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Core Knowledge NPLEX 2 > Dermatology > Flashcards

Dermatology Flashcards

1
Q

Acne Rosacea

Epidemiology

A

Found in all skin types but with the highest prevalence in fair-skinned individuals

30-50 years old; F>M

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2
Q

Acne Rosacea

Etiology

A

Inflammatory reaction of the pilosebaceous unit of the skin on the face

Hyperplasia of the sebaceous gland

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3
Q

Acne Rosacea

Pathophysiology

A

Unknown

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4
Q

Acne Rosacea

Clinical Features

A
  • Pustules and flushing with a burning sensation is common initially on the cheeks, forehead, nose and chin, causing a ruddy complexion. Worsened by alcohol, stress, eating spicy food, heat, cold, wind, sun
  • Flushing, non-transient erythema, and telangiectasia
  • Characterized by remissions and exacerbations
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5
Q

Acne Rosacea

Treatment

A
  • Trigger avoidance is key to long tern management
  • Avoid topical corticosteroids and make up
  • 1st line tx: oral tetracycline ( doxy) and topical Metronidazole gel, topical azelaic acid
  • oral retinoids, topical sulfur
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6
Q

Acne Vulgaris

Epidemiology and Etiology

A
  • Chronic inflammation of pilosebaceous gland
  • age of onset is puberty (9-11 years) that increases in severity in teenage years among men, severity decreases in adulthood
  • family history of severe, cystic acne
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7
Q

Acne Vulgaris

Clinical Features

A
  • Inflamed papules, pustules, nodules and cysts

Non-inflamed Comedones:

  • plugging of hair follicle, nodules and cysts
  • open comedone= blackhead
  • closed comedone= whitehead

Inflamed type:
- increased sebum production
bacterial lipase produces irritating fatty acids causing an inflammatory reaction

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8
Q

Acne Vulgaris

Treatment

A

Systemic Antibiotics:

  • mild acne: Clindamycin ( lincosamine antibiotic that inhibits protien synthesis)
  • Moderate acne: doxycyclin ( tetracycline that inhibits protien synthesis)
  • Severe acne: Isotretinoin ( retinoid that inhibits sebaceous gland function and regulates keratinization)

Hormonal therapy:
- oral contraceptives( reduce free testosterone levels in women)

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9
Q

Candidiasis

Etiology

A
  • many species of Candidia

- opportunistic infection with predisposing factors

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10
Q

Candidal Paronychia

A
  • painful red swelling of periungal skin ( toenail, fingernail)
  • Management: oral antifungals if topicals are not effective
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11
Q

Candidal intertrigo

A
  • erythematous rash in body folds
  • predisposing factors: obesity, diabetes, systemic antibiotics, immunosuppression, malignancy
  • KOH shows pseudohyphae and yeast
  • management: keep area dry, topical antifungals (terbinafine) until rash clears
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12
Q

Carbuncles

Etiology

A

most commonly caused by staphylococcus aureus

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13
Q

Carbuncles

Clinical Features

A
  • Abscess larger than a boil, may have multiple openings to drain pus onto the skin
  • Deep- seated abscess from multiple coalescing furuncles; mass may be deep enough so it cannot drain
  • red, irritatied, and may be painful when touched
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14
Q

Carbuncles

treatment

A

I&D to relieve pressure and pain

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15
Q

Cellulitis

Etiology

A
  • Group A strep, Staph A (large sized wounds)

- often occurs where ther is skin damage ( blisters, burns, bites, surgical wounds, injection sites)

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16
Q

Cellulitis

Clinical Features

A
  • Inflammation of the dermis and subcutaneous fat caused by bacterial infection
  • Involves lower dermis/ subQ fat
  • symptoms of erythema, warmth, swelling, and pain
  • borders are not elevated, poorly demarcated vesicles
  • the legs are the common cite of infection, regional lymphadenopathy is present
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17
Q

Cellulitis

Investigations

A

Clinical diagnosis usually

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18
Q

Cellulitis

Treatment

A
  • Antibiotic: Cephalexin as 1st line treat

- If patient is diabetic: prescribe trimethoprim-Sulfamethoxazole

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19
Q

Felon

Definition

A

Subcutaneous abcess in the fingertip that commonly occurs after severe paronchyia or puncture wounds into the pad of the digit

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20
Q

Felon

Treatment

A
  • elevation, warm compress

- Antibiotics, I&D

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21
Q

Folliculitis

Definition

A

Inflammation of the hair follicle due to superficial infection

22
Q

Folliculitis

Etiology

A
  • Normal non-pathogenic Bacteria

- Staph Aureus is most common

23
Q

Folliculitis

Clinical Features

A
  • lesion has a dome-shape pustule at the hair follicle where it will eventually rupture to form an small crust
24
Q

Folliculitis

Treatment

A

Topical antibacterials ( Mupirocin); antiseptic

25
Q

Furuncles

Etiology

A
  • most commonly causes by staph aureus resulting in painful and swollen area on the skin from the accumulation of pus and dead tissue
26
Q

Furuncles

Clinical features

A
  • AKA Boil
  • Deep folliculitis, infection of the hair follicle
  • Common sites are hair-bearing skin areas such as highs, neck, face, axillae, groin, buttocks
  • red, hot, tender and inflammatory nodules
  • a yellow or white point at center of the lump that can rupture and drain pus
27
Q

Furuncles

Treatment

A

Topical Antibiotics I&D

28
Q

Herpes Simplex

Clinical Presentation

A
  • Vesicles on an erythematous base on skin due to HSV

Transmitted through contact with erupted vesicles or through asymptomatic viral shedding

29
Q

Primary Herpes Simplex

A
  • Affects children and young adults
  • Malaise, high fever, regional lymphadenopathy
  • Antibody formation and latency of virus in the dorsal nerve root ganglion
30
Q

Secondary herpes simplex

A
  • recurrent form seen in adults, triggered by emotional stress, URI, fever, physical trauma
  • Tingling, Pruritus, pain
31
Q

HSV- 1

A
  • seen as a cold sore that are typically seen on the face, lips but not on mucous membranes
  • painful, small fluid-filled vesicles that burst leaving a yellowish crust which heals 12-21 days after outbreak
32
Q

Herpes simplex

Investigation

A

Tzanck Smear with Giemsa stain shows multi nucleated giant epithelial cells

33
Q

Herpes simplex

Treatment

A

Anti viral meds: Acyclovir or Valacyclovir

34
Q

Impetigo

A

Bacterial infection of the epidermis

most common bacterial skin infection and the third most common skin disease among children

35
Q

Impetigo Vulgaris

Etiology

A
  • Group A streptococcus, Staph Aureus

- After preschool/ young adults- usu due to poor hygiene

36
Q

Impetigo Vulgaris

Clinical Features

A
  • Vesicle or pustule that ruptures and becomes yellow “honey crusted’ exudate over erosion that is surrounded by erythema.
  • Common sites are face, arms, legs and buttocks
  • rapid spread follows by contiguous extension or to distal areas through inoculation of other wounds from scratching
37
Q

Impetigo Vulgaris

Investigations

A

Gram stain and culture of lesion fluid

38
Q

Impetigo Vulgaris

Treatment

A
  • Saline compress and topical antiseptic soak to remove crusts
  • Topical antibacterial (e.g mupirocin)
  • Systemic Antibiotics ( cephalexin)
39
Q

Bullous Impetigo

Etiology

A

Staph Aureus

40
Q

Bullous Impetigo

Epidemiology

A

Neonates and older children

41
Q

Bullous Impetigo

Clinical Features

A
  • small, or large, superficial fragile, thin-walled bullae
  • appear quickly and spontaneously rupture and drain a clear yellow turbid fluid with no surrounding erythema
  • Lesions spread usually on the face, trunk, extremities, butt and groin
42
Q

Bullous Impetigo

investigation

A

Gram Stain and Culture lesion fluid

43
Q

Bullous Impetigo

Treatment

A
  • topical antibacterial ( mupirocin)

Oral antibiotics

44
Q

Molluscum Contagiosum

Etiology

A
  • Poxvirus (DNA Virus)- molluscum contagiosum virus
  • Can be transmitted sexually, direct contact or auto- inoculation by scratching the infective viral particles out of the crater
  • Common in children and sexually active young adults, common in AIDs
45
Q

Molluscum Contagiosum

Clinical presentation

A
  • Dome-shaped lesions with central crater containing white papule. Depression contains Viral Molluscum Contagiosum virus
  • Common sites: eyelids, beard (likely spread by shaving), neck, axillae, trunk, perineum, buttocks
46
Q

Molluscum Contagiosum

Investigation

A
  • Non required, however can biopsy to confirm diagnosis
47
Q

Molluscum Contagiosum

Treatment

A
  • cryothperapy
  • curettage
  • immunocompetent, there can be spontaneous remission in 6-9 months
48
Q

Necrotizing Fascitis

Definition

A
  • rapidly progrssive inflammatory infection of the fascia, with secondary necrosis of the subcutaneous tissue
  • infection spread rapidly enough that it is limb and life threatening!
49
Q

Necrotizing Fascitis

Etiology

A
  • Numerous causes ( Surgical proceedures, insect bite, intramuscular injections, local ischemia)
  • Type 1 ( polymicrobial, areobes and anaerobes- e.g aures, bacteroides, Enterobacteraceae)
  • Type 2: Monomicrobial, usually beta- helolytic strep
50
Q

Necrotizing Fascitis

clinical features

A
  • Pain out of propotion to clinical findings that reaches past the border of erythema
  • Crepitus can be heard as anaerobes produce gas
  • Edema
  • Infection spread rapidly
  • May appear well initially, but will become very sick later
  • appearance of skin becomes black and blue( secondary to thrombosis and necrosis)
  • Gangrene
51
Q

Necrotizing Fascitis

Investigations

A
  • diagnosed clinically - begin treatment right away, do not wait for investigation
  • blood and tissue culture and sensitivity (C&S)
    Plain film X-ray ( soft tissue gas may be visualized)
    -Extreme elevation in CK which means a late sign of myonecrosis
52
Q

Necrotizing Fascitis

Treatment

A
  • IV antibiotics with penicillin clindamycin

- Emergency surgical debridement to confirm diagnosis and remove necrotic treatment

Core Knowledge NPLEX 2 (28 decks)

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