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Skin/Musculoskeletal > SM: Week 3 > Flashcards

SM: Week 3 Flashcards

1
Q

What is the appearance, duration, and histopathology of urticaria?

A
  • Appearance: pruritic, transient raised red or white wheals of various sizes
  • Duration: persist for less than 24 hours
  • Histopathology: dermal edema
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2
Q

How is urticaria treated?

A
  • Acute urticaria is treated with a series of antihistamines, starting with non-sedating H1-blockers
  • Chronic urticaria improves slowly over 1-2 years, cause is undetermined in 75-80% of cases; frustrating for patients
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3
Q

What is the general progression of antihistamine treatment for urticaria?

A
  • First choice: second generation, non-sedating H1-blockers
  • Second choice: add first generation, sedating H1-blockers
  • Third choice: add H2 blocker
  • Fourth choice: add H1 and H2 blocker combo
  • Fifth choice: add leukotriene modifier
  • Sixth choice: add oral corticosteroid
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4
Q

Angioedema has what as its characteristic hallmark?

A

It appears as intense swelling of the dermis and subcutaneous layers and can cause pain and burning.

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5
Q

Where are angioedemas typically located/.

A

Lip, eye, groin, palms/soles

Laryngeal involvement = EMERGENCY!!!

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6
Q

What causes Urticaria and Angioedema to form?

A

Thought to be either immune or non-immune related.

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7
Q

What are some immune related causes of urticaria and angioedema?

A 
- Type IgE mediated (urticaria)
     o Foods such as shellfish, fish, peanuts, eggs, soy, milk, wheat, tree nuts
     o Latex
     o Insect stings
     o Medications
- Auto-immune
     o Hashimoto's immune thyroiditis
     o SLE
     o Vasiculitis 
- Infectious
     o Viral (cytomegalovirus, EBV, HIV, Hep A,B,C)
     o Parasitic, Fungal, Bacterial
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8
Q

What are some non-immune related causes of urticaria and angioedema?

A
  • Physical Urticarias:
    o Cholinergic (sweating vs. heat) - small papular urticaria after exercise, sweating, or hot showers
    o Cold - hives begin during cold exposure, maximal upon re-warming
    o Dermaographism
  • Direct mast-cell degranulation:
    o Narcotics, aspirin, NSAIDs, dextran, ACE inhibitor angioedema, vancomycin (“red man” syndrome)
  • Foods containing histamine:
    o Strawberries, tomatoes, shrimp, lobster, cheese, spinach, eggplant
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9
Q

What are some laboratory tests that can be ordered to evaluate urticaria and angioedema?

A
  • CBC, ESR, TSH, basic chemistry panel (BUN, creatinine, electrolytes)
  • throat culture, monospot (if Hx warrants)
  • anti-thyroid Ab titer and FANA (women)
  • punch biopsy
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10
Q

What is the treatment of urticaria and angioedema?

A

Generally, avoid the allergen, extremes of hot/cold, exercise, and alcohol (vasodilation, flares, hives).

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11
Q

What is the appearance of Erythema Multiforme (EM) and which dermal layers does it affect?

A

Erythema multiforme appears as multiple circular papules with an erythematic periphery, classic “target” lesion, reaction follows blood vessels in dermis
- affects the epidermis and dermis

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12
Q

What is the etiology of EM?

A
  • Drugs: sulfonamides, phenytoin, barbituates, phenylbutazone, penicillin, allopurinol
  • Infection: herpes simplex virus (HSV), mycoplasma pneumonia
  • Idiopathic: more than 50% of cases unknown cause
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13
Q

What are the different forms of EM?

A
  • EM Minor: <10% epidermal detachment

o Toxic Epidermal Necrolysis (TEN): 2+ MM, 30% epidermal detachment

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14
Q

What is the appearance and etiology of SJS?

A
  • Appearance: skin tenderness, erythema of skin and mucosa followed by extensive cutaneous and mucosa epidermal necrosis and sloughing
  • Etiology: mucocutaneous drug-induced, or idiopathic reaction patterns
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15
Q

What are some risk factors associated with SJS/TEN?

A
  • SLE, HLA-B12 (human leukocyte antigen - immune response), HIV
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16
Q

How is SJS/TEN treated?

A
  • Early diagnosis and withdrawal from Rx
  • Management of IV fluids/electrolytes
  • Systemic glucocorticoids
  • High dose Ig’s for TEN
  • Debride only clearly necrotic skin
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17
Q

What is the appearance, location, and treatment of fixed drug eruptions?

A
  • Appearance: localized, sharply demarcated erythematous patch that can itch, burn, or be asymptomatic; hyperpigmented, will occur in same location if re-challenged
  • Location: predisposition for face and genitals
  • Treatment: eliminate offending drug
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18
Q

What is the appearance of Panniculitis?

A

Panniculitis appears as an erythematous or violaceous (purple) nodule in the SQ fat and is either lobular or septal depending on where disease process begins. It also has SQ inflammation.

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19
Q

What is the appearance and location of Panniculitis Erythema Nodosum?

A
  • Appearance: erythematous tender nodules, septal panniculitis
  • Location: anterior shins
  • Symptoms: painful, very tender nodules accompanied by malaise, fever, and arthralgia (often in ankle joint)
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20
Q

What are some risk factors for developing Panniculitis Erythema Nodosum?

A
  • Infection (strep, TB, fungal)
  • Medications (Oral contraceptive pill - OPC, fungal, NSAIDs)
  • Autoimmune (IBD, Sarcoid)
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21
Q

How is Panniculitis Erythema Nodosum treated?

A
  • Rest, ice, pain control, removal of offending drug, treatment of infection
  • Spontaneous resolution seen within 6 weeks; lesions do not break down or ulcerate
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22
Q

What is the appearance of Panniculitis Erythema Induratum?

A
  • Appearance: tender red nodules, lobular panniculitis and vasiculitis; chronic, recurrent SQ nodules and plaques with ulceration
  • Location: posterior legs (more so than anterior)
  • Associated with TB infections
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23
Q

What is the appearance of Herpes Simplex 1 & 2 and what virus causes the diseases?

A

Both types present as groups of vesicles on a red base which rapidly becomes purulent and crusted.
- Epstein-Barr Virus (EBV)

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24
Q

What are some characteristics of HSV 1?

  • how it’s transmitted, recurrence of infection, seropositivity
A
  • Transmitted during childhood via nonsexual contact
  • 90% of recurrent HSV 1 causes orofacial lesions called herpes labialis
  • Seropositivity rate = 85%
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25
Q

What are some characteristics of HSV 2?

A
  • STD of adults involving the genital area (sometimes oral as well)
  • Recurrent, lifelong disease with no cure; greater recurrence than HSV 1
  • viral culture is preferred for diagnosis
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26
Q

What is the treatment of HSV 1 & 2?

A
  • Anti-viral (Zovirax) and contagion prevention
  • Oral acyclovir
  • Recurrent treatment with acyclovir, famciclovir, and valacyclovir
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27
Q

What is the clinical presentation of Varicella Zoster (Chickenpox) and what is its incubation period, prodrome, and type of spread?

A
  • Presentation: eruption of successive crops of 2-3 mm size vesicles, “dew drop on a rose petal,” lesions rapidly become pustules and crust
  • Incubation period: 14 days
  • Prodrome: fever, chills, malaise, 2-3 days before onset of rash
  • Spreads via respiratory droplets
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28
Q

What is the major complication associated with Varicella?

A

Encephalitis, pneumonia, hepatitis, Reye’s syndrome (use of aspirin with varicella causes Reye’s syndrome which leads to encephalopathy)

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29
Q

What virus does the varicella vaccine immunize against and what are the immunization recommendations for children and for those who have never had chickenpox that are over 13 years old?

A
  • Virus = Varicella Zoster Virus (VZV)
  • Children:
    o 1st dose at 12-15 months
    o 2nd dose at 4-6 years
  • Over 13 y/o without chickenpox/vaccine:
    o receive 2 doses at least 28 days apart
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30
Q

What virus causes Herpes Zoster and what is its prodrome?

A
  • Varicella Zoster Virus (recurrence from chickenpox)

- Prodrome: radicular pain along nerve root up to 5 days prior to rash

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31
Q

What does the rash for Herpes Zoster look like and where does it appear?

A
  • The vesicular rash follows the nerve root which manifests in a single dermatome, unilaterally. It may cross the dermatomal spread with up to 30 vesicles in the next dermatome. This dissemination rules out immunosuppression (cancer, HIV, CT disease)
  • Involvement of the tip of the nose (Hutchinson’s sign) is a clinical predictor of ocular involvement.
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32
Q

What is the treatment for Herpes Zoster?

A
  • Immunization: Zostavax = a live, attenuated vaccine for prevention of herpes zoster in patients aged 50 and older.
  • Acyclovir, Prednisone, IV acyclovir (most effective after eruption)
  • treat within 48 hours to decrease postherpetic neuralgia
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33
Q

Non-bullous impetigo has what kind of clinical presentation?

A
  • Begins as a single red macule or papule which quickly becomes a vesicle. The vesicle ruptures to form an erosion. The contents dry up to form the characteristic honey-colored crusts that may be pruritic.
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34
Q

What is non-bullous impetigo caused by?

A
  • Group A strep pyogenes, coagulase positive Staph aureus, mixed infection
  • Host response to infection, direct contact
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35
Q

What causes bullous impetigo and what is its clinical presentation?

A
  • Caused by phage group II Staph aureus (epidermolytic toxin)
  • Blisters (bullae) occur in the axillary, groin, and fold areas. Superficial vesicles progress to rapidly enlarging, flaccid bullae with sharp margins and no surrounding erythema. When bullae rupture, yellow crusts with oozing result.
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36
Q

How is impetigo (nonbullous and bullous) treated?

A
  • hygenic measures
  • topical antibiotics
  • oral antibiotics
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37
Q

What is the appearance of candida albicans (yeast) in cutaneous and mucosal infections?

A
  • Erythematic, small pustules with fringe of white scale
  • bright beefy red dermatitis surrounded by satellite micropustules
    o commonly seen in skin folds and mucous membranes
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38
Q

What appearance do dermatophyte infections result in?

A
  • Infections can produce superficial blisters or pustules with positive dermatophyte in the stratum corneum producing a subcorneal or introepidermal blister
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39
Q

How are fungal infections treated?

A
  • Antifungal agents for dermatophytes (griseofulvin, terbinafine, azoles, ampiterocin B/nystatin, caspofulvin)
  • treat tinea corporis, cruris, and pedis with azoles and terbinafine
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40
Q

What is the clinical presentation of bullous pemphigoid, how is it diagnosed, and what is the typical age of onset?

A
  • Presentation: numerous tense bullae in clusters on normal or erythematous skin
  • Diagnosed based on histological exam
  • Age of onset: between 60 and 80 years
  • Autoimmune disease
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41
Q

How is bullous pemphigoid treated?

A
  • Prednisone, topical cortisone for mild cases
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42
Q

Dermatitis herpetiformis is an ________________ condition which arises as a consequence of _________ _____________ which is associated with ___________ __________ .

A

autoimmune
gluten sensitivity
celiac disease

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43
Q

How does dermatitis herpetiformis present in clinic?

A
  • Typified by clusters of erythmatous papules, excoriations, and vesicles
  • Pruritic and distributed symmetrically along extensor surfaces
44
Q

What is the age of onset of dermatitis herpetiformis?

A

Between the ages of 20 and 40 years (typically when celiac disease is diagnosed), but condition can occur at any age

45
Q

What is the clinical presentation of pemphigus vulgaris and what membranes does it affect?

A
  • this autoimmune disease affects skin and mucous membranes
  • Presentation:
    o skin lesions are flaccid blisters which are located on the head, trunk, and intertriginous areas (axilla, groin, etc)
    o Associate with Nikolsky sign – skin finding in which the top layers of skin slip away from lower layers when rubbed slightly, may create a blister
46
Q

Porphyria Cutanea Tarda results from what deficiency and has what associated risk factors?

A
  • deficiency in heme-synthesizing enzyme

- Risk factors: Hep C, hemochromatosis, alcoholism

47
Q

What is the clinical presentation of Porphyria Cutanea Tarda?

A
  • blistering of skin occurs on sun-exposed areas (hands, forearms, face)
  • may exhibit hypertrichosis (increased hair growth), skin hyperpigmentation, and urine discoloration
48
Q

What is the hallmark feature of psoriasis?

A

Silvery scaled region with underlying erythema

49
Q

What are some other characteristics of psoriasis?

A
  • Sharply demarcated erythema, usually with thick micaceous scale.
  • Auspitz sign: bleeding after removal of scales
  • Koebner phenomenon: lesions induced by trauma
  • Rarely pustular
50
Q

What is the pathogenesis of psoriasis?

A
  • T-cell mediated autoimmune disorder
  • Environmental factor-T cells produce cytokines which stimulate keratinocyte proliferation and production of antigenic adhesion molecules in the dermal blood vessels. These adhesion molecules stimulate further production of cytokines.
51
Q

What are some risk factors for psoriasis?

A
  • First degree relative with psoriasis, stress, medications, infection, chronic HIV
  • Precipitated by infection, trauma, stress, alcohol, systemic steroids (particularly withdrawal from), beta blockers, lithium, antimalarials, indomethacin
52
Q

What are the different types of psoriasis?

A
  • Chronic plaque
  • Inverse
  • Guttate
  • Pustular
53
Q

What areas does chronic plaque psoriasis affect?

A
  • affects the scalp, extensor surfaces, palms, and soles
54
Q

What areas does inverse psoriasis affect?

A
  • intertriginous areas (folds) - gluteal, axillae, glans of penis; may not have scale
55
Q

What causes guttate psoriasis and what is its clinical presentation?

A
  • caused by post strep infection, usually in children/young adults
  • Presentation: eruptive trunkal dermatosis; sudden tear drop shaped scaled spots of trunk and proximal extremities
  • Has a tendency towards spontaneous resolution
56
Q

What is the appearance of pustular psoriasis and where is pustular psoriasis of Barber located?

A
  • Appearance: small pustules become generalized with fever, potentially life-threatening
  • Pustular Psoriasis of Barber is localized to the hand (palm) and foot (sole)
57
Q

How is psoriasis treated and what are the diseases complications?

A
  • Treated with combination topical steroid + PUVA (light) if > 20% of body
  • Complications:
    • Psychiatric/self-esteem
    • Increased risk of non-melanoma skin cancers and lymphoma
    • Psoriatic arthritis
    • Nail pitting and onycholysis (separation of nail from the nail bed)
58
Q

What are the hallmark features of Lichen Planus?

A
  • Wickham’s stria (lacy, reticular white lines)

- 6 Ps: planar, purple, polygonal, pruritic, papules, plaques

59
Q

What are the histopathologic characteristics of Lichen Planus?

A
  • interface dermatitis (occurs at junction of epidermis and dermis)
  • saw tooth acanthosis
  • shaggy deposits of IgM along basement membrane zone (whereas lupus has IgG)
60
Q

What are the different forms of Lichen Planus and what are they?

A
  • Hypertrophic: very thick plaques of scale over lichen planus, especially over the extremities and extensor surfaces
  • Bullous: blisters that occur under the lichen planus due to severe interface dermatitis
  • Scalp: Lichen Planopilaris - scarring alopecia of the scalp due to lichenoid infiltrate
  • Oral: Tender red patches, surface (with Wickham’s striae) does not wipe off like thrush would. Can occur by itself or with classical
61
Q

How is Lichen Planus treated and typically, where are the lesions located?

A
  • Cutaneous may resolve spontaneously in 1-2 years
  • Topical or oral steroids
  • Phototherapy
  • Stop drug if drug induced (often thiazide, sulfa-related, beta blockers, captopril)
  • lesion located on wrists, shins, mucosal membranes
62
Q

What are the different types of Systemic Lupus Erythematosus and what are the histopathologies that correspond?

A
  • Acute: Pauci-inflammatory interface dermatitis; prominent dermal edema and dermal mucin
  • Subacute: Prominent suprabaslar exocytosis of lymphocytes, prominent epidermal atrophy; lymphocytic infiltrate.
  • Discoid: Very thick basement membrane, follicular plugging; Dense perivascular and peri-adenxal infiltrate
  • Generally, immunofluorescence shows IgG at basement membrane (may also have IgM)
63
Q

What are the different risk factors for SLE?

A
  • More common in women and in African-Americans, Hispanics, and Asians
  • Age 14-40
64
Q

What is the hallmark feature of SLE?

A

butterfly rash across face

65
Q

What are some other characteristics of SLE?

A

• Photosensitive erythema
• Red rash on sun exposed upper chest and extensor areas
• May become bullous in these areas
• Non-specific skin lesions
o Vascular (50-70%) e.g. telangiectasia, vasculitis, thrombophlebitis, ulcers, Livedo reticularis
o Alopecia (40-60%): frontal, diffuse
o Other: Urticaria, mucous membrane, pigment changes
• May have non-specific features like digital infarcts, Raynaud’s syndrome

66
Q

What is the appearance of subacute SLE and what causes it to occur?

A

o Erythematous and usually scaling rash in psoriasis plaque-like form or annular polycyclic form
o Due to SSA or SSB antibody

67
Q

What is the appearance of the different types of chronic SLE: discoid, tumid, panniculitis, verrucous?

A

o Discoid Lupus: scarring lesions of skin (especially pinna)
o Tumid Lupus: erythematous indurated plaques in sun exposed areas
o Lupus Panniculitis: infiltration and destruction of adipose tissue, especially upper extremities, unlike erythema nodusum which is usually lower extremities
o Verrucous Lupus: very thick hyperkeratotic discoid lupus like lesions that usually occur on the extensor sun exposed surfaces

68
Q

How is SLE treated?

A

NSAIDs, antimalarials (Plaquenil), corticosteroids, immunosuppressants

69
Q

What are the risk factors for SLE?

A

Sunlight, medications (anti-seizure, antibiotics, blood pressure meds)

70
Q

What pathogen, tick vector, and host animals are associated with Lyme Borreliosis?

A
  • Pathogen: B. burdorferi (micro-aerophilic spirochete)
  • Tick vector: I. pacificus, I. scapularis – needs to be attached for > 36 hours for bacterial activation and passage
  • Animal hosts: white-talied deer, white-footed mouse
71
Q

What time of year do Lyme Borreliosis infections most often occur and what are the incidence rates for MN and WI?

A
  • Peak incidence = July and August because I. scapularis feeds from March through November
  • MN: 24.4 cases per 100,000/year
  • WI: 44.0 cases per 100,000/year
72
Q

What are the clinical stages of Lyme Borreliosis?

A
  • Early localized, 1-2 weeks
    • Erythema migrans seen in 60-80%; must have diameter of 2 inches in size
    o “bullseye” rash only seen in 15-20% of patients
    • Low grade symptoms: fever, headache, muscle aches
    • Nonspecific CBC and LFT changes, ESR and CRP may be elevated
  • Early disseminated, weeks-months
    • Systemic complications
  • Late (persistent), month to years
    • Chronic arthritis: HLA DR 2,3,4
    • Acrodermatitis chronicum: B. afzelii atrophicans
    • Neurological impairments
73
Q

What tests should be ordered to diagnose Lyme Borreliosis?

A
  • IFA
  • ELISA: test positive for C6 peptide (found on surface of B. burgdorferi
  • EIA - quantitative assay for detecting biological peptides
    o need to have a confirmatory Western Blot:
    • IgM - 23, 39, 41 – positive with > 2 bands
    • IgG - 18, 23, 28, 30, 39, 41, 60, 66, 93 – positive with > 5 bands
  • Antibodies (IgG) tends to persist for decades. Difficult to tell if old or new infection
74
Q

What is the treatment for Lyme Borreliosis?

A
  • Doxycycline

Others: amoxicillin, cerfuroxime (2nd gen cephalosporin), axetil
Adjunctive therapy: NSAIDs, muscle relaxants, bicyclic antidepressants, tricyclic antidepressants

75
Q

What is the pathogen, tick vector, and host animals for RMSF?

A
  • Pathogen: Rickettsia rickettsii
  • Tick vector:
    o Dermacentor spp. (Wood tick); only adult Dermacentor tick bites humans
    o Amblyomma americanum (Lone Star tick)
    o Rhipicephalus sanguineus (Brown dog tick): AZ
  • Host Animal: rodents, dogs
76
Q

What is the clinical presentation of RMSF?

A
  • Incubation period = ~7 days
  • Abrupt Symptoms: fever, chills, myalgias, headache, nausea, vomiting
  • Day 4: onset of centripetal, petechial rash
    o longer have the rash, more severe the disease becomes
    o rash starts at the extremities and goes towards trunk
  • Splenomegaly in 50% of patients
77
Q

What is the treatment for RMSF?

A

Doxycycline

can also use Tetracycline, Chloramphenicol, Rifampin

78
Q

What is the pathogen, tick vector, and host animal(s) for Babesiosis?

A
  • Pathogen: Babesia = hemato-parasites
    o B. microti, dominant pathogen in USA
    o B. duncani, rare infections found in CA and WA
  • Tick vector: I. scapularis (“deer tick”)
  • Host animal: white-footed mouse, white-tailed deer
79
Q

What is the Clinical presentation of Babesiosis?

A
  • gradual onset of illness with non-specific influenza-like symptoms: fever, headache, malaise, myalgias, arthralgias, weakness, nausea
  • NO rash or eschar at bite site
  • Physical exam may reveal hepatosplenomegaly, occasionally jaundice due to RBC destruction
80
Q

What lab tests are used to aid in diagnosing Babesiosis?

A
  • Blood-smear (perform a giemsa stain) to see the trophozoites formed by Babesiosis
  • IFA: look for IgG levels, 1:1,024 suggest active infection
  • PCR of 18S rRNA
81
Q

How is Babesiosis treated?

A
  • Quinine PLUS Clindamycin, for two weeks

- Atovaquone PLUS Azithromycin

82
Q

What is the pathogen, vector, and animal host(s) that cause Tularemia?

A
  • Pathogen = Franciscella tularensis
  • Vector: ticks, deer flies, mosquitoes
  • Host Animals: rabbit > deer > other rodents
83
Q

What is the incidence of Tularemia?

A
  • Exposure occurs due to inhalation, contact with fresh blood, or flesh
  • Incubation time = 1 day - 3 weeks
  • Scatter occurrence throughout the US
84
Q

What is the clinical presentation of Tularemia?

A

o Abrupt onset of fever and chills; headache, myalgias, sore throat
o Bite site ulcerates and forms a black eschar with non-healing ulcer
o Regional lymphadenopathy, nausea and vomiting common

85
Q

What might lab tests reveal if a person is infected with Tularemia?

A
  • Elevated WBC, ESR, and LFTs
  • Thrombocytopenia seen occasionally
  • F. tularensis grows in blood-culture
  • Antibodies may persist for > 10 years…
86
Q

How is Tularemia treated?

A
  • Antibiotics: Streptomycin, Gentamycin, Doxycycline
  • Alternative therapy: Ciprofloxacin, Moxifloxacin, Chloramphenicol
  • Combo therapy: Doxy and Cipro
  • Treat for 7-14 days
87
Q

What are the different pathogens that cause Ehrlichiosis and Anaplasmosis?

A

o E. chaffeensis – Human monocytic ehrlichiosis (HME)
o A. phagocytophilum – Human anaplasmosis (HGA, or HGE)
o E. ewingii – Human granulocytic ewingii ehrlichiosis
o E. muris-like agent – E. muris ehrlichiosis
- gram negative bacteria, obligate intracellular organism
- form morulae

88
Q

What is the vector and the host animals for Ehrlichiosis and Anaplasmosis?

A
  • Tick vector – transmission occurs due to exposure to animal blood (mice, deer, human) or infected blood transfusion
  • Animal host – white-footed mouse, white-tailed deer
89
Q

What is the clinical presentation of Ehrlichiosis and Anaplasmosis?

A
  • Incubation period = 2-14 days
  • Frequent complaints (>80%): fever, chills, headache, myalgias
  • Less common complaints (30-80%): arthralgias, nausea, cough, confusion
  • Uncommon complaints: rash (HME ~20%, HGA - rarely)
90
Q

What findings are expected from lab tests that are ordered to test for Ehrlichiosis and Anaplasmosis?

A
  • CBC non-specific but it can show: leukopenia, thrombocytopenia, lymphopenia, and relative granulocytosis
  • Mild elevation in AST and ALT
  • Elevated ESR, CRP
  • Blood-smear (need manual differential) to visualize morulae using light microscopy:
    o HME - very low (<5%)
    o HGA - sensitivity varies (~20-60%)
91
Q

How are Ehrlichiosis and Anaplasmosis treated?

A

Active antibiotics: Tetracycline, Doxycycline, Rifampin

92
Q

Drug delivery depends on…?

A
  • Skin type (location and quality, i.e. thin vs thick)
  • Skin condition (inflammed, cracked, healthy)
  • Lipid vs. water-based vehicle
  • Charge of drug molecules
  • Concentration gradient
93
Q

What are some key points to remember about derm therapy?

A
  • stratum corneum = “bricks and mortar” barrier; rate limiting step to topical therapy absorption
  • Hydration of skin increases absorption making the stratum corneum more penetrable
  • Vehicle of therapy determines level of occlusiveness and absorption
94
Q

What are the actions, uses, and adverse effects of corticosteroids?

A
  • Actions: anti-inflammatory, immunosuppressive, anti-proliferative, vasoconstrictive
  • Uses: eczema, contact dermatitis, psoriasis, lichen planus, pruritis
  • Adverse effects: SKIN ATROPHY, striae, acne
95
Q

What is the mechanism, actions, uses, adverse effects, and examples of retinoids?

A
  • Mechanism: retinoids are Vitamin A analogs which cause alteration of gene transcription through nuclear receptors on DNA
  • Actions: regulates cell growth, inhibits carcinogenesis, alters enzymes involved with cellular differentiation
  • Uses: acne, psoriasis, cosmetic skin improvement (lessens wrinkles)
  • Adverse effects: dryness, irritation, sun sensitivity
  • Examples: tretinoin (Retin-A), tazarotene (Tazorac), adapalene (Differin)
96
Q

What are the actions, uses, adverse effects and examples of Calcipotriene?

A
  • Action: Vitamin D analog that acts through DNA receptors to alter skin differentiation
  • Uses: psoriasis, eczema
  • Adverse Effects: irritation, increased serum Ca
  • Example: Dovonex
97
Q

What are the actions, uses, adverse effects, and controversy surrounding Topical Calcineurin Inhibitors (TCIs)?

A
  • Action: works through calcineurin to alter T-cell activation
  • Uses: eczema, dermatitis
  • Adverse effects: limited, local irritation or burning
  • Controversy around safey – FDA added “black box” due to possible risk of lymphoma
98
Q

What are the active ingredients of sunscreen?

A

Avobenzone/Helioplex or Mexoryl

Titanium dioxide and Zinc oxide

99
Q

Imiquimod (Aldara cream) works through what kind of mechanism and is used for what conditions?

A
  • Mechanism: “immune response modifier” – increases inflammation to draw on immune system by increasing local immune activity through Toll receptors
  • Uses: Condyloma (genital warts), actinic keratosis, BCC, common warts, molluscum, in situ cancer
100
Q

What is 5-FU used to treat?

A

Actinic Keratosis

- Examples: Carac, Efudex

101
Q

How should wounds be cared for?

A
  • keep the wound covered with vaseline and nonstick dressing to allow natural cytokines to facilitate healing, monitor for infection
102
Q

What is the action, uses, adverse effects, and labs to check for dapsone (a sulfone)?

A
  • Action: inhibits myeloperoxidase in PMNs (neutrophils)
  • Uses: treat leprosy, dermatitis herpetiformis, linear IgA disease, bullous lupus, etc.
  • Adverse effects: hemolysis (esp. w/ G6PDH deficiency), methemaglobinemia, motor neuropathy
  • Labs: G6PDH, CBC
103
Q

What are the three stages of Alopecia?

A
  • Anagen (growth stage, lasts 2-7 years)
  • Catagen (transition stage, lasts 3 weeks)
  • Telogen (falling out stage, lasts 3 months)
104
Q

What is the cause, location, and treatment for androgenetic alopecia?

Also called: “Simple Baldness”, “Hereditary Alopecia”, “Pattern Alopecia”

A
  • Cause: genetically determined miniaturization of follicles triggered by androgens
  • Area: top of scalp
  • Treatment: minoxidil (topical), finasteride (oral), hair tranplants
105
Q

What is the cause, area, triggers, and treatment for telogen effluvium?

Also called “stress hair loss”

A
  • Cause: disrupted growth cycle of hairs causing premature shift from anagen to telogen phase
  • Area: diffuse scalp involvement - “comes out in bunches”
  • Triggers: pregnancy, surgery, high fever, extreme diet, emotional stress
  • Treatment: remove trigger, minoxidil, time, reassurance
106
Q

What is the cause, area, and treatment of Alopecia Areata?

A
  • Cause: autoimmune, T-cells attack the hair bulb - appears as a “Swarm of bees” upon microscopic exam
  • Area: circular patches on scalp or beard
  • Treatment: topical or intralesional steroids, minoxidil, anthralin,protopic/elidel, watch and wait
107
Q

What is pediculosis and what is it’s treatment?

A
  • Pediculosis = head or pubic lice

- Treatment: kill lice (Nix), suffocate lice (vaseline, cetaphil), remove nits and live eggs, wash fomites

Skin/Musculoskeletal (5 decks)

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