COMMON DERMATOLOGICAL PROBLEMS LECTURE NOTES
COMMON DERMATOLOGICAL PROBLEMS LECTURE NOTES
DERMATOLOGICAL
PROBLEMS
PRESENTERS;
MRUMA E, ROBERT E, MWANGANIKANI E.
SUPERVISOR;
PROF. PALANGYO
Outline
• Introduction
• Common dermatological conditions
• Skin infections
• Eczema⁄ Dermatitis
• Papulo-squamous eruptions
• Vesiculobullous eruptions
• Inherited skin disorders
• Pigmented lesions
• Malignancy
• references
Introduction
• Skin diseases have a high prevalence throughout the world. In
developing countries infectious diseases such as TB, leprosy
and onchocerciasis are common whereas in developed
countries inflammatory disorders such as acne and eczema are
common
Primary lesions are either the first visible lesion or involve the initial
skin changes. The terms used to describe primary skin lesions include
the following:
• Macules are nonpalpable lesions ≤1 cm that vary in pigmentation
from the surrounding skin, Patches are nonpalpable lesions >1 cm.
• Papules are palpable, discrete lesions measuring ≤5 mm in diameter.
They may be isolated or grouped.
• Plaques are large (>5 mm) superficial slightly raised lesions, often
formed by a confluence of papules.
• Nodules are palpable, discrete lesions measuring ≥5 mm in diameter.
They may be isolated or grouped. Tumors are large nodules.
• Telangiectasia is a dilated superficial blood vessel.
• Purpura are red-purple lesions that do not blanch under pressure,
resulting from the extravasation of blood from cutaneous vessels into
the skin. Purpuric lesions can be macular or raised.
Secondary lesions of the skin represent evolved changes from the skin
disorder, due to secondary manipulation or as a result of infection.
Examples include:
• Excoriation describes superficial, often linear skin erosion caused by
scratching
• Lichenification is increased skin markings and thickening with
induration secondary to chronic inflammation caused by scratching
or other irritation.
• Edema is swelling due to accumulation of water in tissue .
• Scale describes superficial epidermal cells that are dead and cast off
from the skin.
• Crust is dried exudate, a "scab".
• Fissure is a deep skin split extending into the dermis.
• Erosion is a superficial, focal loss of part of the epidermis
• Ulceration is focal loss of the epidermis extending into the dermis.
Lesions may heal with scarring
• Atrophy is decreased skin thickness due to skin thinning.
• Scar is abnormal fibrous tissue that replaces normal tissue after skin
injury.
• Hyperpigmentation is increased skin pigment; hypopigmentation is
decreased skin pigment; and depigmentation is total loss of skin
pigment.
SKIN INFECTIONS
BACTERIAL INFECTIONS
Infections of epidermis; Impetigo.
Infections of the dermis; Erysipelas and cellulitis.
Common hair follicle infections; Superficial folliculitis, furuncles(Boils) and
Carbuncles.
IMPETIGO
Clinical Presentation; acute purulent infection which appears vesicular;
progresses to golden yellow “honey-crusted” lesions surrounded by erythema.
Can present with bullae
Common sites: face, arms, legs, and buttocks
Etiology; GAS, S.aureus, or both
Epidemiology; preschool and young adults living in crowded conditions, poor
hygiene, neglected minor trauma
Differential Diagnosis; infected eczema, HSV, VZV
Investigations; Gram stain and culture of lesion fluid or biopsy
Management;
Remove crusts, use saline compresses, and topical antiseptic soaks
twice a day
Oral antibiotics for 7-10 days: flucloxacillin 500mg 6 hrly or
erythromycin 250-500mg 6hrly, mupirocin cream 2% 12 hrly
Isolation
Prevention:
Good personal hygiene particularly washing hands with soap
Cellulitis
Presents as tender erythema, edematous and warm area of the skin due to
infection in the deep subcutaneous layers of the skin.
Often affecting lower limbs causing an upward spreading. Occasionally with
blister especially if edema is persistent
It may also occur on the face affecting one side.
• Aetiology
GABHS, rarely staph, and sometimes community acquired MRSA.
In immunocompromised or diabetic patients gram negative organisms,
anaerobes should be suspected
• Diagnosis
Confirm infection serologically-ASOT.
Swabs are usually unhelpful
• Treatment
oral flucloxacillin or erythromycin 500mg 6 hrly 5-7 days.
If cellulitis is wide spread give iv antibiotics 5-7 days followed by oral therapy 2
weeks.
Treat any identifiable underlying cause
Erysipelas
• Erysipelas is a type of superficial cellulitis with dermal
lymphatic involvement
• It is characterized clinically by shiny, raised indurated and
tender plaque-like lesions with distinct margins
• Most common caused by group A beta hemolytic streptococci
most frequently on the legs and face.
• Erysipelas of the face must be differentiated form herpes zoster
and contact dermatitis
• Commonly accompanied by fever chills, and malaise
• It may be recurrent and may result in chronic lyphoedema.
• Erysipelas and cellulitis overlap so it is often impossible to
distinguish
Diagnosis
Characteristic appearance
Blood culture in toxic patients
Management
• Penicillin V or erythromycin 500mg oraly 6hourly for two weeks
or more
• Penicillin G 1.2 million units IV 6h which can be replaced by oral
therapy after 36 to 48h is indicated in severe cases
• In case of resistance to these antibiotics cloxacillin or
cephalexin can be used
• Cold packs and analgesics for relieving discomfort and pain
Folicullitis
• Folliculitis-inflammation of hair follicles presents as
itchy/tender, erythematous papules and pustules.
• Aetiology: staph aureus
• Extensive itchy folliculitis on the upper trunk and limbs- suspect
HIV
• Treatment
Topical antibiotic i.e mupirocin, oral antibiotics;
flucloxacillin/erythromycin 500mg 6 hrly 2-4 wks
prevention
Suspected irritants should be avoided e.g.. Shaving agaist
direction of hair growth, long term use of antibiotics for acne,
exposure to heated swiming pools
Boils(furuncles)
• Herpes simplex
• Herpes zoster
• Human papilloma virus
Herpes simplex
• Two genomic subtypes exist; HSV type 1 and HSV type2. the
hall mark of all herpes infection is the ability of the virus to
establish latent infection that persist for life in an individual.
• HSV 1 major cause of herpetic stomatitis ~ 70% of the
population is infected whereas HSV 2 is responsible for genital
and systemic infections. This division is however not rigid.
Clinical presentation:
• Primary infection may be subclinical or produce severe
inflammatory reaction with cluster of vesicles formation on the
face or gingival stomatitis, genital skin surface which coalesce
and form painful shallow ulcers
• Systemic symptoms vary, may include fever, myalgia, inguinal
lymphadenopathy and headache
• Clinical manifestations in immunosuppressed patients may be
more severe.
Reactivation of the virus is facilitated by several stress stimuli
such as
• Febrile illness
• Uv radiation
• Surgical trauma to the neurones
Diagnosis
• High suspicious index of the disease from history and physical
examination and a firm dx is made by detection of the virus
from within the skin lesions through HSV DNA PCR
Treatment
• Primary infection: Drug of choice is acyclovir 400mg 8 hrly for
7-10 days. Is useful when the vesicles are still forming. If the
lesions are crusting antiviral therapy will do a little to change
the clinical course
Treatment
Clinical presentation
• Warts which develop around the external genitalia and
perianal area, vagina and cervix may also be involved in
women.
• In males penile shaft and sub preputial space are commonly
affected.
Diagnosis
• Is essentially clinical. Its crucial to differentiate it from
condylomata-lata of secondary syphilis. Unusual lesions should
be biopsied if the dx is in doubt.
Treatment
Medical therapy
• Podophyllum resins 25% soln or Podophyllotoxin 0.5% soln are
cytodestructive therapies that can be applied topically to kill
the wart cells
• Trichloroacetic acid-destroys cell via chemical coagulation of
tissue proteins
surgical therapy( ablation and excisional procedures)
• Cryoablation (with liquid nitrogen destroys warts tissue via cell
lysis)
• Laser ablation ( lasers produces light that leads to thermal
damage and resultant ablation)
Prevention
• Vaccination- two vaccines exist against hpv one is effective
against hpv typ 16 & 18. the second against type 6,11,16 &
18.
• Regular cervical screening for women with male partners
with warts
• Practice of protected sex. use of condoms up to 8 months
after treatment
FUNGAL SKIN INFECTIONS
• Psoriasis
• Lichen planus
Psoriasis
• Psoriasis is an immunologically mediated chronic inflammatory
skin disease.
• Characterized by well-defined salmon-pink plaques bearing
large adherent silvery centrally attached scales.
• Affects 1-3% of most populations, and it is most prevalent in
European and north American whites.(Light skinned people)
• People between 15-40years of age are affected more, rare
under 10yrs.
• There are two peaks of onset of psoriasis.
• Type I has onset in the second and third decade and a more
common family history of psoriasis.
• Type II has onset in late adulthood in patients without obvious
family history.
• Its course is unpredictable but is usually chronic with
exacerbations and remissions.
Etiology
Differential diagnoses
• Discoid eczema, Seborrheic eczema, Pytiriasis rosea
• Secondary syphilis, Cutaneous T-cell lymphoma,Tinea unguium
Management & treatment
Treatment
• If drugs are suspected as the cause, they should be stopped.
• Potent topical steroids will sometimes relieve symptoms and flatten the
plaques.
• Systemic steroid are recommended only in special situations (e.g. unusually
extensive involvement, nail destruction or painful and erosive oral lichen
planus).
• Photochemotherapy with psoralen and ultraviolet A
(PUVA) or with narrowband UVB may reduce pruritus and
help to clear up the skin lesions.
• Oral ciclosporin or acitretin have also helped some
patients with stubborn lichen planus.
• Antihistamines may blunt the itch.
Complications
• Nail and hair loss can be permanent.
• The ulcerative form in the mouth may lead to squamous
cell carcinoma.
• Ulceration, usually over bony prominences, may be
disabling, especially if it is on the soles
ECZEMAS/DERMATITIS
Definition
inflammation of the skin
Clinical Presentation
• poorly demarcated erythematous patches or plaques
• symptoms include pruritus and pain
acute dermatitis: papules, vesicles
subacute dermatitis: scaling, crusting, excoriations
chronic dermatitis: lichenification, xerosis, fissuring
Atopic eczema
Atopic eczema is the most common type - usually develops by
early childhood and resolves during teenage years (but may
recur)
Epidemiology; frequently affects infants, children, and young
adults, almost 15% of children in developed countries under the
age of 5 are affected
Causes; Not fully understood, but a positive family history of
atopy (i.e. eczema, asthma, allergic rhinitis) is often present
• Exacerbating factors such as infections, allergens (e.g.
chemicals, food, dust, pet fur), sweating, heat and severe stress
Presentation; Commonly present as itchy, erythematous dry scaly
patches
• More common on the face and extensor aspects of limbs in
infants, and the flexor aspects in children and adults
• Acute lesions are erythematous, vesicular and weepy (exudative)
• Chronic scratching/rubbing can lead to excoriations and
lichenification
Management; General measures - avoid known exacerbating
agents, frequent skin moisturizers +/- bandages and bath oil/soap
substitute
• Topical steroids eg. 1% hydrocortisone
• Oral therapies - antihistamines eg cetirizine for symptomatic relief,
antibiotics (e.g. flucloxacillin) for secondary bacterial infections,
and antivirals (e.g. aciclovir) for secondary herpes infection
• Phototherapy and
immunosuppressants (e.g.
oral prednisolone,
azathioprine, ciclosporin) for
severe non- responsive cases
Complications; Secondary
bacterial infection (crusted
weepy lesions)
• Secondary viral infection -
molluscum contagiosum
(pearly papules with central
umbilication), viral warts and
eczema herpeticum
Contact Dermatitis
• Pemphigus vulgaris
• Bullous pemphigoid
• Dermatitis Herpetiformis
• Steven-johnson syndrome (sjs) and toxic epidermal
necrolysis (ten)
Pemphigus Vulgaris
Clinical Presentation; autoimmune blistering disease characterized by
flaccid, non-pruritic intraepidermal bullae/vesicles on an
erythematous or normal skin base
• may present with erosions and secondary bacterial infection
• sites: mouth (90%), scalp, face, chest, axillae, groin, umbilicus
• Nikolsky’s sign: epidermal detachment with shear stress
• Asboe-Hansen sign: pressure applied to bulla causes it to extend
laterally
Pathophysiology; IgG against epidermal desmoglein-1 and -3 lead to
loss of intercellular adhesion in the epidermis
Epidemiology; 40-60 yr old, M=F, higher prevalence in Jewish,
Mediterranean, Asian populations
Investigations
• immunofluorescence: shows IgG and C3 deposition intraepidermally
• circulating serum anti-desmoglein IgG antibodies
Prognosis; lesions heal with hyperpigmentation but do not scar
• may be fatal unless treated with immunosuppressive agents
Management
• prednisone 1-2 mg/kg until no new blisters, then 1-1.5 mg/kg until
clear, then taper ± steroid-sparing agents (e.g. azathioprine,
methotrexate, cyclophosphamide and cyclosporine
Bullous Pemphigoid
• Hyperpigmentation
• Lentigos
• freckles
Vitiligo
• Acquired progressive disorder in which some or all of the
melanocytes in the interfollicular epidermis, and occasionally
those in the hair follicles, are selectively destroyed.
• Focal loss of melanocytes results in the development of
patches of hypopigmentation.
• Incidence: 1% - 30% of cases have family history
• onset is most commonly observed in persons aged 10-30
years.
• The pathogenesis is unclear and, but it is thought that
melanocytes may be the target of a cell-mediated
autoimmune attack
• A positive family history of vitiligo is relatively common in
those with extensive disease, and this type is also associated
with other autoimmune diseases
• Can be clinically
• Localized
• Focal - One or more macules in 1 area.
• Segmental - One or more macules in a dermatomal pattern
• Mucosal - Mucus membrane alone
• Generalized (more symmetrical)
• Acrofacial - Distal extremities and face
• Vulgaris - Scattered macules
• Mixed - Acrofacial and vulgaris involvement, or segmental and
acrofacial and/or vulgaris involvement
• Universal - Complete or nearly complete depigmentation
Vitiligo
Treatment modalities
Topical therapies
• Topical corticosteroids-Mid- to super-high-potency topical
corticosteroids are commonly used as a first-line therapy for the
treatment of limited vitiligo. Their efficacy is attributed to
modulation of the immune response
• Topical calcineurin inhibitors — Tacrolimus and pimecrolimus are
topical immunomodulatory agents that affect the T-cell and mast-
cell function and inhibit the synthesis and release of multiple
proinflammatory cytokines.
• Systemic corticosteroids — Low-dose oral corticosteroids are
generally utilized for the stabilization of rapidly progressive vitiligo,
often in combination with NB-UVB phototherapy.
Phototherapy
• Narrowband ultraviolet B phototherapy — NB-UVB involves the use
of UV lamps with a peak emission of approximately 311 nm.
• These shorter wavelengths provide higher-energy fluences and
induce less cutaneous erythema.
• NB-UVB induces local immunosuppression and apoptosis; and
increases melanocyte proliferation and melanogenesis.
• PUVA photochemotherapy — Historically, photochemotherapy with
topical or systemic PUVA radiation was the "gold standard" treatment
for the repigmentation of vitiligo but has been largely replaced by
NB-UVB phototherapy dueto its phototoxicity.
• Surgical therapies — Surgical therapies have been used for vitiligo for
the past 25 years and remain viable options for patients with
localized depigmented areas that have been unresponsive to medical
intervention.
• It includes skin grafting which transfers a reservoir of healthy
melanocytes to vitiliginous skin for proliferation and migration into
areas of depigmentation.
Increased pigmentation
• Albinism
• neurofibromatosis
OCULOCUTANEOUS ALBINISM
• There is no one overall treatment for NF1 nor are there any
therapeutic agents specifically approved for patients with NF1.
Rather, the individual manifestations are treated as they arise.
• For example :The approach to treatment of the various tumors
associated with NF1 depends upon the type of tumor, its effect on
adjacent tissues, and related complications.
• The management of patients with NF2 is complex, and involves
multiple disciplines to prevent or treat the various complications that
may develop. including Tumor surveillance and follow-up, Treatment
of vestibular schwannomas and meningiomas and spinal tumors.
References
• Kumar & Clark's clinical medicine 8 th edition
• Davidson’s principles & practice of medicine 23 rd edition
• Toronto notes 2017
• Dermatology Handbook for medical students 2nd edition
2014
• Old lecture notes
• Medscape
• Roderick J. Hay et al. The Global Burden of Skin Disease in
2010: An Analysis of the Prevalence and Impact of Skin
Conditions- journal of investigative dermatology.
published on Nov, 2013