Dernatology Flashcards

1
Q

What is Cellulitis ?

A

Acute spreading infection of the skin.
(involved dermis & subcutaneous tissue.

Erysipelas - is the superficial form with notable lymphatic involvement.
(typically affects face , lower limbs - bright red raised skin (well demarcated (bordered))

CHARCTERISTICS

  • acute onset of red , painful , swollen skin.
    (area usually has poor borders and is diffuse but may have good borders - but if there are multiple lesion with good border suggests something else)
    (MOSTLY OCCURS ON LEG) - usuallly unilateral - bilateral leg cellulitis is rare.
  • Orange peel appearence (Peau d’orange- pits appear on the skin link on an orange peel - caused by superficial oedema around hair follicles)
  • blisterring within areas of cellultis
  • Bleeding (superfical - may present as petechiae or ecchymoses (bruising occurs from bleeding underneath)
  • Fever (above 38 indicates severe infection)
  • Malaise
  • swollen lymph nodes
  • Lymphangitis - indicates spread along lymphatics to lymph nodes.

if there toe - web abnormalities e.g . tinea pedia , fissures , scaling - could indicate point of entry of pathgen .

RISK FACTORS

  • Injury
  • Weakened immune system
  • Skin condition e.g eczema , athlete’s foot , shingles
  • chronic swelling of arms or legs.
  • Obesity
  • Diabetes (Diabetic foot infections)
  • Hx of cellulitis.

Cellulitis can develop into sepsis if untreated.

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2
Q

Diagnosis of Cellulitis ?

A
FBC 
0 ESR
0 CRP
0 U & E
0 Blood culture & sensitivities. (if the patient needs admitting & is systemically unwell : fever , hypertension , tachycardia etc) , immunocomprimised , may have unusual organisms (immersion injury))

CONSIDER:

Skin swab - when showing systemic illness & obvious open wet wound , skin break , ulcer.
and :

There is a :

0 penetrating injury,

or

0 exposure to water-borne organisms,
or

0 infection acquired outside the UK.

(this applies also skin aspirate (withdrawal of skin fluid from lesion)

SKIN BIOPSY ARE RARELY TAKEN - may be done for differential diagnosis .

X RAY

Cellulitis can develop into osteomylelitis (infection of the bone ) ——–> so X ray can be used if Osteomyelitis suspected .

if Underlying Osteomyelitis present do MRI.

THERE IS OVERLAP BTW OSTEOMYELITIS & CELLULITIS.

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3
Q

Treatment of cellulitis ?

A

(if there is a star , and then another star it means this is where that text continues)

SUSPECTED SEPSIS -

1ST LINE

  • follow sepsis protocol

SEVERE - ANY SITE (NOT NEAR NOSE OR (EYES)

  • Empirical antibiotics
    (1ST LINE - IV Flucoxacllin
    if penicillin allergy (IV Clarithromycin) *

(For site near ears and eyes (ANY SEVERITY)
(1ST LINE - Amoxicillin/clavulanate
2ND LINE - Clarithromycin (or another macrolide antibiotics)- if allergic to penicillin or 1st line combination not possible.) - whether it is IV or oral depends on severity and where oral is tolerated) - if systemic symptoms (IV)

NON SEVERE - ANY SITE NOT NEAR EARS & EYES.

  • Oral Flucoxacllin
    if penicillin allergy (Clarithromycin , Doxycycline) *

The following applies to both the severe & non- severe any site section and areas near ears and eyes.

*
Consider :

  • Analgesia (Para , NSAIDS first and susquent pain analgesia ladder)

-MRSA cover
(Vancomycin
Teicoplanin
Linezolid (for specialist use only).)

  • Fresh water exposure - aeromonas hydrophilla antibiotic cover
    (Ciprofloxacin
    Doxycycline
    Trimethoprim/sulfamethoxazole.)
  • Saltwater exposure
    (Vibro vulnificus anti-biotic cover)
    (Doxycycline)

Re - assess patient for after 48hrs of oral anti-biotics before discharging (if considering discharge)

also re - assess if :
Symptoms worsen, for example:
Significant redness and swelling spreading beyond 48 hours after initial presentation
Pain becomes severe
You suspect systemic involvement
There is no improvement within 2 to 3 days.

ONGOING -

Frequent relaspses

manage predosping factors increasing risk of cellulitis e.g. tinea pedia , eczema , obesity etc.

Consider :

  • Antibiotic prophylaxis.
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4
Q

Caution with Fluoroquinone antibiotics ??

A

They use has been restricted due to irreversible adverse effects : Musculoskeletal or nervous system.

restricted to serious life threatening infections only (not used for self limiting infections)

Should be discontinued at the first signs of a serious adverse reacttion e.g. tendon pain , tendinitis , tendon rupture, inflammation.

EX -
- Ciprofloxacin 
-  Levofloxacin
-moxifloxacin
olofloxacin
etc. 
(end in floxacin)

Avoid use with corticosteriods - could exacerbate fluroquinolone induced tenditis

Report adverse reactions to yellow card scheme.

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5
Q

What is Erythema nodosum ?

EN

A

Type of panniculitis ( inflammatory disorder effecting subcantaneous fat) - self limiting ( if no underlying cause)

CHARACTERISTICS

Erythematous (red ) , tender nodules
(nodule - growth of abnormal tissue (lump above 1cm - can be felt)
Found most commonly at shin / pre tibial area—————————————————–>
These areas then fade into pigmented patches before resolving.
(these different types of lesion can co-exist at different stages as new nodules form and old fade)

Nodule locations

  • Shin/ pre-tibial area
  • thighs
  • calves
  • buttocks
  • upper extremities
  • face.
  • Areas do ulcerate & completely heal

Can be accompied by :

  • Fever
  • joint pain
  • malaise

RISK FACTORS

  • Streptococcal infection - most common cause

0 Sarcoidosis ( EN can be a symptom of this )

0 Tuberculosis - common cause in developing countries

0 Opportunistic infections - all 3 edemic to US

  • Histoplasmsosis
  • Blastoycosis (fungi infection - pulmonary disease (fungi spores inhaled ) - least common of 3 opportubistic infections
  • Coccidiomycosis ( valley fever - endemic to US and those with history of dessert camping or digging) - caused by Coccidioides immitis (fungi)
-Behcet's disease - rare inflammation oof BV and other parts of the body 
typical signs :
O Mouth ulcers
O genital ulcers
O recurrent eye inflammation. 
EN can be a cutaneous manifestation
  • leprosy

-

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6
Q

Diagnosis of EN?

A

FBC ( Leuckocytosis - often present)

Anti - streptolysin - O - titre - elevated in streptococcal infection.

CXR -
Bilateral hilar adenopathy - inidactes sacrodosis

Unilateral hilar adenopathy indicates Tubercolosis , HIstoplasmosis , Coccidiodomycosis brucellosis.

(hilar adenopathy = enlargement of the lymph nodes of the pulmonary hila) - found along bronchi.

Tubercullin skin test , inferferon gamma release assay - postive -Tuberculosis

CONSIDER

Serum ACE levels - elevated in sarcodosis.

skin test for other organsism if other opportunistic infection suspected

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7
Q

Treatment of EN ?

A

Mild to moderately severe

1ST LINE
Bed rest & leg elevation + NSAID + Treatment of underlying cause.

  • have to assess for risk of DVT & if needed give compression socks.

2ND LINE

Oral Potassium Iodide
(Thyroid function should be monitored with long term use due to risk of hypothyroidism due to iodide uptake)

Hyperkalemia -also possible side effect

3RD LINE

Intraleasional corticosteriod injection - Triamcinolone acetonide.

ADJUNCT - Analgesia (aspirin & NSAIDS preffered to Para)
relevant for all above lines of treatment

ERYTHEMA NODOSUM MIGRANS
(variant - nodules migrate )

1ST LINE - Systemic corticosteriods - oral prednisolone

SEVERE REFRACTORY SYMPTOMS

1ST LINE

  • Systemic corticosteriods + treatment of underlying cause (oral prednisolone)

PLUS

Bed rest & leg elevation

ADJUNCT - Analgesia

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8
Q

What is paroncyia ?

A

Paronchyia (Inflammation of the nail appartus)

TYPES

Acute version - Infection on nail folds & periungal tissues (occur around the fingernail/toenail - periungual)
(acutely painful, purulent infection)

Chronic - Barrier damage to nail tissues (cuticle , prximal & lateral nail folds.———————-> this predisposes nail to irritant dermatitis from soap, water , chemicals & microbes etc.

CAUSATIVE ORGANISM

  • Staphylococcus aureus (most common) - can be caused by others , strptococcus & Virus (Herpes Simplex virus ) & Fungi (Candida albicans)

SIGNS /SYMPTOMS - ACUTE

0 Pain
0 Swelling
0 Purulent nail fold.
0

CHRONIC

0 Nail plate irregularities
0 Swelling / redness of nail folds.
0 Missing cuticle
0 Underlying nail plate abnormaities.

RISK FACTORS

  • Micro/macroscopic injury to nail folds - ACUTE
  • Occupational risks (work related trauma (portal of entry) or disruption to nail barrier due to exposure to chemicals )
  • Barrier damage to nail folds , cuticle (CHRONIC)
  • Ingrown nail
  • Chemotherapeutic agents.
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9
Q

Diagnosis of Paronchyia ?

A

0 Swab for gram stain , culture & sensitvity.

0 Swab for Tzank smear - Checks for Herpes Simplex Virus

CAN CONSIDER :

0 Potassium hydroxide or fungal culture ( looking for candida colonisation (not infection)

0 X - ray /MRI -(atypical / resistant cases - checking for osteomyelitis)

Skin / bone biopsy - resistant / atypical cases - check for maligancy & to remove chronically inflame tissue.

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10
Q

Treatment of Paronychia ?

  • ACUTE
A

Acute

Mild bacterial inflection

1ST LINE - Soaks
(warm saline or aluminium acetate soaks)

+ Topical antibacterial - (mupirocin, - bacitracin,

  • fusidic acid
  • polymyxin B/bacitracin/neomycin

+ incision & Drainage (of pus - this the sent for gram stain , culture & sensitivity)

If MRSA positive culture - Oral antibiotic therapy

Severe bacterial infection or more tissue involved

1ST LINE - same as mild but Oral antibiotics are defintely used.

Herpertic infection

Ora; antiviral therapy (aciclovir , valaciclovir , famiciclovir (clovir’s))

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11
Q

Treatment of Paronychia ?

CHRONIC

A

Moisture & irritant avoidance

+ Topical corticosteriof
(Fluocinonide , Clobetasol.)

Treatment of secondary colonisation by yeast or bacteria.
(Clomrimazole solution , ciclopirox suspension - until nail normalised)

2ND LINE
- intra-lesional corticosteriods
(Triamcinolone acetonide)

3RD LINE- Surgery

  • IF UNRESPNOSIVE TO ALL THERAPIES - BIOPSY INDICATED TO RULE OUT MALIGANCY (squamous cell or amelanotic melanoma)
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12
Q

What is retronchyia ?

A

ingrowth of the proximal nail plate into the proximal nail fold.

-suspected when there is peristent paronchyia

TREATMENT

1ST LINE - Nail plate avulsion (remobe nail plate & relieve pressure)
+/- NSAID (Ibu)

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13
Q

Penicillin allergic signs / symptoms ?

A

0 Riased , itchy skin (Hives /uticaria)

0 Coughing
0 Wheezing
0 Tightness of throat - can cuase breathing difficulties.

Severe - analphylaxis reaction - life threatening.
may see:

  • lightheadness
  • breathing difficulties (fast, shallow)
  • wheezing
  • a fast heartbeat
  • clammy skin
  • confusion & anxiety
  • collasping/losing conciusness.
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14
Q

Which groups are susceptible to amoxicillin induced skin rash ?

A

People with:

  • Glandular fever (infectious mononuclesis )
  • Chronic / acute lymphocyctic leukaemia

prescribe with caution - if occurs stop.

rash in this group does not indicate a true penicillin allergy

  • note - amoxicillin is contra-indicated in renal failure.
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15
Q

Treatment of vitiligo ?

A

SEGMENTALL OR LIMITED VITILIGO (cover 2-3% of body surface)

1ST LINE

Topical corticosteriod and/or tarcolimus

mometasone topical , clobestasol topical , taroclimus

2ND LINE - phototherapy

3RD LINE - Surgery e.g punch grafting, epidermal blister grafting , ultrathin epidermal sheet grafting.

WIDESPREAD VITILIGO - more than 3%

1ST LINE - Phototherapy + topical or oral corticosteriod or topical tarcolimus

2ND LINE

Oral cortiosteriod

3RD LINE - Surgery

4TH LINE - Depigmentation therapies
(mequinol/tretinoin topical or monobenzone topical ) -last option or if very widespread (>50 %) or recalcitrant & high visible i.e. face , hands.

PLUS-Supportive therapies - cosmetic camoflage etc. (For all lines of treatment. Limited & widespread)

Diagnosis is clinical.

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16
Q

What is Virtiligo ?

A

Aquired loss of melanocytes causing areas of depigmentat .

RISK FACTORS

<30 years
0 Fhx of vertilgo
0 auto - immune disease
0 chemical contact.

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17
Q

Signs of infected atopic dermatitis?

Complications of infected AD?

A

Infected AD can present with widespread erythema in usual sites of AD.

Infected AD is painful & itchy while normal AD is just itchy.

Bacterial infection

0 fluid oozing from the skin

0 a yellow crust on the skin surface

0 small yellowish-white spots appearing in the eczema

0 Swollen , sore skin

0 feeling hot and shivery and generally feeling unwell

Viral infection

Herpes simplex virus - usually causes cold sores ————————> can develop into ezcema herpeticum (SERIOUS - EMERGENCY- ADMIT TO HOSPITAL IF SUSPECTED)

Ezcema herpeticum (Clusters of itchy blisters or punched out lesions - most common around mouth. )

Ezcema herpeticum is often condused with impetigo ( pl impetigo are often do not feel unwell)

0 areas of painful eczema that quickly get worse

0 groups of fluid-filled blisters that break open and (leave small, shallow open sores)

0 feeling hot and shivery and generally feeling unwell, in some cases

Treatment - Antiviral therapy - aciclovir etc.

may be given antibiotic prophylaxis - if damage to skin normally harmless bacteria on skin can infect it. (secondary bacterial infection)

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18
Q

Treatment of infected AD?

A

Bacterial infection

In people who are not systematically unwell antibiotics are not given rountinely but can be given if thought to be of benefit.

1ST LINE- Flucloaxcillin (or clarithrymocin - in penicillin allergies or resistance to flucloxacillin)

if pregnant & allergic to penicillin - erythromycin

if 1st line does not work prescribe alternative.

IF LOCALISED AREAS OF INFECTION - Topical fuidic acid.

  • prescribe topical emollients , steriods for use after infection has cleared up.

REFER URGENTLY IF Infection not responded to treatment.

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19
Q

Treatment of atopic dermatitis / eczema ?

I have another card that says something different.

A

MILD
1ST LINE

Emollients
+ consider mild corticosteriod

MODERATE

Emollients + topical corticosteriods

2ND LINE - calneurin inhibitors (tarcolimus , pircolimus (pircolimus-mainly used for face & neck ezcema where further steriod use ca cause atrophy etc)

SEVERE

Emollients + topical corticosteriods

2ND LINE - Calneurin inhibitors

3RD LINE - systemic immunosuppressie agents ( Oral corticosteriod)

ADJUNCT - if severe itch or utritcaria (non - sedating anti-histamine e.g. certirizine, loratadine, fexofenadine)

ADJUNCT- consider antiobiotics if infection suspected
(BEWARE OF EZCEMA HERPETICUM)

CONSIDER : IF resistant to corticosteriods (after increasing potency ) or calcneurin inhibitors use UV Light therapy. )

20
Q

What is kerion

A

Abscess caused by fungal infection

- can be seen as a complication of tinea capitis , corporis.

21
Q

What is rosacea ?

A
Long term skin condition - mainly effects face. 
(can resemble acne)
Primarily effects :
- central face
(cheeks, chin, nose , forehead) 
 but can extend upper trunk

SIGNS/SYMPTOMS

  • Facial flushing
  • Redness (eythema) (can be transient but may become persistent as condition develops)
  • papules & pustules
  • Telangiectases (superfical capillaries - hallmarks of condition)
  • roughened skin
  • rhinophyma

0 ocular manifestation (describe having foerign body sensation in eye with tearing , pain and blurry vision.

  • Keratitis
  • episcleritis (inflammation of the episcleral tissue btw conjunctiva and sclera)
  • scleritis
  • horedeolum (stye - small lump caused by infection of glands of eyelid)
  • conjunctivitis
  • Blepharitis (red , swollen , itchy eyes)

Some experience :
telangiectases and erythema of eyelid margin with scaling or none.

  • ## plaque formation
  • MAY OR MAY NOT CO-EXIST WITH ACNE VULGARIS

RISK FACTORS

  • Fair skin
  • hot baths / showers
  • temperature extremes
  • sunlight
  • hot drinks, emotional stress (trigger for flushing)
22
Q

Diagnosis of Rosecea ?

A

Clinical

Consider :
skin biospy

  • antinuclear antibody titre - rule out SLE.
23
Q

Treatment of roseca ?

A

ERYTHEMA SUBTYPE -

1ST LINE

Topical brimonidine 0.5 gel.

MILD TO MODERATE PASTULES / PAPULES

  • Topical ivermectin (antihelminthics - kill helminthics - worm like parasites e.g tapeowrms , roundworms , flukes etc)

2ND LINE - Tpical metronidazole , azeliac acid
(if ivermectin - not possible /tolerated e.g pregnancy)

IF MODERATE - use Ivermectin + oral doxcycline.
(if Iver not possible metro or azeliac) (If doxy not possible - oxytetracycline , tetracycline , or ethyromycin for pregnant or breastfeeding)

PHYMATOUS PHENOTYPE -

1ST LINE - Antibiotic
( Oral doxycycline)

OCUCLAR MANIFESTATIONS

  • lid hygeine measures ,
  • artifical tears (eye dryness present)
24
Q

What is Seborrhoeic Keratosis ?

A

Multiple benign tumours of the skin

COMMON LOCATION

0 Forehead
0 Torso ( Chest & back)

APPEARENCE

(Overall - well - circumscribed stuck on plaques or papules or may look like warts- not usually need treatment (bcc benign) but if they become irritated , itchy or displeasing can be treated.

0 Multiple Lesion - stuck on appearence

  • can be slightly raised or flat.
  • lesions are normally painless

0 Wart-like texture

0 Yellow to light brown colour
(can also be grey black)

0 can sometimes see some yellow white horn pearls on surface of esions

0 Itchy

  • CAN LOOK LIKE MALIGANT MELANOMA - Some features differientitate it .

RISK FACTORS

  • Age over 50 years (80-100%)
  • White skin
  • family history
  • sun/UV expsoure
25
Q

Diagnosis of SK?

A

Dermoscopy -n
(looks for features of seborrhoeic keratosis (e.g horn pearls / Mila -like cyst (white or yellowish round structures that are intra-epidermal keratin filled cysts.)

0 Biopsy & histopathology examination

0 Reflectance confocal keratosis (RCM) form of non-invasive imaging

  • RCM features that indicate the diagnosis of seborrhoeic keratosis are: cerebriform surface structures; keratin-filled invaginations; corneal pseudocysts; a regular honeycomb pattern at epidermal layers; cords and polymorphous papillae at the dermo-epidermal junction; melanophages and looped vessels at the papillary dermis; and the absence of RCM features suggestive of malignancy.
26
Q

Treatment of SK?

A

Treatment is not usually needed unless irritated , itchy or dispeasing to patient.

Irritated or itching lesions

1ST LINE - corticosteriods

RAISED SEBORRHOEIC KERAROSIS

1ST LINE - Curettage or cautery

FLAT SK

1ST LINE -Cryotherapy

2ND LINE - Curettage

3RD LINE - laser , dermabrasion , chemical peels or tretinoin.

27
Q

SK VS Malignant melanoma ?

A

Shape

0 SK - round or oval shaped

0 MM - may have sides that do not match in size or shape.
- borders fuzzy , ragged , blurred edges.

0 COLOUR

SK - Can be light brown , yellow (flesh coloured ) & brown or black .

MM - Brown or black
(can be a variety of colours within the same mole.

EVOLUTION

0 SK - lesions typically stays the same colour & shape

0 MM - Clour & size can change over time

OTHER FEATURES

0 MM - may bleed or ooze

0 SK - can have horn pearls in lesions

28
Q

What is Leukoplakia

A

White plaques of the mouth - pre-maligant condition.

(diagnosed when other conditions causing white lesions have been ruled out. - DIAGNOSIS OF EXCLUSION

0 Candida & linchen planus *( are differential diagnoses- these white lesions can be wiped/rubbed off whilst leukplakia cannot.

linchen planus - rash affects body including mouth - leaves white patches in gums , tounge , cheeks also raised , shing red purple blotches on arms , leg/body etc amongst other things.

LOCATION - in mouth

0 e.g . Tounge , inside cheeks , buccal / labial mucosa , under tounge etc.

TYPES

0 Homogeneous Leukoplakia - uniform white lesions - most common

0 NON HOMOGENOUS

0 Speckled leukoplakia - (predominately white lesion - fissured appearence with area of red atrophic areas ireehuarly scattered with keratotic white comonent

0 Nodular - red & white lesion

0 Erythroleukoplakia (white and red lesions)

0 Ploliferative verrucous leukoplakia ( most risk of maligant transformation )
- LEAST COMMON TYPE

0 Sublingual Leukoplakia.

other types

  • Oral hairy LP - caused by EBV (epstein barr virus) - patches look hairy.
  • the higher the degree of dysplasia (change in cells - & maligant transformation , the more dangerous and potential for cancer development)

RISK FACTOR

  • Male
  • Age > 40 years
  • tobacoo use]- alchohol
  • genetic pred isposition
  • Immunosuppression
  • Fanconi’s anaemia.
29
Q

Treatment of Leukoplakia ?

A

1ST LINE

Removal f contributory factors ( somking cessation , alcohol abstinence / reduction. , emilation of bete lquid use (some sort of smoking concotion)

30
Q

Treatment of Leukoplakia ?

A

1ST LINE

FOR ALL

Removal f contributory factors ( smoking cessation , alcohol abstinence / reduction. , emilation of bete lquid use (some sort of smoking concotion)

HOMOGENEOUS LP

1ST LINE
Removal of CF + Observation with biopsy as needed (can do repeat incisional biopsy if changes occur - with excision of any confirmed dysplasia.

SUBLINGUAL LP

1ST LINE

Removal of CF + excision or ablation e.g scalpel excision , laser ablation , cyrotherapy.

SPECKLED OR PLOLIFERATIVE VERRUCOUS LEUKOPLAKIA

1ST LINE

  • Removal of CF + Excision or ablation.
31
Q

What is Molluscum contagiosum?

A

Skin infection caused by Molluscum contagiosum virus (MVS) causes lesions .

  • Contagious (skin to skin , sexual transmission , indirectly - formite surface e.g towels , flannels.
    (THIS CONDITION COMMON IN CHILDREN , YOUNG ADULTS)

SELF - LIMITING , SPONTANEOUS RESOLUTION usually IN 1-2 YEARS.

APPEARANCE -

0 Pinkish , pearly white papules

0 Umblicated lesion (have a central depression)

0 up to 5mm in diameter.

0 erythema can surround papules

0 can have pruritus

RISK FACTORS

  • Close /sexual contact with infected individual
  • Atopic dermatitis (impaired skin barrier)
  • Immunocomprised
  • Tropical climate
32
Q

Diagnosis of M contagiosum?

A

0 Dermoscopy - can be used to confirm diagnosis .

0 Cutterage isopsy - can be used to confirm Diagnosis.

0 Hematotoxylin and eosin staining - provides definite diagnosis (find henderson - patterson bodies)

Full sexual health screen (including HIV)- for anogenital lesions & refractory/extensive disease.

33
Q

Treatment of M contagiosum?

A

1ST LINE

Observation - self limiting condition .

2ND LINE - Topical treatment (for those who desire treatment (anxiety , discomfort , appearence etc).

  • Potassium hydroxide topical (1st)

other options - salicyclic acid , benzoyl peroxide topical, tretinoin topical.

3RD LINE - Cryotherapy

IF THEY HAVE ANOGENTITAL LESIONS -

34
Q

Treatment of M contagiosum?

  • anogenital lesions
A

1ST LINE - conservative measures + sexual health screen

2ND LINE - Cryotherapy , cautery or curettage

(conditions for treatment of anogential lesions include if patient prefernce , extensive/persistent disease , cosmetic , fearing of spreading /scarring , symptomatic e.g itchy , inflammation)

3RD LINE - Topical treatment e.g. potassium hydroxide , imiquimod , podophyllotoxin.

35
Q

Treatment of M C ?

  • Atopic dermatits ?
  • eyelid lesions
A

1ST LINE - Optimise treatment of dermatitis

  • adjunct - consider referral to dermatology

Eyelid lesions - observation and consider referral to ophthalmology.

36
Q

Treatment of M C?

- Immuncomprised
and those who are immunocomprimised with anoogenital lesions , eye lesions , atopic dermatitis

A

can be immunocomprised sue to HIV infection , immunosupression , SLE , sarcodosis , neoplasia.

JUST IMMUNOCOMPRISED

1ST LINE - Treat underlying condition

  • consider topical treatment or physical (cutterage , cautery , cyrotherapy )
    e. g

IF HIV cause - ART - Antiretroiral (cidofovir topical) can also use other topicals e.g. podophyllotoxin therapy used. —–> if does not work physical treatments.

ANOGENITAL LESIONS -

1ST LINE - Treat Underyling cause

Adjunct - topical or physical therapy
( if few , discrete lesions - physical therapy more apporiate)

IF HIV Cause - treatment said earlier.

ATOPIC DERMATITIS - optimal treatment of AD.

  • refer to dermatology

EYELID Lesion

  • refer to opthalmology
37
Q

Shingles treatment ?

A

MILD pain - paracetamol , co- codamol or NSAID.

Oral antiviral treatment
e.g aciclovir , valaciclovir , famciclovir with 72 hours of rash onset- (if 72hours not possible within 1 week), if have not be admitted to hospital or need specialist treatment .
ALSO need any of this criteria:

0 Immunocomprimised

0 Non-truncal involvement (e.g involves the neck , libs or perinum)

0 Moderate to severe rash

0 Moderate to severe pain
(SO DONT TREAT IF PAIN/RASH IS MILD)

  • Consider oral corticosteriods in combination with oral antiviral (only used together) in first 2 weeks in immunocomptent people with localised shinges & severe pain
  • also consider in over 50s to reduce risk of post - herpetic neualagia ( pain persistin or appearing more than 90 days after rash onset) - most common complication of shingles

(Shingles caused by Herpes Zoster)

MILD pain - paracetamol , co- codamol or NSAID.
(SEVERE pain - if treatment with opiod is being considered e.g morphine refer to specialist)

2ND LINE - Amitriptyline , duloxteine , gabapentin or pregabalin.

In childern - trail of Para , aviod NSAIDS.

38
Q

When do you admit someone with shinges to hospital ?

A

0 Immunocomprimsed child

0 Immunocomprised adult , with or without severe rash , widespread rash , systemically unwell.

0 Visual symptoms

0 Unexplained red eye

0 Shingles in opthalmic part of trigeminal nerve especially if :

  • Hutchinson’ sign - rash on tip of nose , side , root of nose (in dermatome of nasocillary nerve —————–> can lead to eye inflammation & permanent corneal denervation)
39
Q

Define these key terms ?

  • Exanthem

- Macule

A

Exanthem - rash or eruption of rash.

macule - flat , distinct discoloured area of skin.

40
Q

What is Verruca Vulgaris

A

OTHER NAMES - Common warts

Verruca - wart of any kind

vulgaris (means the normal / most common form a certain disease e.g. most common wart disease)

CAUSES

  • HPV - human papillomavirus

SIGNS / SYMPTOMS

0 (Appearence)

  • Round raised papule (characteristic appearance of common wart )
  • Rough , scaly appearence e.g. Hyperkeratosis (thickening of outer layer of skin) - MAY BE SEEN
  • Fissuring (fissure , bleeding —> pain) - MAY BE SEEN

0 Colour - greyish - white , light brown - characteristic.

0 Size - average 5mm ( up to 1 cm)

0 Location - most commonly found around hand, fingers or periungual area (around finger nail or toenail)

  • can have sati;ite lesions (smaller ones around bigger one )
  • may see tiny black dots - thrombosed capillaries.
  • immunocomprised patients - tend to have more lesions , increased lesions size , different morpholgies.

RISK FACTORS

  • Water immersion (swimming , regular dishwashing etc.)
  • Occupations involving handling meat or fish.
  • Nail biting (risk of periunginal lesions)
    (may cause warts to spread to mouth & face also)
  • Age - under 35 (most common in children & young adults ) - CAN HAPPEN AT ANY AGE.
  • Immunocompromised
41
Q

Diagnosis of Verruca vulgaris ?

A

Clinical diagnosis

if unsure - consider :

0 Skin biopsy - Histopathology- G - to rule out other differential diagnosis (HPV - induced squamous cell carcinoma , seborrhoeic keratosis , fibrokeratoma etc.

0 Immunoperoxidase stain - presence of HPV antigen

0 Skin culture - done to rule out deep fungal , bacterial etc in immunocomprimsed patients with severe lesions.

42
Q

Treatment of Verruca vulgaris ?

A

Most people do not need treatment ( may resolve spontaneously within months/2 years. (can take much longer for some)

If treatment needed (due to pain , being unslightly , persisting , requested by patient:

1ST LINE

0 Cryotherapy with liquid nitrogen (only for adults & older children) - NOT YOUNG CHILDREN

or Topical salicyclic acid (up to 12 weeks )

2ND LINE - (Often 1st tried in primary care - if dont work refered to secondary care and these methods can be used :

  • Physical ablation (surgery , laser treatment , photodynamic treatment)
  • Immunomodulatory treatments e.g. Topical Imiquimod 5% , intralesional interferon , topical sensitizers (Squaric acid)
  • Anitimiotic agents (disrupting mitosis ) e.g.
    0 Topical /oral retinoids
    0 Topical Podophyllotoxin
    0 intralesional Bleomycin
  • Virucidal treatments - fomaldehyde and Glutaraldehyde.
  • Cantharidin (potent blistering agent )
  • Advice to avoid
  • sharing towel , socks (contagious)
  • biting nails

FACIAL WARTS NOT ROUTINELY TREATED IN PRIMARY CARE - REFER TO DERMATOLOGY

43
Q

What is Haemanigioma?

A

OTHER NAMES :

  • Cherry angioma
  • Campbell - De Morgan spot
  • Senile Angiomas

Type of Benign vascular lesions

PATHOPHYSIOLOGY - Hemangiomas are bright red birth marks that show up at first weeks of life - looks like RUBBERY RED BUMP (made up of extra BV in skin)

start of as blue /pink macules / patches then become elevated above surrounding skin (Prolifertative phase) (DIFFERENT COMPARED TO OTHER VASCULAR LESIONS) - stage usually ends at 5 months.

Infantile haemangiomas/ strawberry marks - (described in above paragraphs)

Congential haemangiomas - fully formed at birth

Haemangiomas - also used to describe acquired lesions in adults (cherry Haemgiomas /angioma) - DO NOT REALLY UNDERGO INVOLUTION.

Some of the angiomas will be INVOLUTING (skrink & lighten over time ) while others are NON - INVOLUTING.

SIGNS/ SYMPTOMS

  • Red , pink blue colour (sign vascular lesion present)
    (can also be dark red (look slightly purple ) - cause it to look like early melanoma)
  • Flat patches / macule or nodular character
  • Rapid growth (infantile Haemangiomas - proliferate rapidly )
  • can be ulceration & bleeding .
    (ulceration can cause significant painful lesions , other haemangiomas not usually painful)
  • Lesions in lumbar sacral area - may signal underlying spinal dysraphism (baby’s spine / cord do not form properly - defects)
  • Lesions in bread area / lower face / neck - may associated with laryngeal involvement - May present with Stidor.

RISK FACTORS

0 Hx of low birth weight
0 Premature birth 
0 White 
0 Female 
0 Maternal multiple gestation (twins , triplets etc - highter risk of lower birth rate , premature )

0 Advanced maternal age - risk of LBW , premature.

44
Q

What is multifocal infantile haemangiomas ?

A

More than Five Haemangiomas on the skin

increased risk of internal involvement (affect internal organs - extracutaneous involvement e.g LIVER , GI)

45
Q

Diagnosis of Haemangiomas ?

A

0 Doppler ultrasound - Used to distinguish haemangiomas from vascular malformations e.g. ( Venous / arterial /lymphatic malformations )

CONSIDER -

0 MRI of angioma - to determine extent & assess relationship with other stuctures (e.g. organ involvement)

0 Biopsy of lesion (if maligant tumour with significant vascular component is suspected/is possible )

46
Q

Treatment of Haemogiomas?

A

Corticosteriods - oral / topical (cream) / injectable
e.g.
0 Pred oral
0

47
Q

Treatment of Haemogiomas?

A

1ST LINE

Corticosteriods - oral / topical (cream) / injectable
e.g.
0 Pred oral
0 Triamcinolone acetonide - intra lesional

type used depends on whether angioma is superfical or deep
if well localised without deep extension - (intralesional can be used)
oral / systemic are avoided if possible - more side effects.

0 Beta blockers -

  • Timolol topical (can be considered if oral not warranted or contraindicated ( good for superficial lesions)
  • Propranolol oral ( be careful in those with PHACES syndrome - propanolol induced hypotension)

2ND LINE

0 Surgery (excision ) - if other measure inadequate & lesions threatens functional & cosmetic intergrity.

  • sometimes used for patients where involution is complete to improve cosmetic appearence if needed. (e.g. unsightly fibro - fatty tissue)

or

0 Laser treatment

ADJUNCTS

  • Emollient creams
  • Topical antibiotics (metronidazole - 1st, mupirocin topical)
  • Analgesia (para , topical lidocaine (local anesthetic )
  • Dressings