry appearance
Telangiectasias
Papulopustular Rosacea
Papules and pustules of central face
Inflammation can be confluent
NO comedones
Phymatous Rosacea
Tissue hypertrophy causing irregular contours
Mostly nose but can involve cheeks, forehead and chin
Mostly affects men
Ocular Rosacea
Often coincides with other types of rosaceas
> 50% of those with other types
Children and adults
May precede, coincide, or follow
Dry eyes, pain, itching, blurry vision, photosensitivity, blepharitis (An inflammation of the eyelid that affects the eyelashes or tear production), keratitis (Inflammation of the clear tissue on the front of the eye (cornea).), conjunctivitis, stye.
Treatment of Erythematotelangiectatic Rosacea
First line: behavior changes
- avoid trigger
- sun protection
- gentle skin care
Second line
- laser and pulsed light therapy
- topical brimonodine
Treatment of Papulopustular Rosacea
Mild-Moderate
1st Line topicals: (Metronidazole, Azelaic acid)
2nd Line topicals: ivermectin and sulfacetamide-sulfur
Moderate-Severe or failed topical tx
Oral abx:
- Tetracyclines: doxycycline, minocycline, tetracycline
- Macrolides: clarithromycin, azithromycin, erythromycin
Treatment of Phymatous Rosacea
Early Disease: Isotretinoin
Advanced Disease: surgical debulking and/or laser ablation
Treatment of Ocular Rosacea
Refer to Ophthalmologist
Topical abx, cyclosporin (immunosuppressive drug), oral abx
Degree of Envenomation
Grade 1: Local pain and paresthesias at the sting
Grade 2: Local symptoms as well as remote pain and paresthesias
Grade 3: EITHER cranial nerve OR somatic skeletal neuromuscular dysfunction
Grade 4: Both cranial nerve dysfunction AND somatic skeletal neuromuscular dysfunction
Characteristic Signs of Envenomation
Local pain exacerbated by tapping near the sting site (tap sign)
Cranial nerve dysfunction •Hypersalivation •Abnormal eye movements •Blurred vision •Slurred speach •Tongue fasciculations
Somatic skeletal neuromuscular dysfunction
–Fasciculations
–Shaking and jerking of the extremities
–Opisthotonos (arching of the back)
–Emprosthotonos (tetanic forward flexion of the body)
–Fever up to 104°F from excess motor activity
Severe envenomations require monitoring for…
•Respiratory compromise –Suctioning of oral secretions –Endotracheal intubation •Myocardial infarction •Hyperthermia •Rhabdomyolysis
Common Clinical Presentation of Bee Stings
Commonly result in a local reaction
Swelling, erythema lasting a few hours to 1-2 days
Treat with cold compress
Large Local Reaction (LLR)
Bee Stings will cause a different response about 10% of the time
–Exaggerated erythema and swelling
–Gradually enlarges over 1-2 days
–Resolves in 5-10 days
–Cold compress, prednisone, antihistamines, NSAIDs
Widow Bites
Cause a small local reaction
- Often cause few symptoms because no venom injected
- Blanched circular patch, surrounding red perimeter and a central punctum
•Venom causes catecholamine release
–Intermittant radiating pain
–Abdominal/chest/back pain and muscle spasm
–Local/regional diaphoresis, HA, N/V
Common Recluse Bites
Often painless initially
•Progress to severe pain in 2-8 hours
•Usually a red plaque or papule with central pallor
•May see two small puncture marks within the erythema
•Vesiculation can occur
•Resolves in a week
Rare Recluse Bites
severe ulcerative necrosis can occur
•Dark, depressed center develops after 1-2 days
- Systemic symptoms
•N/V, h/a, fever, chills
•Rarely, renal failure, hemolytic anemia, hypotension, DIC, rhabdomyolysis can occur
Vitiligo
an acquired skin depigmentation via an autoimmune process directed against melanocytes
Epidemiology of Vitiligo
–1% of worldwide population –Affects males and females equally –Onset peaks in 2nd/3rd decades –Subtype (generalized vitiligo) can be associated with other autoimmune disease in 20-30% of patients –Family history in 20-30% of patients
Clinical Presentation of Vitiligo
presents as milk-white macules with homogenous depigmentation and well-defined borders
- Slowly progressive
- Spontaneous repigmentationin 10-20%
Diagnosis of VItiligo
- Consider screening for other autoimmune diseases
* Skin biopsy will show epidermis devoid of melanocytes
Treatment of Vitiligo
Treatment focuses on prevention and repigmentation therapy
- Treatment
- Topical and systemic corticosteroids (first line)
- Calcineurin inhibitors
- Narrowband ultraviolet B phototherapy (extensive disease)
- Skin grafts
- Sunscreen
- Makeup (Covermark, Dermablend)
- Ask about psychological distress
Hidradenitis Suppurativa (Acne Inversa)
Chronic inflammatory skin disorder involving the hair follicle
Results from the cycle of follicular occlusion, rupture, and the associated immune response
- Occurs in the axillary, inguinal and anogenital regions
- 1-4% prevalence
- Female > male; no racial predilection
- Avg age of onset = 23 –Rarely before puberty or after menopause
Other factors: genetics, mechanical stress, obesity, smoking, diet
Progression of Hidradenitis Suppurativa
Begins with a single, deep-seated, inflammatory nodule
- More nodules form as disease progresses
- May form an abscess that opens to the skin
- Purulent drainage occurs if ruptured
As the disease progresses:
- Sinus tracts
- Comedones
- Scarring
Diagnosis of Hidradenitis Suppurativa
Based on lesion, location, chronicity, and relapse
Treatment of Hidradenitis Suppurativa
•Local tx: –topical clindamycin –Intralesionalcorticosteroids •Systemic antibiotics –Doxycycline or minocycline •Anti-androgenic agents •Surgery –Punch debridement (nodules) or wide excision (scarring) •Severe, refractory cases –TNF inhibitors –Oral retinoids
Used in conjunction with lifestyle modifications
Complications of Hidradenitis Suppurativa
- Fistulae
- Strictures and contractures
- Lymphatic obstruction
- Infectious complications
- Squamous cell cancer
- Malaise, depression, suicide
