Derm Tx Flashcards

(196 cards)

1
Q

Atopic Dermatitis Tx

A
  1. Education: to avoid exacerbating factors and hydrate the skin
    - vasline is best or other ltion -BID and after bathing
  2. Topical Corticosteroid
    -mild: low potency 1-2x per day x2-4 wks
    -moderate: med-high pot
    -acute: med-very high pot for up to 2wks then replaced with lower potency.
  3. Topical Calcinereurin Inhibitors -
    Pimecrolimus(Elidel) cream and Tacrolimus(protopic)
    -steroid sparing and antiinflammatory because they imped production of proinflammatory cytokines.
    -.1% for adults
    -.03% for 2-15
    -BID for mild eczema on face, eyelids, skin folds
    -2-3x per week for maintanance
    may have bruning or itching during the first week of use
  4. Oral antihistamines prn pruitis, antibiotics for 2nd infection, oral steroids for severe or wide spread cases.
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2
Q

Topical Corticosteroid warning

A

Face, groin, and skin folds have higher absoprtion so use caution when applying to those locations
-skin atropy, rosacea, striae, bruisng, telangiectasis, hypertrichosis

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3
Q

Lichen Simplex Chronicus Tx

A

Want patient to stop the rubbing!
1. High Potency topical steroid
then:
2. Moisturizers
3. Antidepressants: Paroxetine(paxil) or Sertraline(zoloft)
4. for nocturnal pruritis: 1st gen antihistamine, hydroxyzine(Visatril) or Tricyclic antidepressent

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4
Q

Dyshidrotic Eczema Tx

A

Primary:
1. Reassurance -usually resolve in 2-3wks
2. Topical Steroids (maybe at night with occlusion)
Secon:
3. Wet dressings (burow’s soaks)

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5
Q

Keratosis Pilaris Tx

A

No really good treatment

pt. may try: exfoliating scrubs, topical retnoid, salicylic acid, alpha-hydroxy acids

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6
Q

Contact Dermatitis Tx

A

Discontinue exposure or decrease hand washing
and wear protective clothing
- use a bland emollient like vasaline or aquaphor
*Topical corticosteroid 1-2 days x 7-14days
or oral corticosteroid if on face or more than 20% of the body

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7
Q

Tx for common cutaneous drug reactions

A

Discontinue drug!!!
-sytemic corticosteroids to come the immune system
-topical steroids or antihistamines prn for pruitis
-cousel to avoid crossreactive drugs in the future
Typically resolved in 5-14 days
may be left with post inflammatory hyper-pigmentation

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8
Q

SJS and TEN Tx:

A
Discontinue Medication!!!!
Hospital admission if severe usually to ICU or Burn Unite
Supportive care:
-nutritional and fluid replacement( B/C mouth sores)
-Temperature maintance
-Pain relief
-Occular managment 
-Wound care and sterile handling
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9
Q

Tinea Capitis at risk populations

A

Children, african americans, homeless, poor hygeine, low SES, and overcrowding

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10
Q

Tinea Capitus Cause/Presentation

A

Fingual infection (Trichophyton/Microsprorin)
From direct contact
-Scaly patches with alopecia
-black dots with alopecia
-widespread scaling with subtle hair loss
- Kerion
-Favus (multiple cup shaped yellow crusts): usually with immunocomp pt.

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11
Q

Tinea Capitus Associated Signs

A

Cervical adenopathy, Dermatophydid reaction ( eczema like,in response to treatment), and rerely erythema nodosum (tender nodules)

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12
Q

Tin Cap Dx

A

KOH prep, physical exam, culture, dermascope,woods lamp

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13
Q

Tin Cap Tx

A

Systematic antifungal therapy

  1. Griseofulvin x 6-12wks for microsporin or empiric tx
  2. Terbinafine x2-4wks if tricophyton
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14
Q

Tine Corporis Risk factors

A

Cargivers of children c tinea cap
athletes with skin contact (tinea corporis gladiatroum)
immunocomp

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15
Q

Tinea Corporis Presentation

A

Pruritic, annular, erythematous plaque

with a central clearing , raised advancing border

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16
Q

Tinea corp,cruris,pedis Dx

A

Physical exam. KOH prep, and culture

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17
Q

Tinea Corp,Cruris,Pedis Pharm Tx

A

Topical antifungus
-Cotrimazole at least 2 wks (4wks if pedis)
Systemic only in special circum
-Intraconazole

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18
Q

Improper treatment of Tinea infections can lead to what?

A

Usually if you accidentally use steroids

  • Tinea Ingognito
  • Mojpcchi’s granuloma
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19
Q

Tinea Cruris Risk factors

A

Male, sweaty/humid, obese/skinfolds, athletes foot, and occulusive clothing

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20
Q

Tinea Cruris Presentation

A

Begins at the inguina folds
well marginated, scaly, annular, with raised border
scrotum is typically spared
-Pruritis, pain

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21
Q

Tinea Cruris tx non Pharm

A

Drying powder, avoid tight clothing, weightloss

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22
Q

Tinea Pedis Risk Factors

A

occlusive footwear, communal baths or showers

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23
Q

Acute Tinea Pedis presentation

A

self limited, intermittnet, recurrent infection

  • itchy/pain vessicles following sweating
  • secondary staph infections may occur*
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24
Q

Chronic Tinea Pedis Presentation

A

slowly progressive that may persist indefinatly

  • erosions between the toes (oft bw 3-4)
  • interdigital fissures
  • May progress to Mocassin Ringworm (along the whole bttom of the foot, with shapr demarcations of accumulated scale
  • Tinea Manuum ( two feet one hand)
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25
Tinea Pedis non pharm Tx
Burrows wet dressing 20min BID-TID Treat secondary infections Food powers, proper footwear
26
Onycomycosis Etiology
Nail infection caused by fungus, yeast, or non-dermatophyte molds - typically yeast(candida albicans) with fingernails
27
Onycomycosis Risk factors
Old Age, Tinea Pedis, Genetics, Immunodeficiency, Household infection
28
Onycomycosis Presentation
Typically Cosmetic but may be painful - brown/yellowing of the nail and nail thickening 1. Dista Sugungual: most common and starts from distal corner and moves proximal. Distal nail bed may break exposing nail bed 2. Proximal Subungual: near cutical and extends up usualy seen in immunocomprimised patients 3. White superficial: begins with dull white spots that will extend out. These spots are soft
29
Onycomycosis Dx
KOH prep, culutre, histopathology
30
Onycomycosis Tx
Not neccessary but considered if Hx of cellulitis, diabetic, desires cosmetic improv, or discomfort - topical meds inefffective and high rate of failure 1. Dermatophye:Oral Terbinafine (6wks fingernails, 12wks toenails 2. Non-Dermatophyte: oral intraconazole (same duration as above)
31
What drugs treat both Onycomychosis and Tinea infections
Terbinafine- tinea capitus | Intraconazole - other tinea inf
32
Candidial Interrigo etilogy and Risk Factors
infectious or noninfection skin condition of two closely opposed skin surfaces -moisture, skin friction, immunocompromised
33
Candidal Interrigo Presentation
typically affects the groin,mammary/ab folds, web spaces, and axilla - erythemous, maccerated(soggy) palques or errosions - sattelite papules/pustules - fine peripheral scaling
34
Candidal Intertrigo Dx
-Physical Exam, KOH prep, culutre
35
Candidal Intertrigo Tx
Prevent: -drying agents, weight loss, address underlying med cond. Pharm: Topical x2-4 wks: Nystatin (for yeast) Syestemic for resistant/severe: Fluconazole 2-5wks
36
Tinea Versicolor Cause/ Risk Factors
Caused by malassezia- normal skin flora of the skin that becomes pathologic Seen in tropical climates, adolecents/ young adults, hyperhidrosis, genetics, immunosupression *NOT contageous*
37
Tinea Versicolor Presentation
Macules, patches/plaques of the trunk and UE, can coalesce, often have fine scale, maybe erythemous - often asymptomatic but may be mildly itchy - often hypopigemented on dark skin and hyperpigmented on lighter skin
38
Tinea Versicolor Dx
Physical, KOH prep, Woods lamp (sometimes yellow/green flourescense)
39
Tinea Versicolor Tx
Topical - Clotrimazole (2wk), Selenium sulfide( lotion, foam, shampoo x1wk), or Zinc Pyrinthione shampoos x2wk Systemic -oral intraconazole 5-7days - only insevere cases and failed topical, not used in children *note pigmentation can persist for months which makes it hard to nknow if the treatment has worked
40
Scabes etilogy/ risk factors
Parasitic infection- sarcoptes scabiei mite - female mites and their eggs - eggs hatch in 10 days All groups affectes and it is transfered through direct contact
41
Scabes Presntation
Intial lesion and burrow (pathonomonic) - locations: groin, rists, waist severe pruritis which is often morse at night In immunocomprimised people: Norwgian or crusted scabies -will have severe fissures and requires oral medication
42
Scabies Dx
-Visualization of the burrow , microscopic identifcation of the mite, eggs, or fecal pellates with dermatoscope
43
Scabies Tx
Permethrin 5%- first treatment and then 2nd dose 10-14 days later Oral Ivermectin- single dose repeated 2 weeks later Edu: treat house and close contacts simulaneously, itching may persist for 2 wks( can treat with antihistamines and emoilliants), wash linens under high heat
44
Pubic Lice etilogy/ presentation
Parasites that are larger than Scabies - crab louse (phthirus pubis) - transmitted through sexual contact - presents as itching in the groin or axilla
45
Pubic Lice Dx/Tx
Visualize the lice or nits with a microscope Tx: Permithrin 1% cream and repeat in 10 days and treat sexual partners * often have another type of STI*
46
Important things to note when diagnosing acne vulgaris
- possible workup for hyperandrogenism for female patients with other sx - rapid acne with other signs of virilication may be becuase of ovarian or adrenal tumor - medication history may reveal acnes causing medications
47
Comedonal (non-inf) acne Tx
Topical retnoid
48
Mild papulopustuar and mixed acne Tx Moderate Sever
BP +/- topical antibiotic and topical retnoid BP + topical retnoid+ oral abx (tetracycline class) BP+ top ret+Oabx OR oral isotrtinoin monotherapy
49
What acne meds are teratogenic ? What are okay?
Topical retnoid and not okay during pregnancy and BP is not really known - oral erythromycin, topical clindamycin, and topical azelaic acid
50
Solar Lentigo
Age spot or freckles - local proliferation of melanocytes and from UV damage - well circumscribed - brown macules - often found in group - no treatment required
51
Seborrheic Keratosis (SK)
-benign epidermal lesion proliferation of immature keratinocytes - usually after age 50 warty, waxy, stuck on apperance -well circumscribed -back,head, neck
52
Irritated SK
caused by rubbing of friction of the SK | - may have pruitis, pain, or bleeding
53
Leser-Trelat sign
sudden onset of multiple SK +skin tahs + acanthosis nigrican - possible associated with GI and Lung cancer
54
SK eval and managment
Dx- clinical presentation and biopsy if necessry | Tx: reassurance and possible removal for some ISKs. Shave off or use cryotherapy.
55
Keratoacanthoma Presetation
rapid growth- 6-8wks - round, flesh colored nodule with central keratin plug - same risk factors as skin cancer - benign but some say it pseudo-malignancy
56
Karatonacanthoma Managment
Majority will resolve on their own in 6-9mo Difficult Dx: requires biopsy and treatment - typically excisional biopsy is typically preferred
57
Actinic Keratosis etiology andRisk Factors
AK "pre cancer" may progress to SCC M>F light skin, history of UV exp, immonsuppression, ^age
58
AK presentation
- Erthematous, scaly/gritty macule or papule - may be tender - often felt easier than seen
59
AK dx
clinical dermatoscope Shave or punch biopsy if unable to differentiate from SCC (>1cm, rapid growth, ulcer) *if >6mm then we just consider it SCC in situ
60
AK tx
may spont resolve but usually treat anyway - Cryotherapy or surgical intervention Field Treatment: if you have multiple lesions -topical flourouracil cream (preferred) -Photodynamic therapy (PDT) -Imiquimod (Aldara)
61
Basal Cell Carcinoma Etiology
Most common type of skin cancer | - arised from the basal layer of the epidermis
62
BCC presentation
nodular - flesh colored - pearly* papule - has telangiectasia* - may have central ulcer with *rolled boreder - most common on the head and neck * may be pink patch to AK or SCC in situ.
63
BCC tx
``` Surgical is preffered -currettage or desiccation -excision within 4mm margins -Mohs for high risk or cosmetic Nonsurgical -radiation if poor surgical canidate -Imiquimod cream -5% fluoroiracil cream -Photdynamic therapy ```
64
Squamous cell carcinoma etilogy
2nd most common -originated from keeratinocytes and AK M>F - can arise from previous area of skin injuries like scars
65
SCC presentation
papule, plaque, nodule - not as sandpapery as a AK pink, red, skin colored - get a scaly appearance, friable, indurated -not as nice of a border -often asymptomatic but van be very irritable
66
SCC tx
``` Surgical - wide excision or mohs Non surgical - Radiationfor poor surgical canidate or residual tumor -Curettahe and Desiccation or cryotherapy ( good for SCC in situ which is low risk) -5-fluorouracil therapy -Imiquimod -PDT ```
67
Malignant Melanoma Etiology + Risk
high morbidity and Mortality >5 atypical nevi or >25 nevi in gen Risks: fair skin, blue eyes, red/blonde hair, freckling, immunosupression, family history
68
Melanoma presentaion
-usually asymptomatic and arise usually de novo but some can arise from pre-existing nevus - pigmented papule, plaque, or nodule ABCDE
69
Superfiial spreading melanoma
- most common - confined to epidermis - often in younger pop - radial spread> verticle spread
70
Nodular Melanoma
Rapid verticle growth and minimal radial growth - very agressive - nodule is inflammed and friable
71
Lentigo Maligna
Elderly pt with chronic sun exposure - slightly less common - slowl progression and usually spead radially and remains superficial
72
Acrak Lentiginous
More in darker skin and AA pop - M>F - spreads superficial more than verticle
73
Breslow depth and Melanoma
How deep the lesion is related to the prognosis of the skin cancer
74
Melanoma Tx
``` Wide surgical clearing -2cm margins - typically dont use Mohs -regional lymph node dissection If really large or advanced: radiation, chemo, immuno 3mo follow up ```
75
Erthymatotelangiectatic rosacea
Chronic redness of central face, flushing (wet or dry), skin sensitivity, dry appearance, telangiectasias
76
Papulopustular rosacea
papules and pustules inflammation can be confluent but there are no comedones
77
Phymatous rosacea
only rosacea that is more common in men than women - tissue hypertrophy causing irregular contours - mostly on nose and can involve cheeks, forehead, and chin
78
Occular rosacea
in addition to one of the other 3 types - may preceded, coincide, or follow - dry eyes, pain, itching, blurry vision, photosensitivity
79
Erythematotelangiectatic rosacea Tx
1. Modify behavior to avoid triggers, gentle skin care, and avoid sun exposure 2. Laser pulse light therapy or topical brimonodine (vasoconstrictor)
80
Papulopustular rosacea Tx
Mild: - metronidazole - Azelaic acid - then: ivermiectin or sulfacetamide-sulfur
81
Phymatous rosacea Tx
Early- Isotretinoin( retinoid) | Advnced- surgical debulking or laser ablation
82
Scorpion sting Grades 1-4
1: local pain c paresthesiaa at sting site 2. local symp + remot pain and parasthersias 3. Either cranial nerve or somatic skeletal neuromuscular disfunction 4. Both cranial and somatic skeletal dysfunction
83
Scorpion Sting Dx
-clinical Tap Sign: local pain made worse by tapping near the stinging sight cranial nerve disfunction: hypersalivation, abnormal eye move, blurred vision, slurred speech, tongue fascicilations Skeletal dis: fasiculations, shaking or jerking, emprosthotonos (tetanic forward flx), fever
84
Scorpion tx
``` Pain managment cleansing of sting site tetanus prophylaxis observe for 4hrs Severe cases: -treat for respiratory comprimise, MI, Hyperthermia, Rhabdomyolysis, multiple organ failure -fentanyl for pain -IV benzodiazepines -Antivenom** cannot use with the benzos ```
85
Bee sting LLR
Rare - exagerated erythema and swelling -gradually elnarges over 5-10days Tx; cold compress and prednisone, antihist, NSAID
86
Bee sting complications
1. Secondary bacterial infection- worsening after 3-5 days of it getting better 2. Anaphylaxis - treat with epinephrine and refer to speciallist
87
Widow bites
-found near human habitats - small local reaction (often no venom inj) -blanched circular round patch with central punctum - venom causes catacholamine relase> intermitant radiating pain, ab/chest/back spasm, sweating, HA/N/V Tx: local wound care, antiemetics, narcotic analgesics, tentanus, muscle relaxers, maybe antivenom
88
Recluse spider bite
usually happen indoors -painless initially> red plaque/papule c central pallor> possible vessiculation - necrosis can occur +N/V/Ha>> rareley renal failur, rhabdo, anemia, hypotension Tx: cleansing, cold compress, analgesics, antibiotics, surgical excision for necrosis only fter the wound has stabilized
89
Tx of vitiligo
- screen for other autoimmune disorders Tx: topical and systemic corticosteroids, calcineurin inhibitors, narrow band UV B phototherapy, skin grafts - edu on sunscreen
90
Hidradenitis Supprativa etiology/ risk factors
chronic inflammatory skin dis of the hair follicle female>males usually around 23 genetics, mechanical stress, smoking obesity from a cycle of occlusion and rupture
91
Hidradenitis Supprativa presentation
``` Nodules in the axilla and groin more form as the disease progresses may form abscess(collection of pus) -sinus tracts can form -comedomes -scaring ```
92
Hidradenitis Supporativa Dx
Clinical based off lesion, location and history of relapse
93
hidradenitis supprativa Tx
1. Lifestyle Mod: avoid skin trauma, hygeine, no smoking, weight managment, diet 2. Pharm: - Topical clindamycin -intralesional corticosteroids -anti-androgenic agents -Surgery ( punch debredment or wide exicion) Super sever> TNF inhibitors, oral retnoids
94
Complications asso. c Hidradenitis supprative
fistulae, contractures(melted skin appearance), Lymphatic obstruction, infection, SCC, depression
95
Measles Etiology
Rubeola -Virus Paramyxovirus highly contageous- maintain in an area for 2hrs spread via cough sneezes, close breathing
96
Measles Clinical Stages
1. Incubation: 2-3 wks - typ asymptomatic 2. Promodone: anorexia, malaisw, fever 105+ followed by *3C's cough, coryza, conjunctivitis* 3. Enanthem: *Koplik spots 4. Exanthem: blanching and maculopapular - starts on face head to toe and spares the hands and the feet
97
Measles Dx
Reportable disease! - serum and throat swab for histologic analysis * serology: measles specific IgM
98
Measles complications
Common: -diarrhea > ottis media Severe and less common: -Pneumonia ( common in children), Encephalitis, subacute sclerosing panencephalitis (1-2 yrs later) High risk: preg, immunocomp, young or old
99
Measles Tx
``` Symptomatic treatment nly - vitamin A may lessen severity Patient education - avoid contact with pregnant women *vaccination!!!! ```
100
Erythema Infectiosum Etiology
Fifths disease- parovirus B-19 - transmitted by respiratory secretions - common in children
101
Erythema Infectiosum Presentation
can last from weeks to years 1. Incubation : 7-14 day 2. prodorome: no specific flu sx - low grade fver, coryza, HA, Nauseae, diahreeha, malaise, sorethroat 3. Facial Rash***- Slapped Cheek*** 4. Body Rash: 2-3 days later - *lacey rash*- paink macular rash on extensor surfces - may get polyarthropath (pain in joins)
102
Erthyema indectiosum Dx/ complications
- based on clinical presentation Compl: - transient aplastic crisis - in preg: *hydrops fetalis
103
Erthyema Indectiosum managmentn
reassurance and tell them to avoid pregnant women - will go away on its own - a lot of people have already had it
104
Rubella
German Measles Rubella virus - large particles in the air
105
Rubella presentation
1. Incubation 12-23 days 2. Prodorone 1-5 days - may have rash during - low fever, *lymphadenopathy, cold symptoms 3. Rash appears - erythemous papules and purpura- pin point pink - can be contageous for 7 days * * head to toe progresson**
106
Rubella Dx
clinical presentations - often resolve on its own | - may do serology if you cant tell
107
Rubella Complications
Congenital rubella syndrome- in pregnant women and is lethal to bany *blue berry muffin rash*
108
Rubella Managment
treat symptoms and avoid pregnant women - rubella titer is drawn at first prenatal visit! - prevention via immunization
109
Roseola Infantum etiology
Herpes virus 6 is most common - infants and younger children - transmission is not understood
110
Roseola Infantum present
- high fever that comes and then resolves abruptily - then a rash comes out of nowhere * this story is very classic 1incubation: 9-10 days 2. Prodrome: febrile maybe higher than >105 with abrupt end 3. Rash: *neck to trunk and then it will go toface* - blanching, pink, maculopapular rash - not itchy usually
111
Roseola Infantum Dx/ tx
Clinical presentation - serology is the pt is immunocomprimised Tx: suppotive treatment -antipyretucs
112
Hand, Foot, and Mouth Disease Etiology
Cozsackie A16 virus - mostly children 1-5 - fecal oral or oral respiratory secretions
113
HFM disease presentation
1. incubation: 3-5 days 2. Prodorome 12-24 hrs - no symptoms, fever, fussiness, abdominal pain, diarrhea 3. Oral enanthem/exanthem- oral more - sore throat and vessicles on buccal mucose and toungue - vessicles on hands* feet* and buttocks
114
HFM dx/Tx
Dx: clinical presentation - usually by based on location Tx: symptomatic maybe litocaine gel and prevent with good hygeine
115
Molluscum Contagiosum etiology/risk factors
Poxvirus common in children/ immunocomp -direct physical contact with fomites (towel, lines etc.) or skin - can also autoinoculation via scratching or clothing or shaving
116
Molluscum Contagiosum Presentation
Lesions: flesh colored and *umbilicated* located anywhere except palms and soles! - usually no associated symptoms - self limiting but super duper contagious
117
Molluscum Contagiosum Dx/Tx
Clinical presentation Tx: you dont really need treatment - home: podophyllotoxin cream ( not in preg) -office: quick cyotherapy, currettage, canatharidin
118
HPV types
1. mucosal: condyloma acuminata | 2. Cutaneous: common, plantar, and flat wart
119
HPV condyloma accuminata etiology/pres/Dx/tx
genital warts - most commonanorectal infection in MSM transmission- sexual contact Present: *cauliflower like lesions*, perianal growth, mild pruritis Dx; clinical presentation may need to evaluate for internal lesions (anoscopy or proctosigmoidoscopy) Tx: Topical posophyllin, electrocautery, laser, cryother. excision
120
HPV verruca Vulgaris etiology
``` more common in kids and younger adults Common Warts -transmission skin to skin contact - spont resolution 1-2 yrs - reoccurance is common Present: raised rough surfaced lesions wih tiny pigmented **thrombosed cappillaries** "seeds". Common on hands and feet. ```
121
HPV verruca vulgaris dx/tx
Dx: clinical presentation- may scrape of with 15 blade to visualize the thrombosed cappilaries Tx: may spont resolve, salicylic acid, cryotherapy, electrodessication,
122
Varicella etiology/transmission
Chicken pox Varicella Zoster virus- a herpes vaccine - through aerosolized droplets and is highly contagious - reoccurance can occur
123
Varicella Presentations/Dx
1. incubations 10-21 days 2. Prodorome 2-5 -fever, malaise, paryngitis, anorexia 3. Rash *vesicular rash* -pruritic rash occurs in stages paipule> blister> ulcer Dx: clinical typically but a Tzanck smear will show mononucleated giant cells
124
Varicella complications
- group A strep - Encephalitis and reye syndrome (uncommon) - most complications occur in immunocomp pt.
125
Varicella tx:
sypotomatic treatment - contagious until all lesion have crusted over - avoid pregnant females!! - acyclovir in imminosup pts. - vaccines
126
Herpes Zoster presentation
1. Prodrome: - acute neuritic pain precedes eruption 3-5 days - throbbing stabbing burning senstions - itching fever, headade, allodynia 2. Rash Active - development of grouped vessicles on a erythematous base - follows dermatome and unilateral most often - thoracis distribution most common
127
Herpes Zosters chronic complications
1. . post herpetic nerualgia: lanciating pain that lasts months after resoltution of lesions 2. Herpes Zosters Qphthlmicus- sight threatening linked to trigemial ganglion - begins with sign on nose (hutchinsons sign) 3. Other retinal problems or nerve palsies
128
Herpes Zosters Tx
treat early -72hrs ( lower pain/severity) Antiviral: Famciclovir 500mg TID 7days Valacyclovir 1g TID x 7days - hydration, keep skin clear, pain managment - NSAIDs, narchotic, topical anesthetics for acute - Chronic; tricyclic antidepressets, gabapentin, pregablin * if ocular involvment send right away to an eye doctor (emergency)
129
Herpes Zosters Infectious precautions
- can transmit virus to give someone chickenpox but can not give shingles - avoid pregnent women, infants, and immunocomp - infectious until crusts have healed Prevention: Zostavax or Shingrix** vaccines - approved >50 yo and recommended for >60
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Herpes Symplex Virus -1 | -location and transmis.
Most common oral- cold sores and transmitted by direct contact during viral shedding - can have a very severe primary presentation ( Pharygitis, mouth pain, fever )
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Herpes symplex Virus II | -location and trans.
Most often genital - sexually transmitted - pt may be asymptomatic and still spread the disease - genital herpes can also comes from HSV-1
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HSV presentation
Prodrome: burining, tingling, or pruritis Lesions appear: grouped vesicles on an erythematous base> may crust later - can have lymphadenopathy
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HSV dx
1. clinical presentation 2. Can do viral culture 3. Direct microscopy via Tzanck smear use wright stain> see giant mononucleated cells ( just pos for herpes)
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HSV tx
Start early!!- 72 hours Valcyclovir, Famciclovir, or Acyclovir - can treat before outbreak or chronic suppression which decreases recurrences and asymptomatic sheading
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Epidermal Inclusion Cyst Presentation/ Tx
``` epidermpid cyst - soft, mobile, often central punctum - if infected> erythema and pain Tx: - may spontaneously go away but recur often -kenalog injection, I&D, excision - if infected then I&D, oral abx ```
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Lipomas
Composed of adipose tissue and most common soft tissue tumor Present: soft, mobile, non tender Tx: surgical removal - there is a concern of maligncancy with deeper tumors
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Sarcoma
Rare malignant tumor -usually of soft tissue Presentation: enlarging, painless mass of extremities or trunk Managment: imaging of primary lesion MRI, core needle biopsy, surgical resection, chest CT to rule out metastasis
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Seborreheic Dermatitis risk factors
infants and then again as teenagers M>F in 3rd 4th decade - cause is unknown but possibly a fungus malessezia furfur
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Seborrehic Dermatitis presentation | Infants
Dandruff common, chronic, relapsing dandruff or inflammation - gets worse with stress and when it is cold and dry Infants: yellow greecy scale "cradal cap" and you will see it in the diaper region and axilla Adults: erythematous coalescing macules, patches or plaques areas where there is hair, scalp, eybrows ^ with HIV and parkinsons
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Seborrheic Blepharitis
dandruff around the eyelid - have yellow crust with a greasy appearing flakes and edges are pink Tx: warm compress and eyelid scrubs
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Sebhorrheic Dermatitis Dx Tx
Clinical diagnosis Tx: warm compress for cradal cap and baby shampoo. Can use olive oil to losen up Scalp: antifungal shampoo and topical steroid Ketoconazole (shampoo or cream) Senlenium Sulfide or antidandruff shampoo Face: low pot top steroid, topical antifungal, or combination
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Pityriasis Rosea Etiology
Benign viral exanthems | - common in teens and young adults in the spring or fall
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Pityriasis Rosea Present
Possible prodroms- fver or malaise Herald patch (2-5cm) as primary lesion which is larger than the other ones on the trunk and secodnary lesion 1-2 wks later -pink or slamon, fine scale (collarette scale), oval papulaes and plaques -Christmas tree pattern - usually asymptomatic possible itching
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Pityriasis Rosea Dx/ Tx
Tx: self limiting and will go away on its own - antihistamine for itching and possibly topical steroid ( just for itching) - sun helps it go away faster - can do a KOH prep to make sure its not funcgal
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Lichen Planus presentation
Prurutuc, purple, polygonal, papulaes (4 Ps) -papulosquamous eruption - skin (itchy) genitals nails, scalp, most common- wrist, ankles, shins back and MOUTH (painful) Wickhams striae- tiny white lines running through papules
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Lichen Planus cause
idiopathic: dont know why - 30-60yr olds - immune mediated response - drugs can cause association with hep C Koebner phenomenon- development of lesions in site of trauma
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Lichen Planus Dx/Tx
Dx: punch or shave biopsy Tx: self limiting disorder and resolved 1-2 yrs - topical steroids (high pot) - injection intralesional triamcinolone then: oral steroids, phottherapy, oral retinoids
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Psorisis Etiology/ Risks/
hyperproliferation inflammatory skin disorder -overactive T cells to cause inflamation which shortens skin cell cycle so skin pile up. M=F 20-30 and 50-60 yo genetic- usually have 1st degree relative Risks: genes, infections (strep), medications, stress/skin inj, weather(cold and dry), tobacco or heavy alch
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Psorisis presentation
erythematous with silvery white scale - itchy or burning - can be local or generalized may also have nail pitting and psoriatic arthritis
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Psorisis Vulgaris
most common form - plaques with scale and defined margins - the plaques are symetrical on the body and smaller ones can clump together Koebner phenomenon and auspitz sign
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Guttate Psorisis
Strep infection often preceded this onset - will often resolve on its own but you may get plaque psorisis - little droplets
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Pustular psorisis and palmplantar psorisis
Pustular- such wide spread inflamation may have fever> treated in hospital Palm- debilitating becuase fissures will form so hard to walk and use hands and usually require more exstensive treatment
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Psorisis Tx
sunshine, warm baths, emollients (reduce pruritus), occlusive dressing, rest, ***** do NOT use oral steroids***** Topical: 1.Group 1 or II corticosteroids (high pot) 2-3wks [ good if small TBSA and not in genitals, hand, face] 2.steroid sparing agents [can be used in combination therapy] - synthetic vIt D - coal tar - topical retinoids- tazarotene -totcal caliceurin inhibitors (tacrolimus and pimecrolimus) > use topicals after soaking 3. Phototherapy Moderate to sever: >5% TBSA requires care by derm and wil need photo therp or systemic
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Psoriatic Arthritis Etiology/ present
inflamatory arthritis - 1/3 of pt with psorisis will have this - pain and stiffness usually worse in the morning - usually asymetric - typically of the smaller joints (hands fingers) but also spine - enthesitis and dactylitis (sausage digets)
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Psoriatic arthritis Dx
``` lab findings non-specific - will have elavated sedimentation rate and leukocytosis - usually negative for RF factor lab tests are just to rule out other Dx ***usually just a history and physical - possbile additional immaging ```
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Inverse psorisis
Will often appear in the axilla, genitals | - often not as scaly as other types
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Folliculitis Cause/ presentation
itchy Inflammation of the hair follicle with pustules and papules Infectious: -s. aureus (most common) -"hot tub folliculitis) - gram neg Pseudomonas possibly from a drug interaction
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If folliculitis gets worse what can happen?
can turn in a furnucle and then possibly a carbuncle abscess
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Folliculitis Tx - saphylococcal - gram neg
``` Usually no tx (self limiting) Staphylococcal folliculitls - topical: mupirocin - oral abx: cephalexin If MRSA: clindamycin or doxycyclin Gram Negative folliculitis - Ciprofloxacin ```
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Impetigo eitology and risks
Contagious superficial bacterial infection Kids>adults 1.S. aureus- bullous and non bulllous 1. Ecthyma is usually strep
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Impetigo types
Honey colored crusting- typically on face neck and extremities 1. Nonbullous: most common papules. vessicles> pustules> hone colored ccrusting 2. Bullous- vesicles enlarged and forms bulla 3. Ecthyma- punched out ulcers with overlying crusts - like cigarrette burns
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Impetigo Dx/Tx
``` typically clinical possible culture TX: 1. non bullous and bullous: - - mild abs : mupirocin - mod/sever: dicloxicillin cephalexin 2. Ecthema is always oral therapy (ones above) ```
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Cellulitis etiology and risks
Risks: skin trauma, lymphedema, venous indufficency, obesity, immunosup 1. pus- strep 2. no pus- s. aureus - caused by beta-hemolytic strep, staph
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Types of cellulitis
Expanding redness and not really well demarcated. Pain and swelling 1. Nonpurulent (non pus)- cellulitis or erysipelas - erythema edema warmth 2. Purulent: absess or purulent cellulitis painful fluctuant and erythematous nodule
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Erysipelas
``` Type of non-purulent cellulitis -streptocci bacteria Well demarcated and perfect border of erythema -usually on cheeks and lower extremities - warm. with fever and chills usually in the elderly ```
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Abscess etiology
Type of purluent cellulitis enclosed collection of pus -painful fluctuant erythematoud nodule
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abscess Dx/ Tx
clinical diagnosis- maybe U/S | Tx: I and D - sometimes we test with culture and may need additional abs ( IC, very red
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Cellulitis tx Erysipelas purulent
Cellulitis: oral cephalexin or IV cefazolin Erysipelas: beta-hemolytic strep therapy -cefazolin, ceftiaxone Purulent infection: 1. abscess- I&D +/- abx - trimethoprim-sulfamethoxazole, doxycycline, clindamycin 2. Purulent cellulitis- sim abx to above
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MRSA prevention and control
Hand hyfeine, enviornmental cleaning, contact precautions | - decolonization with chlorohexidine wash and mupirocin ointment intranasally
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MRSA risk factor
Abx, invasive device, chronic wound, hospitalization, group settings, colonization of MRSA,
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MRSA tx
Oral abx: trimethoprim-sulfamethoxazole, doxycycline, clindamycin - tailored to culture results IV abx may be necessary (vancomycin): -if extensive involvement, toxicity, rapid progression, failure PO tx, immunocomp
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Systemic Lupus Cutanious manifestations
1. Discoid lupus: scaly plaques, annular on sun exposed areas 2. Malar/butterfly rash - erythema on cheeks and bridge of the nose - nasolabial folds are spared !
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Lupus Rash DX/Tx
Dx: autoimmune connective tissue disease workup sun protection and smoking cessation - topical or intralesional steroids - Hydroxychloroquine * some people are on medications that cause a lupus rash*
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Erythema Multiforme
acute, immune mediated conditions distinct target like lesions can be associated with viral, bacterial or functions - herpes is most common - can be associated with NSaIDS or abx
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Erythema Multiforme Dx/Tx
Dx: clinical dx may have labs will be non specific inflammatory markers, leukocytosis Tx: symptomatic tratment - usually self limiting -topical steroids, oral antihistamines, anestetic mouthwash - antiviral meds are not indicated
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Dermatitis Herpetiformis etilogy
autoimmune skin condition associated with gluten sensitivity (possibly celiac disease) Sx: pruruitic papules and vesicles herpeticform pattern- forearm, knees, scalp, butt Dx: markers for seriological, biopsies of the lesions (looking through direct immunoflourescence)*** Tx: gluten elimination and dapsone
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Pemphigus Etioogy
life thretening blistering disorder on epidermis - autoimmmune:antibodies can cause acantholysis - genetic, idopathic, drug induced
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Pemphigus presentation
Accantholysis: separation of the epidermis Mucosal involvment - flaccid bullae Nikolsky sign: gentle pressure causes superficial layer to slough off
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Pemphigous Dx/Tx
Physical: acantholysis and Nikolsky sign -biopsy and **perilesional skin biopsy** later can do IIF and ELISA Tx: always indicated **systemic corticosteroids and immunosupressive agents**
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Pemphigoid etilogy
Chronic autoimmune subepithelial blistering condition
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Pemphigoid Presentation
- begin with prurirtis eczematous or uticarial lesions Classic: *tense bullae**urticarial erythematous plaque. on trunk and extremities +/- mucosal involvment
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Pemphigoid Dx/Tx
Dx: biospy *perilesional direct immunoflourensense** Tx: *topical and/or systemic corticosteroids* - immunosupressive agents
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Melasma/Cholasma
aquired hyperpigmentation of the skin. - often with hormones like the pill of pregnancy - regresses within a year Tx: skin lightener and sun protection
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Acanthosis Nigricans
hyperpigmentation velvety plaques | - associated with insulin resistance
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Hirsutism
male pattern hair growth in women | - caused by a variety of things
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Adrenal excess on skin
Cushing syndrome | - increase sebum, acne, androgenic alopecia, hirsutism, striae
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Adrenal insufficency of skin
Addisons disease | - hyperpigmentation of the gums, buccal mucosa, elbows, knees, palms, genitalia
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Thyroid effects on skin
Hyperthyroidism: warm moist skin -pretibial myxedema - non pitting, scaly, orange peel skin Hypothyroidism: dry cool skin
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Porphyria Cutanea Tarda cause /Sx/ risks
deficiency of uroporphyrinogen decrarboxylase- suppose to break down porphyrins Sx: painless sub-epidermal blistering on sun exposed areas Risk: genetic, tobacco, etoh, estorgens, liver disease
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Porphyria Cutanea Tarda Dx/TX
Dx; ^ serum/ urinar porphyrins, ^ liver tests irons stores Tx: discontinue potential cause phlebotomy for the the ^iron wear sun protective clothing
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Pressure injury stages
1: intact skin with localized erythema 2. partial thickness loss with exposed dermis - no adipose visible and no eschar 3. full thickness - adipose is visible with rolled edges but no facia or muscle visible 4. Full thickness skin and tissue loss with esposed muscle, tendon or bone - eschar with rolled edges
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Pressure injury tx:
- redistiribute pressure - local wound care 1. transparent film for protection 2. dressings that maintain moisture 3. debridement of necrotic tissue with appropriate dressing +/-abx
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Tick removal
- grasp tick as close to skin surface - wash area >36hrs ^ risk for lymes RMSF can be after only 6 hrs
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Erythema Migrans
Etiology: borrelia Burgdorferi Pres: bulls eye rash - fatigue, HA, arthralgia,fever - later: cardiac, arthritis, beuro, bells palsy Tx: doxycycline or amoxicillin - can do 200mg dose of doxycycline for prophylaxis is >36hrs
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Rocky Mountain Spotted Fever
Etiology: rickettsia rickettsia 1. non specific symptoms: Fever, HA, arthralgias, nausea 2-14 after tick bite * do not wait for the rash becuase some people dont get it Rash: petechial lesion on ankles wrists then trunk
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Rocky Mountain spotted fever Dx and Tx
Dx: clinical because the serology is retrospective Tx: doxycycline