Transcript f24c081643806e5

Assistant Professor Family Medicine
Qassim Medical College
1429 - 1430
Learning Objectives
To enable the student to:
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Approach the most common skin lesions
Diagnose and differential diagnosis of the most
common skin problems.
Management of these cases in Family Practice
Impact of psychological effect of these problems.
When to refer
CASE STUDY
 A I5-year-old female comes to your office with " zits.“
She has been attempting to treat these with frequent
washings with a buff puff and avoidance of cosmetics.
She is very distressed and breaks down crying.
She is afraid that "no boys will ever go out with
someone with such an ugly face.“
Her past history is unremarkable.
She is taking no medications at present.
She has no allergies.
Her family history is unremarkable.
On physical examination the patient has multiple
maculopapular-pustular lesions with comedones on her
face and back.
No other abnormalities are found on examination.
What is the diagnosis in this patient?
a. rosacea
b. drug eruptions
c. Acne vulgaris
d. Eczema
e. folliculitis
 A disorder characterized by comedomes,
papules and pustules centered on the pilosebaceous follicles.
Affects
most teenagers, usual age of onset
is between 12 – 14 yrs
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androgens stimulates sebum secretions.
Genetic
The
factors may be important
role of corynebacterium acnes is
uncertain
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the face (most common)
 Neck
 Chest
 Back
 Shoulders
 The upper arms
 They can also occur on scalp
and legs.
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Environmental factors: humidity and heavy
sweating .
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hormonal components of milk and/or other
bioactive molecules in milk could exacerbate
acne
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acne severity did appear to have some
correlation with stress around the time of
school examinations ? !
consists of small lesions,
such as:
 Black heads,
 White heads or
 pustules,
which appear at or near
the surface of the skin
- Mainly comedones,
- With an occasional small
inflamed:
. papule or,
. Pustule;
- No scarring present
This photo shows comedones, papules and
pustules on the face of an acne patient
In moderate to moderately severe
acne, numerous whiteheads,
 blackheads,
 Papules
 Pustules
 comedones
- Cover from ¼ to ¾ of the face
and/or
- Other affected area
is characterized by:
-deep cysts,
- inflammation,
- extensive damage to the
skin and scarring
- It requires an aggressive
treatment regimen and
- should be treated by a
dermatologist
 The
tendency to develop acne is an inherited.
 Acne can’t be prevented,
 Careful cleanliness and gentle skin care can
help to lessen the effects .
Treatment protocol for mild to moderate acne
a. Begin with topical benzoyl peroxide 2.5 %. Increase to 5% and
10% rapidly. apply twice a day.
b. Add topical tretinoin, applied at bedtime.
Remember to tell your patient:
 To expect redness and irritation of the face initially.
 Urge them not to discontinue.
c. Add topical erythromycin or topical clindamycin.
a systemic antibiotic from the beginning.
d. You may need to prescribe a systemic tetracycline to the
topical benzoyl peroxide and topical tretinoin. Continue the
topical antibiotic.
About Acne Treatment approach
 The
key to getting rid of acne lesions and
preventing new ones.
 Psychological Support.
 Resolution takes time.
 What works for one person may not work
for another.
 A dermatologist’s help may be required.
Treating Mild Acne
 Gently washing the affected area(s) with
warm water and a mild soap twice a day to
remove dead skin cells and excess oil.
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A topical over-the-counter acne treatment
containing benzoyl peroxide or salicylic acid.
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Acne medications can cause an initial
worsening of symptoms.
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Following the Acne Skin Care Guidelines
Good skin-care program
 cleansing
gently and non abrasively.
 using oil-free products,
 leaving the skin lesions alone.
 It is also important to match the vehicle
(lotion, cream, gel, or solution) with the
skin type.
 Gels and solutions tend to be more drying,
whereas lotions and creams are
somewhat more emoliant .
Patients with acne should avoid
 occlusive
clothing
 rubbing face or picking skin .
 Oily cosmetics
Treatment measures:)summary)
A.
Non-pharmacologic:
Gentle face washing, avoidance of manipulation of acne lesions, using
water based cosmetics only, and using oil-free moisturizers only.
B. Pharmacologic:
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Step 1: Begin with benzoyl peroxide gel.
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Step 2: Add topical tretinoin or adapalene (Consider using step 1 in the
morning and step 2 in the evening)
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Step 3: Add topical antibiotic (erythromycin, clindamycin). (Consider using
step3 along with a combination of steps1 and 2)
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Step 4: Add systemic antibiotics, such as tetracycline, minocycline,
doxycycline, erythromycin, clindamycin,or trimethoprimsulfamethoxazole).Consider using a combination of steps 1, 2, 3, and 4(.
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Step 5: For severe nodular-cystic acne only,
use oral isotretinoin (associated with serious, dose-related side effects)
Common myths believed by patients
:
A. Acne is caused by failure to wash away dirt. Not true –
Acne can be made worse by washing too vigorously.
B. Too much junk food causes acne. Not true –
No connection between diet and acne.
C. Stress can cause acne. Not true –
However,stress can increase a nervous tendency to pick, squeeze,
and/or rub pimples and make them worse.
D. Acne is a normal adolescent problem of no consequence that should
be allowed to run its course. Not true –
Prompt treatment can prevent severe outbreaks and avoid physical
and emotional scarring.
E. Acne vulgaris always clears up after adolescence.Not true,
More than 10% of individuals continue to have this form of acne well
into adulthood.
Definition:
 Acni-form eruption that affects middleaged patients.
 It is characterized by papules and pustules
occurring on a background of erythema and
telangiectasia of facial skin.
Complications:
Thick skin forms on face (especially on
nose). This condition is called rhinophyma.
Treatment:
a. Step 1: topical metronidazole
b. Step 2: systemic therapy: tetracycline,
erythromycin, minocycline, doxycycline,
metronidazole, or isotretinoin
c. surgery for severe rhinophyma.
Rosacea is distinguished from acne
vulgaris by:
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Affects cheeks, nose, center of forehead
and chins
Sparing of periorbital
Intermittent flushing followed by fixed
erythema & telengectasia
No comedones, but papules, pustule and
nodules.
Rhinophyma and lymph edema may occur
Occular complications ( blephritis, keratits
and corneal ulceration)
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Chronic less vesicular and exudative, more scaly,
pigmented and thickened.
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More likely to be lichenified and have fissures.
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Asthma and rhinitis are often associated with the atopic
form.
Etiology:
 Constitutional or exogenous,
 frequently both,
 and impossible to differentiate
on clinical appearances alone
 Atopies are more prone to
irritant hand eczema.
Clinical Patterns: Constitutional
patterns of hand eczema
include:
 recurrent pompholyx;
 vesicular/hyperkeratotic hand
eczema and
 hyperkeratotic hand eczema.
Exogenous patterns of hand eczema include
1- Irritant patterns · 'Ring' eczema from wet work/detergents:
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'Web' eczema/dorsum of
hands from wet work.
'Finger-tip' and 'palmar'
patterns due to wet cloths,
frictional factors, etc.
'Patchy' / 'discoid' patterns.
Exogenous patterns of hand eczema include
2- Allergic patterns :
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'Non-specific'. Most cases, e.g.
with perfumes, preservatives,
etc., will be missed unless
routine patch testing is
performed.
'Specific patterns', e.g. rubber
glove dermatitis, ring dermatitis
and fingertip eczema.
Atopies may also develop type I
contact urticaria or protein
contact dermatitis from food
handling and preparation.
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Identify the cause.
Patch testing is helpful.
Provide hand care advice, e.g. cottonlined PVC gloves for wet work and
frequent applications of emollients.
Potent steroids with or without
antibiotics can be used for secondary
infection.
Atopies with a history of eczema should
be given employment counselling.
Investigations . Usually clinical
diagnosis
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Atopic: patch testing, serum IgE
levels, specific antigen detection
(Radio Allergo Sorbent Test=RAST(
 Contact: search for any possible
sensitizing antigen (patch test if
necessary).
 Biopsy may be required. Exclude
fungal
 infections by culture of scrapings
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Acute:
apply wet dressing impregnated
with 1% ichthamol in calamine
lotion.
Each dressing followed by a
smear of corticosteroid cream or
lotion.
Systemic antihistamines can be
used to control itch.
Subacute: steroid creams or
lotions (dose depends on the
severity of the attack.
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Chronic:
steroids in an ointment base and zinc
cream.
Treat the associated dry skin with
emollient (e.g. oilatum).
Avoid perfumed soaps.
Bacterial super-infection can often be
controlled by the incorporation of
antibiotics (e.g. neomycin)
A short course of systemic
corticosteroids may be needed in severe
attacks.
Avoid precipitating antigen if possible.
Complications:
 Higher incidence of warts and fungal
infections in the atopic form.
 Occasionally widespread viral infections
e.g. herpes simplex.
 Time may be lost from work or alternative
employment may be necessary.
Fungal Infections
Etiology:
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Ringworm (tinea) infections enzymaiically digest keratin.
Obtain scrapings for microscopy and culture before beginning
treatment.
Infections are classified as follows:
Tinea pedis (athlete's foot) is due to Trichophyton rubrum, T.
mterdigiiale and Epidermophyton fioccosum.
It is precipitated by communal showering, swimming pools and
occlusive footwear.
Fungal Infections
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Tinea manuum is predominantly due to T. rubrum.
Tinea cruris is caused by the same organisms as tinea
pedis.
Tinea corporis is caused by all types of ringworm.
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Tinea pedis scaling, fissuring or
irritation, especially between 4th
and 5th toes. It may
 also be caused by bacteria,
Candida or sweating, and may
 produce erythema, scaling and
occasionally
 vesicles /pustules on sole of foot
 Tinea manuum characteristically
unilateral
 with scaling of the palm.
 Exaggerated skin markings are
also seen.
Contd
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Tinea cruris:
occurs predominantly in young men.
there is well demarcated erythema and scaling in the groins
with central clearing and an 'active' edge
Tinea corporis:
 discoid, scaly areas which spread slowly
 with central clearing. The edge of the lesion may bevesicular
Treatment
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Topical antifungal agents e.g. Whitfield's
ointment or imidazole creams/lotion, Castellani's
paint for interdigitai maceration.
Giriseofulvin 500 mg daily (with food) for 4- 5
weeks or,
 one of the newer oral anti-fungals such as
terbinafine or miconozole may be necessary for
T, rubrum or more extensive infections.
Etiology:
 Candida albicans-, moisture, warmth,
occlusion,
 antibioucs, steroid treatment, pregnancy
and immuno-suppression all predispose.
 Clinical features:
 Erythema with scaling and papular or
pustular satellite lesions at and beyond a
well defined irregular edge,
 affecting skin folds, especially in obese
patients (intenrigo).
 It may be itchy or sore.
Treatment:
 Nystatin or imidazole creams;
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eradication of gut and vaginal yeast
carriage, oral fluconasole in resistant
cases.
Tinea Versicolor Pityriasis
versicolor
Etiology: Pityrospavm orbiculare
• The condition is common in hot,
humid environments.
• The condition presents as hyperpigmenied or hypopigmented macules
• Fine superficial scales mostly on the
trunk or upper limbs and
• Often more conspicuous following
sunbathing.
Treatment
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Selenium sulphide or ketoconazole shampoos and,
 topical imidazole creams.
 Oral miconazole (nizoral) may be used in resistant
cases.
 It may take several months for normal skin color to
return,
and the condition tends to relapse.
CHICKEN POX (VARICElLA)
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DNA herpes virus spread by
droplets or by direct contact with
skin lesions.
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Highly infectious and usually affects
children.
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One attack usually produces
immunity, but;
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reactivation occurs and produces
herpes zoster (shingles).
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Incubation period 14-21 may be
disseminated in the immunocompromised host..
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Clinical features
Mild fever,
The rash appears in crops
 characteristic rash on trunk spreading to the face and
limbs (initially macular, then popular, vesiclar and finally
pustular).
 Investigations .
 Clinical diagnosis.
 Rising antibody titre.
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Complications
2ndary infection, pneumonia
(leaves calcified scar on CXR),
 proliferative glomerulonephritis,
 demyeilinating ecephalitis.
 Manaagement Varicella:
 symptomatic.
 If secondary skin infection occurs
use topical chlorhexidine. Oral
augmentin.
 Human anti-varicella
immunoglobulin can be given to
the immnocompromised
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Etiology Varicella-zoster virus
(dormant in dorsal root ganglion
after childhood chickenpox).
Clinical features:
Pain in the affected dermatome.
After 1- 3 days, there are
clustered, red papules which
become vesicular then pustular.
There may be fever, malaise
and lymphadenopathy. Pain
may persist for months.
Involvement of ophthalmic
division of trigeminal nerve may
cause keratitis/blindness.
Dissemination occurs in the
immuno-suppressed
Treatment:
 Use topical antiseptics, idoxuridine,
 or acyclovir for cold sores,
 and oral acyclovir for severe/generalized
herpes.
For post-herpetic neuralgia,
 use analgesics, carbamazepine, tricyclic
antidepressants
 Oral steroids, if given early.
Etiology:
 Psoriasis affects approximately 2% of the
population.
 Genetic factors are important: 40% of
patients have a positive family history.
 There is a rapid epidermal transit time with
increased epidermal cell production
Clinical features :
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Plaque psoriasis; characterized by:
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well-demarcated, erythematous areas covered with thick, silvery scales
(Pinpoint capillary bleeding occurs when scales are removedSymmetrical plaques commonly affect extensor surfaces, especially the
elbows and knees.
The condition frequently affects the scalp and sacrum but patches may
occur anywhere on the body and,
at site of trauma (Koebner phenomenon) .
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Guttate (and exanthematic) psoriasis:
commoner in the young and
often precipitated by a streptococcal sore throat.
Multiple 'rain-drop' lesions occur suddenly on trunk
and limbs.
 The condition may resolve spontaneously,
 or individual spots may enlarge and turn to plaque
psoriasis
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Pustular psoriasis:
 rare generalized form which can be
facial.
 Patients are often erythrodermic
with sheets of sterile pustules
 associated fever, malaise and
leucocytosis.
 Flexural psoriasis: the affected
psoriatic skin loses its characteristic
silvery scale, but the welldemarcated erythematous areas
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Erylhrodermic psoriasis:
 Persistent palmoplantar
pustulosis:
 Scalp psoriasis:
 Psoriatic arthropathy;
commonly affects the
terminal interphalangeal
joints and sacro-iliac
joints
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Topical steroids: Controversial effective, but
continued use may lead to lessening of effect
 Another treatment modality, e.g. tar; effects of a
coal tar preparation (at night), remain very useful
for intertriginous areas.
 Tar: can be used , but replaced by anthralin or
dithranol (tar stains clothes)!!
 Dithranol: useful for plaque psoriasis inpatients
and replaced tar
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Ultraviolet light (UVB): E0-E1 dose alone or combined
with tar/tar baths.
A newer treatment combining psoralen with UVA (PUVA)
is even more clearing extensive refractory psoriasis
Vitamin D, ointment (calcipitriol): a new topical treatment
for psoriasis, with an efficacy equivalent to topical
steroids.
Systemic therapy: cytotoxic drugs, e.g. methotrexate,
cyclosporin, etc. are treatments normally only initiated by
dermatologists.
Scalp psoriasis regimens: keratolytics, tar shampoos,
topical steroids as lotions/gels.