Rosacea & Insects Flashcards

(46 cards)

1
Q

Driving Factors of Acne Vulgaris

A

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

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2
Q

Microcomedo

A

Considered the precursor for the clinical lesions of acne vulgaris (First stage of acne)

Increased sebum production
Follicular hyperkeratinization

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3
Q

Closed Comedome - Whitehead

A

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

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4
Q

Open Comedome - Blackhead

A

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

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5
Q

Inflammatory Papule (Pimple)

A

Follicular rupture and presence of bacteria contributes to the development of inflammatory lesions

Bacterial byproduct causes inflammation and infection in the surrounding skin

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6
Q

Inflammatory Pustule

A

Immune system sends white blood cells to fight infection and creates pus in the pore

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7
Q

Nodule or Cyst

A

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.

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8
Q

Contributing Factors to Acne Vulgaris

A

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

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9
Q

Topical Retinoids

A

Beneficial for both comedonal and inflammatory lesions

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10
Q

Topical Antimicrobial Therapies

A

Beneficial for inflammatory lesions

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11
Q

Oral Antibiotics

A

For severe inflammatory acne

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12
Q

Benzoyl Peroxide

A

Decreases the emergence of antibiotic resistant bacteria

Often used in conjunction with other therapies (topical retinoids, antimicrobial therapies, oral antibiotics)

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13
Q

Treatment of Comedonal (noninflammatory) Acne

A

Topical Retinoid - Tretinoin

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14
Q

Treatment of Mild Papulopustular and Mixed Acne

A

Benzoyl peroxide +/- topical antibiotic (erythromycin, clindamycin) and topical retinoid

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15
Q

Treatment of Moderate Papulopustular and Mixed Acne

A

Benzoyl peroxide + topical retinoid + oral antibiotic (tetracycline class)

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16
Q

Treatment of Severe Acne

A

Retinoid + oral abx (tetracycline class) + benzoyl peroxide

OR

Oral isotretinoin monotherapy

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17
Q

Treatment of Acne during Pregnancy

A

Some acne medications are teratogenic

Retinoids are super contraindicated in pregnancy

Safe regimen for pregnancy: oral erythromycin, topical clindamycin, topical azelaic acid

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18
Q

Acne Rosacea

A

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
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19
Q

Pathogenesis of Acne Rosacea

A

Not well understood

  • Abnormalities in immunity
  • UV damage
  • Vascular dysfunction
  • Inflammatory reactions to cutaneous microorganisms
20
Q

Presentation of Acne Rosacea

A

Erythema of central face, persisting for months or more

Nose, cheeks, chin, and forehead are commonly affected

Four subtypes:

  • Erythematotelangiectatic
  • Papulopustular
  • Phymatous
  • Ocular
21
Q

Erythematotelangiectatic Rosacea

A

Chronic redness of central face

Flushing (wet or dry)

Skin sensitivity

Dry appearance

Telangiectasias

22
Q

Papulopustular Rosacea

A

Papules and pustules of central face

Inflammation can be confluent

NO comedones

23
Q

Phymatous Rosacea

A

Tissue hypertrophy causing irregular contours

Mostly nose but can involve cheeks, forehead and chin

Mostly affects men

24
Q

Ocular Rosacea

A

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.

25
Treatment of Erythematotelangiectatic Rosacea
First line: behavior changes - avoid trigger - sun protection - gentle skin care Second line - laser and pulsed light therapy - topical brimonodine
26
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
27
Treatment of Phymatous Rosacea
Early Disease: Isotretinoin Advanced Disease: surgical debulking and/or laser ablation
28
Treatment of Ocular Rosacea
Refer to Ophthalmologist Topical abx, cyclosporin (immunosuppressive drug), oral abx
29
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
30
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
31
Severe envenomations require monitoring for...
``` •Respiratory compromise –Suctioning of oral secretions –Endotracheal intubation •Myocardial infarction •Hyperthermia •Rhabdomyolysis ```
32
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
33
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
34
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
35
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
36
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
37
Vitiligo
an acquired skin depigmentation via an autoimmune process directed against melanocytes
38
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 ```
39
Clinical Presentation of Vitiligo
presents as milk-white macules with homogenous depigmentation and well-defined borders * Slowly progressive * Spontaneous repigmentationin 10-20%
40
Diagnosis of VItiligo
* Consider screening for other autoimmune diseases | * Skin biopsy will show epidermis devoid of melanocytes
41
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
42
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
43
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
44
Diagnosis of Hidradenitis Suppurativa
Based on lesion, location, chronicity, and relapse
45
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
46
Complications of Hidradenitis Suppurativa
* Fistulae * Strictures and contractures * Lymphatic obstruction * Infectious complications * Squamous cell cancer * Malaise, depression, suicide