1

DERMATOLOGY
1.

SCABIES:

a. Scabies is caused by the Acarus, Sarcoptes scabiei, with an

estimated global prevalence of 300 million. The infestation causes
considerable discomfort and can lead to secondary infection.
Scabies spreads in households and environments where there is
intimate personal contact.
b. Diagnosis is made by identifying the scabietic burrow and by
extracting the mite using a blunt needle. Inappropriate application
of scabietic treatments can cause considerable irritation in other
conditions.
c. In small children the palms and soles can be involved with pustule
formation Involvement of the genital area in boys is pathognomonic.
The main symptom is itch.
d. The clinical features include secondary eczematisation elsewhere on
the body; the face and scalp are never involved, except in the case
of infants. Even after successful treatment, the itch can continue
and occasionally nodular lesions persist.
e. Topical treatment of scabies is required for the affected individual
and all asymptomatic family members/physical contacts to ensure
eradication.
f. Two applications 1 week apart of an aqueous solution of either
permethrin or malathion to the whole body, excluding the head, are
usually successful.
g. If there is poor compliance, immunocompromise or heavy
infestations (Norwegian scabies), systemic treatment with
ivermectin (200 g/kg) as a single dose is appropriate
2. MUCORMYCOSIS:
a. Mucormycosis is a severe but uncommon opportunistic systemic
mycosis caused by any of the Mucorales, mainly Myocladus
(formerly Absidia) spp., Rhizomucor spp., Mucor spp. and Rhizopus
spp.
b. Disease patterns include rhinocerebral/craniofacial, pulmonary,
cutaneous and systemic disease.
c. All are characterised by the rapid development of severe tissue
necrosis, which is almost always fatal if left untreated.
d. The major predisposing factors are uncontrolled diabetes mellitus,
iron chelation therapy with desferrioxamine, severe burns and, most
commonly, profound immunosuppression from neutropenia or bone
marrow transplant in association with the use of broad-spectrum
azole prophylaxis with agents like voriconazole.
e. Diagnosis is by culture, but histopathological confirmation is
required as the fungi may be environmental contaminants.
f. Treatment requires a combination of antifungal therapy and surgical
dbridement, with correction of predisposing factor(s) if possible.
g. High-dose lipid-formulated amphotericin B is used most commonly,
although posaconazole is active in vitro and has been used
successfully.

3.

PSORIASIS.PAPER I; FEB 2013 PAPER II

1. Psoriasis is a non-infectious, chronic inflammatory disease of the skin,

characterised by well-defined erythematous plaques with silvery scale,
with a predilection for the extensor surfaces and scalp, and a chronic
fluctuating course.
2. The prevalence is approximately 2% in European populations but may be
lower in African and some Asian populations, e.g. Japanese.
3. Psoriasis may start at any age but is unusual before 5 years.
4. There are two epidemiological patterns of psoriasis, sometimes referred to
as type 1 and type 2.
a. The first has an onset in the teenage and early adult years, often
with a family history of psoriasis and an increased prevalence of the
HLA group Cw6.
b. The onset of the second is in the fifties or sixties, when a family
history is less common and HLA Cw6 is not so prominent.
5. Aetiology
a. Psoriasis is genetically complex and a large number of genes are
thought to be important in its pathogenesis.
b. Empirical estimates suggest that if one parent has psoriasis, then
the chance of a child being affected is in the order of 1520%; if
both parents have the disease, this figure rises to 50%.
6. Pathology:
a. There are two key pathophysiological features in psoriatic plaques:
i. The keratinocytes hyperproliferate with a grossly increased
mitotic index
ii. There is a large inflammatory cell infiltrate.
iii. The nails of patients with psoriasis, even when clinically
unaffected, grow more quickly than those of controls.
b. The evidence implicating a key role for an immune pathogenesis
includes the association with HLA Cw6;

7. Factors thought to precipitate exacerbations are:

a. Trauma
i. Lesions appear in areas of skin damage such as scratches or
surgical wounds (Kbner phenomenon) when the condition is
erupting
b. Infection
i. b-haemolytic streptococcal throat infections often precede
guttate psoriasis
c. Sunlight
i. UVR rarely
d. Drugs

3
i. Antimalarials,
ii. b-adrenoceptor antagonists (b-blockers) and lithium
iii. Rebound after systemic corticosteroids or potent local
corticosteroids are stopped
e. Emotion: Anxiety
8. Clinical features
a. There are several different forms of psoriasis.
i. Stable plaque psoriasis
1. This is the most common. Individual lesions are well
demarcated and range from a few millimetres to
several centimetres in diameter. They are red, with a
dry silvery-white scale, which may only be obvious
after scraping the surface. The elbows, knees and
lower back are commonly involved. Other sites of
predilection include: Scalp. Nails Flexures Palms
ii. Guttate psoriasis
1. This is most commonly seen in children and
adolescents, and may follow a streptococcal sore
throat.
2. Individual lesions are droplet shaped, seldom over 1
cm in diameter and scaly.
iii. Erythrodermic psoriasis
1. The skin becomes universally red or scaly, or more
rarely just red with very little scale. As in other forms of
erythroderma, temperature regulation becomes
compromised with a danger of either hypothermia or
hyperthermia.
iv. Pustular psoriasis
1. There are two varieties of pustular psoriasis. The
generalised form is rare but serious. The onset is
usually sudden, with large numbers of small sterile
pustules erupting on a red base. The patient may
rapidly become ill with a pyrexia coinciding with the
appearance of new pustules, and will usually require
urgent assessment and hospital admission.
2. A localised form, which primarily affects the palms and
soles, is more common. This is chronic and comprises
small sterile pustules which lie on a red base, and
resolve to leave brown macules or scaling. The
relationship between pustular psoriasis of the palms
and the soles (palmoplantar pustulosis) and psoriasis
remains disputed, although they commonly coexist.
v. Arthropathy: Between 5 and 10% of individuals with psoriasis
develop a chronic seronegative inflammatory arthropathy
9. Investigations
a. Biopsy is seldom necessary and contributes little.
b. Throat swabbing for streptococci or other evidence of recent
infection may occasionally be useful in suspected guttate psoriasis.
c. Joint symptoms, unless minor, require a formal rheumatology
assessment.
10.
General management of psoriasis

4
a. Explanation, reassurance and instruction are vital.
b. psoriasis is not lifethreatening and therefore, if the treatment is
worse than the disease, it should be stopped.
11.
Treatment
Treatment can be classed in four broad categories:
a. Topical agents
Emollients, corticosteroids, vitamin D agonists, weak tar or
dithranol preparations
b. UV therapies
UVB or PUVA
c. Systemic agents
Methotrexate, retinoids
Immunosuppressives, e.g. ciclosporin, mycophenolate
Newer biological agents, e.g. infliximab, etanercept
d. Intensive inpatient or day-patient care
Topical agents and UVR under medical supervision
12.
Topical agents
a. Dithranol and tar: In Ingrams regimen, the plaques are covered
with low concentrations of dithranol in a zinc oxide paste following a
tar bath and UVR exposure, and then covered in talcum powder and
bandages, which are left in situ for 24 hours.
b. Calcipotriol is a vitamin D agonist. It seldom clears plaques of
psoriasis but reduces plaque thickness and diminishes scaling. It is
applied twice or once daily. It is a mainstay of primary care
management of psoriasis and may be combined with
corticosteroids.
c. Corticosteroids ; Corticosteroids may cause local skin atrophy, and
when they are stopped the psoriasis tends to return.
13. Ultraviolet and PUVA therapy
a. UV therapy
Ultraviolet radiation (UVR) is the mainstay of outpatient management
of those with moderate to severe psoriasis. More recently, a particular
type of UVB radiation produced by the Philips TL01 lamp (narrowband
UVB), delivered 25 times a week on an outpatient basis, has become
a popular treatment.
b. PUVA therapy
Psoralens are natural photosensitisers found in a number of plants.
Psoralen molecules intercalate between the two strands of DNA and,
upon excitation with UVA, photons cross-link the DNA strands. It is thus
a pro-drug that is distributed throughout the body after oral
administration, but only activated by UVR in skin that is exposed to
UVA.
The long-term hazards of PUVA therapy are the result of its
mutagenicity; patients who have received a large amount of PUVA
therapy, particularly maintenance therapy (continuous PUVA lasting
for 6 months to a year), are at increased risk of squamous and basal
cell carcinoma.
14. Systemic treatment
1. Methotrexate

5
a. Methotrexate is highly effective and is given once weekly. Its
mechanism of action is primarily on the immune system rather than
having a direct effect on keratinocyte or epidermal
hyperproliferation. The main hazards are immunosuppression and
bone marrow suppression.
2. Oral retinoids
a. Oral retinoids, such as acitretin, are effective in pustular psoriasis of
the palms and soles, but are potent teratogens.
3. Ciclosporin
a. Ciclosporin is an immunosuppressive used over a 34-month period
to induce clearance or prior to treatment with other systemic
agents.
4. Biological therapies
a. monoclonal antibodies, fusion proteins and cytokines, have been
shown to have striking activity against psoriasis and appear as
effective as classical agents. Eg.
i. etanercept, a human recombinant TNF receptor fusion
protein,
ii. infliximab is a human-murine anti-TNF- monoclonal
antibody.

4.

GUTATE PSORIASIS 2011

1. Guttate psoriasis, a variant that occurs predominantly in children, is

characterized by an explosive eruption of profuse, small, oval or round
lesions that morphologically are identical to the larger plaques of psoriasis.
2. Sites of predilection are the trunk, face, and proximal portions of the limbs.
3. The onset frequently follows a streptococcal infection; a culture of the
throat and serologic titers should be obtained.
4. Guttate psoriasis has also been observed after perianal streptococcal
infection, viral infections, sunburn, and withdrawal of systemic
corticosteroid therapy.
5. Pathogenesis:
a. Psoriatic skin lesions may be induced, in a genetically susceptible
host, by CD4+ T cells that were initially activated by streptococcal
pyrogenic exotoxins acting as superantigens.
b. The source of the streptococcal antigens can be the throat or the
skin.
c. Some of the superantigen-activated T cells recognize streptococcal
M protein in the skin and appear to have cross reactivity with an
abnormal keratin that has homology with streptococcal M protein.
The autoreactive T cells may be responsible for the formation and
maintenance of psoriatic skin lesions.

6
6. D.D: The lesions may be confused with viral exanthems and pityriasis
lichenoides chronica
7. Treatment: refere previos answer.
a. The treatment of psoriasis should be viewed as a 3-tier process. The

1st tier is topical therapy.

b. The 2nd tier of therapy is phototherapy
c. Systemic therapy is the 3rd tier.

5. FOUR CAUSES OF PRURITIS WITHOUT SKIN DISEASE.

Medical conditions associated with pruritus
Medical condition
Cause of pruritus
Treatment
Liver disease
Central opioid effect
Naltrexone
Elevation in bile salts

Colestyramine

Rifampicin
Sedative
antihistamines
UVB
Renal failure
activated charcoal

Unknown; unlikely to

Oral

involve histamine
Blood disease
Anaemia
replacement
Polycythaemia
rubra vera
Lymphoma
Leukaemia
Myeloma
Endocrine disease
Diabetes mellitus
Thyrotoxicosis
Emollients
Hypothyroidism
Carcinoid
syndrome
HIV infection Infection,
Eosinophilic folliculitis
corticosteroids,

Iron deficiency

Iron

Unknown

Unknown

May be associated
Clotrimazole
with genital candidiasis
Generalised due to
dry skin
Localised; may be due
to Candida
5HT-mediated
infestation,
e.g. Candida
Unknown

Treatment of
opportunistic infection
Local
UVB

7
Malignancy
Psychogenic

Unknown
Unknown

Psychotherapy,
anxiolytics,
antidepressants

6. PEDICULOSIS
Head lice
1. Infestation with head louse, Pediculus humanus capitis, is common; it is
highly contagious, spread by direct head-to-head contact.
2. Itching of the scalp leads to scratching which causes secondary infection
and cervical lymphadenopathy.
3. The diagnosis is confirmed by identifying the living louse or nymph on the
scalp or on a black sheet of paper after careful fine-toothed combing of
wet hair that has had conditioner applied.
4. The empty egg cases (nits) are easily seen along the hair shaft and are
characteristically difficult to dislodge.
5. Treatment is recommended for the infected individual and any infected
household/school contacts. Eradication in school populations has proved
difficult because of poor compliance and resistance to certain treatments.
6. The standard treatments are malathion, permethrin and carbaryl in a
lotion or aqueous formulation, which are applied on two separate
occasions at 710 days interval.
7. Many advise rotational treatments within a community to avoid resistance.
Regular wetcombing (physical removal of the live lice by regular combing
of slippery, conditioned wet hair) seems less effective than
pharmacological treatments.
8. Involvement of the eyebrows/eyelashes is treated by topical Vaseline 12hourly for at least a fortnight.

Body lice
1. These are similar to head lice but live on clothing, particularly in seams,
and feed on the skin. They are found on individuals with poor hygiene and
in overcrowded conditions. Itch is the principal symptom. The skin is
excoriated and secondary infection is common. It is managed by dry
cleaning and high-temperature washing or insecticide treatment of
clothes.
Pubic (crab) lice
1. These are usually sexually acquired and cause pruritus. An aqueous-based
treatment of either malathion or carbaryl is the treatment of choice,
applied on two occasions to the whole body, as body hair can also be
infested.
2. Contacts should also be treated.

7. STAPHYLOCOCCAL SCALDED SKIN SYNDROME. (SSSS).

1. SSSS is a potentially serious exfoliating cutaneous disease that occurs
predominantly in children, particularly neonates.
2. It is caused by blood-borne exfoliative toxins from a focus of infection with
Staph.aureus, which specifically cleave desmoglein-1.

8
3. The focus of infection may be the umbilicus or urinary tract, or it may
stem from colonisation of the nasopharynx. The child presents with fever,
irritability, skin tenderness and, in severe cases, erythema, starting in the
groin, axilla and around the mouth. Blisters and superficial erosions
develop within 2428 hours, and can rapidly involve large areas of the skin
with severe systemic upset.
4. Bacterial swabs should be taken from obvious primary sites of infection,
the nose and throat. A skin snip should be taken for rapid histological
examination. This is a sample of the superficial peeling skin removed by
snipping with scissors. No local anaesthetic is required.
5. It shows a split beneath the stratum corneum, and differentiates it from
toxic epidermal necrolysis in which the whole epidermis is affected.
6. Systemic antibiotics (e.g. flucloxacillin) and intensive supportive measures
should be commenced at once. Bacterial swabs from nostrils, axilla and
groin should be taken from the patients relatives to exclude
staphylococcal carriage.
8. SKIN CHANGES IN ENDOCRINE DISEASES. PAPER II AUG 2010
1. Thyrotoxicosis may lead to multiple cutaneous manifestations, including hair loss, pretibial
myxedema, onycholysis and acropachy.

2. In patients with hypothyroidism, there is hair loss, the skin is cold and pale, with
myxedematous changes, mainly in the hands and in the periorbital region.

3. The striking features of Cushing syndrome are centripetal obesity, moon facies, buffalo hump,
supraclavicular fat pads, and abdominal striae.

4. In Addison disease, the skin is hyperpigmented, mostly on the face, neck and back of the
hands.

5. Virtually all patients with acromegaly have acral and soft tissue overgrowth, with characteristic
findings, like macrognathia and enlarged hands and feet. The skin is thickened, and facial
features are coarser.
6. Conditions leading to hyperandrogenism in females present as acne, hirsutism and signs of
virilization (temporal balding, clitoromegaly).
7. A prominent feature of hypopituitarism is a pallor of the skin with a yellowish tinge. The skin is
also thinner, resulting in fine wrinkling around the eyes and mouth, making the patient look
older.
8. Primary hyperparathyroidism is rarely associated with pruritus and chronic urticaria. In
hypoparathyroidism, the skin is dry, scaly and puffy. Nails become brittle and hair is coarse
and sparse.
9. Pseudohypoparathyroidism may have a special somatic phenotype known as Albright
osteodystrophy. This consists of short stature, short neck, brachydactyly and subcutaneous
calcifications.
10. Some of the cutaneous manifestations of diabetes mellitus include necrobiosis lipoidica
diabeticorum, diabetic dermopathy, scleredema adultorum and acanthosis nigricans.

9. PEMPHIGUS VULGARIS. FEB 2010

1. Pemphigus is an uncommon autoimmune disorder that can present with
mucosal symptoms only, usually in the mouth.
2. It is due to:
a. IgG1 and IgG4 autoantibodies, directed against desmogleins-1 and
3 and causing intra-epidermal blistering
b. it can also be drug-induced (e.g. by penicillamine or captopril)
c. It is rarely associated with an underlying malignancy
(paraneoplastic pemphigus).

9
3. In pemphigus foliaceus, a very superficial form, the autoantibodies are
directed solely against desmoglein-1, therefore affecting only the most
superficial epidermis.
Clinical features and diagnosis
1. Flaccid blisters occur on the skin, usually on the upper trunk and back. As
the blisters are superficial, they are fragile and may look like erosions.
2. The Nikolsky sign is positive.
3. Mucosal involvement can be severe, increasing the morbidity and risk of
mortality. Pemphigus can be associated with other autoimmune disorders
and full assessment for these is mandatory.
Investigations
1. In the acute situation, histology from a Tzank smear (taken from the base
of the blister with a scalpel) reveals acantholysis, i.e. separation of the
epidermal cells.
2. Disease activity can be monitored by measuring the level of circulating
autoantibody in serum by indirect immunofluorescence.
3. Investigations should also include full blood count, ESR, urea and
electrolytes, liver function tests, chest X-ray and other imaging,
particularly if paraneoplastic pemphigus is suspected.
Management
1. Systemic treatment with high-dose oral steroids is required, but the
disease is more difficult to control than BP and life-long treatment is
generally required.
2. Azathioprine and cyclophosphamide are alternatives. Intravenous IgG may
be used to gain rapid control in severe cases.

10. URTICARIA Feb 2009 pII

1. Urticaria refers to an area of focal dermal oedema secondary to a transient
increase in capillary permeability.
2. On certain body sites such as the lips or hands, the oedema spreads
deeper and is referred to as angioedema.
3. By definition, the swelling lasts less than 24 hours.
4. Acute urticaria may be associated with angioedema of the lips, face,
throat and rarely wheezing, abdominal pain, headaches and even
anaphylaxis.
5. Whilst severe angioedema can be life-threatening due to respiratory
obstruction, this is extremely rare in a dermatological context
Causes:
Acute and chronic urticaria
1. Autoimmune due to production of antibodies that cross-link the IgE
receptor on mast cells
2. Allergens (in foods, inhalants and injections)
3. Drugs: aspirin; NSAID
4. Contact, e.g. animal saliva, latex
5. Physical, e.g. heat, cold, pressure, sun, water
6. Infection, e.g. viral hepatitis, infectious mononucleosis, HIV
seroconversion
7. Other conditions, e.g. systemic lupus erythematosus (SLE), pregnancy,
intestinal parasites
8. Idiopathic

10
9. Urticarial vasculitis
a. Hepatitis B
b. SLE
c. Idiopathic
Pathogenesis of urticaria.
1. Type I hypersensitivity causing massive degranulation and sometimes
anaphylaxis.
2. Basic pathology is mast cell degranulation and release of histamine and
other mediators like
a. prostaglandins
b. leukotrienes
c. chemotactic cytokines
d. Heparin
e. 5-hydroxytryptamine
f. Proteases
3. Spontaneous mast cell degranulation occurs in chronic urticaria.
4. Chemical mast cell degranulation due to drugs
5. Autoimmunity accounts for 30% of chronic urticaria.
Clinical features:
1. Clinical types:
1. < 24 hours (urticaria)
2. 24 hours (urticarial vasculitis)
3. < 6 weeks (acute urticaria)
4. 6 weeks (chronic urticaria)
2. Knowing the length of time that an individual weal lasts may be of some
use in distinguishing urticaria from urticarial vasculitis. Urticarial vasculitis
is much less common than urticaria, and many patients are unable to
distinguish the development of new weals and disappearance of old ones,
from individual weals which persist for more than 1 day.
3. The physical urticarias can be identified by asking appropriate questions
and subsequent challenge testing.
4. A family history must be sought in cases of angioedema.
5. There is an autoimmune pathogenesis for the most common form of
disease, chronic idiopathic urticaria, which is defined by the presence of
urticarial episodes for more than 6 weeks; self-reacting antibodies appear
to cause cross-linking of the surface IgE receptor on mast cells with
subsequent cellular degranulation.
Investigations
1. Full blood count, including eosinophil count in case of underlying parasites
2. Erythrocyte sedimentation rate (esr): may be elevated in cases of
vasculitis
3. Urea and electrolytes, thyroid and liver function tests:may reveal an
underlying systemic disorder
4. Total IgE and specific IgE to possible allergens, e.g shellfish or peanuts
5. Antinuclear factor: may be positive in chronic urticaria or urticarial
vasculitis
6. CH50: indicates the level of complement activation; C3 and C4 levels may
reveal complement consumption
7. C1 esterase inhibitor: may be quantitatively reduced or more rarely
functionally deficient, as in hereditary angioedema
8. Skin biopsy: helpful if urticarial vasculitis is suspected
9. Appropriate challenge test: to confirm physical urticarias.

11
10.Frequently no cause can be found for acute episodes, whereas in chronic
urticaria an autoimmune pathogenesis will account for the majority of
cases.
Management
1. Non-sedative antihistamines, such as loratadine, fexofenadine or cetirizine,
are effective for one-third of patients with chronic urticaria;
2. H2 -blocker such as cimetidine or ranitidine may be added to antihistamines
3. Mast cell stabilisers or protease and leukotriene inhibitors are used but
efficacy is not clear.
4. Systemic corticosteroids are widely prescribed for urticaria, although there is
little evidence of benefit.
5. Patients with a history of life-threatening angioedema or anaphylaxis, as is
seen in allergy to peanuts and wasp stings, should carry a self-administered
injection kit of adrenaline (epinephrine).
6. Urticaria may be precipitated by aspirin or NSAIDs. If there is a clear history of
these agents precipitating attacks, they should be avoided, and even in the
absence of a clear history it may be advisable to suggest alternatives such as
paracetamol. Codeine and opioids can also induce urticaria.

11. TENIA CAPITIS APRIL 92

1. Dermatophytes are fungi capable of causing superficial skin infections known
as ringworm or dermatophytosis.
2. The causative fungi belong to three genera
a. Microsporum
b. Trichophyton
c. Epidermophyton
3. Clinical forms of cutaneous infection include tinea corporis (involvement of
the body), tinea capitis (scalp involvement), tinea cruris (groin involvement),
tinea pedis (involvement of the feet) and onychomycosis (nail involvement)
4. Pathogenesis
a. Caused by dermatophytic fungi; common etiologic agents are T.
tonsurans (anthropophilic) and Microsporum canis (zoophilic)
b. Transmission is person-to-person or fomites such as combs, clothing,
bedding, toys and furniture Asymptomatic individuals, especially family
members, act as reservoirs for infection (~25% of family members
affected)
5. Clinical features:
a. They are variable due to associated inflammation, with patchy hair loss
and some scaling. Affected individuals should have the area scraped
and affected hairs plucked for mycological microscopy and culture.
b. Endothrix (within the hair shaft) infections, e.g. Trichophyton tonsurans,
cause relatively uninflamed patchy baldness with breakage of the hairs
at the skin surface (black dot).
c. There is no fluorescence under Woods light.
d. Ectothrix (outside the hair shaft) species of fungi, such as Microsporum
audouinii (anthropophilic), show minimal inflammation; Microsporum
canis (from dogs and cats) infections are more inflamed and can be
identified by green fluorescence with Woods light.
e. Kerions are boggy, highly inflamed areas of tinea capitis and are
usually caused by zoophilic (from animals, e.g. cattle ringworm)

12
species of fungi (e.g. Trichophyton verrucosum) painful, inflamed,
crusted mass with purulent discharge; often with associated fever and
regional lymphadenopathy
f. Favus is inflammation and scarring characterized by yellow cupshaped crusts (scutula), around a hair; .
6. Diagnosis
a. Clinical examination
b. KOH preparation: observe spores within brokenoff hairs, rarely hyphae
c. Culture collect specimen by rubbing a sterile cotton swab over the
scalp and inoculating in fungal media or DTM
d. Skin biopsy may be necessary to confirm diagnosis in unusual cases,
especially Majocchi granuloma
7. Treatment
a. It is systemic with oral terbinafine, griseofulvin or itraconazole.
b. Topical therapy, such as an antifungal shampoo, is recommended as an
adjunct and arachis oil is used to remove crusting.
c. Kerions sometimes require short courses of oral corticosteroids in
addition to systemic antifungal therapy to reduce the inflammation.
8. Prognosis
a. Usually resolves without permanent alopecia
b. With severe inflammatory disease, scarring and permanent hair loss
may occur, but tends to be rare and spotty

12. DRUG ERUPTIONS APR 2000

Cutaneous drug reactions are common and almost any drug can cause them.
They should be included in the differential diagnosis of most skin diseases.
Although the mechanisms are poorly understood, drug eruptions may be
classified as shown in Box 27.40.
Clinical features and investigations
Mechanism of drug eruptions:
1. Non-immunological (non-allergic)
a. Pharmacological effect: Striae due to corticosteroids; mouth ulcers
due to methotrexate
b. Drug overdose or failure to eliminate: Morphine rashes with liver
disease/failure
c. Drug interaction: Bruising with warfarin and aspirin
d. Idiosyncratic reaction: Drug-induced variegate porphyria
e. Phototoxic reaction: Chlorpromazine-induced light reactions
f. Altered skin mycology: Tetracyclines and vaginal candidiasis
g. Exacerbation of pre-existing skin condition: Lithium and -blocker
worsen psoriasis
2. Immunological (allergic)
a. Immediate hypersensitivity: Penicillin-induced urticaria
b. Immune complex reaction: Drug-induced vasculitis or erythema
multiforme
c. Delayed hypersensitivity: Drug-induced exfoliative dermatitis or
photoallergic reactions
Clinical patterns of drug eruptions
1. Toxic erythema
a. Erythematous plaques: Antibiotics (especially ampicillin)

13
b. Morbilliform, sometimes with urticarial or erythema multiforme-like
elements: Sulphonamides, thiazide diuretics, para-aminosalicylic
acid (PAS)
2. Urticaria
a. Itchy weals, sometimes accompanied by angioedema:
i. Salicylates, codeine and NSAIDs ;
ii. Antibiotics, dextran and ACE inhibitors
3. Erythema and scaling
a. Small, scaly, pink papules to large, scaly,red papules:
i. Antibiotics (e.g. penicillins, sulphonamides including cotrimoxazole)
ii. Gold, penicillamine and NSAIDs, particularly ibuprofen
iii. Anticonvulsants, ACE inhibitors, barbiturates, anti-thyroid
drugs and cytokine modulators, e.g. adalimumab
4. Allergic vasculitis
a. Painful, palpable purpura developing into necrotic ulcers:
Sulphonamides, indometacin, phenytoin and oral contraceptives
5. Erythema multiforme:
a. Target-like lesions and bullae on the extensor aspects of the limbs:
Sulphonamides and barbiturates
6. Purpura:
a. Widespread purpura in the absence of thrombocytopenia or a
coagulation defect: Thiazides, sulphonamides, sulphonylureas,
adalimumab, infliximab, barbiturates and quinine
7. Bullous eruptions
a. May be associated with erythema and Purpura: Barbiturates;
Penicillamine
8. Exfoliative dermatitis
a. Universal redness and scaling, shivering PAS, isoniazid and gold
9. Acute generalised exanthematous pustulosis/toxic pustuloderma
a. Rapid onset of sterile, non-follicular pustules on an erythematous
base: Ampicillin/amoxicillin, quinolones, sulphonamides,
pristinamycin, terbinafine Diltiazem and hydroxychloroquine
10.
Fixed drug eruptions
a. Round, erythematous, sometimes bullous plaques developing at
same site every time drug is given; Pigmentation on resolution:
Tetracyclines, sulphonamides Quinine and barbiturates
11.
Acneiform eruptions
a. Rash resembles acne
b. Lithium and anticonvulsants
c. Oral contraceptive, androgenic or glucocorticoid steroids
d. Antituberculosis drugs, biological therapy (cetuximab)
12.
Toxic epidermal necrolysis
a. Rash resembles scalded skin: Barbiturates, phenytoin, lamotrigine,
fluoxetine Penicillin, co-trimoxazole, nevirapine and allopurinol
13.Hair loss
a. Diffuse: Cytotoxic agents, infliximab and acitretin Anticoagulants,
antithyroid drugs and oral contraceptives
14.Hypertrichosis:
a. Excessive hair growth in non-androgenic distribution: Diazoxide,
minoxidil and ciclosporin
15.
Photosensitivity:

14
a. Rash limited to exposed skin: Thiazide diuretics and phenothiazines
Tetracyclines, sulphonamides and nalidixic acid NSAIDs, retinoids
and psoralens
16.Pigmentation
a. Amiodarone Slate-grey; exposed sites
b. Arsenic Diffuse bronze pigmentation with superimposed
c. raindrop depigmentation
d. Bleomycin Often flexural; brown
e. Busulfan Diffuse brown
f. Chloroquine Blue-grey; exposed sites
17.
Psoriasiform rash
a. Rash like psoriasis: Lithium, -blockers and anti-TNF- therapy
(infliximab)
Diagnostic clues to drug eruptions
a. Past history of reaction to suspected drug
b. Introduction of suspected drug a few days before onset of rash
c. Recent prescription of a drug commonly associated with rashes (e.g.
penicillin, sulphonamide, thiazide, allopurinol)
d. Symmetrical eruption which fits with a well-recognised pattern caused by
a current drug
Management
a. The first step is to withdraw the suspected drug
b. In the case of suspected drug-induced photodermatoses, phototesting
should be carried out when the patient is on the drug, and then again at a
later date when the drug has been withdrawn.
c. Drug withdrawal may not be easy, or even possible if there is no
alternative available. The decision will depend on many factors, including
the severity and nature of the drug reaction, its potential reversibility and
the probability that the drug caused the reaction.
d. Supportive treatment with antihistamines or a course of systemic
corticosteroids may be indicated, depending on the type of skin reaction.

13. HYPOPIGMENTED SKIN LESIONS AUG 2004

1. The main disorders to consider are albinism and vitiligo. However, a
number of others may produce secondary hypopigmentation:
2. Pityriasis alba, a type of eczema presenting as depigmented areas on the
face, particularly in children, with or without scale
3. Pityriasis versicolor, a yeast infection characterised by hyperpigmentation
early in its pathogenesis but leading to multiple areas of
hypopigmentation on the trunk, particularly the back
4. Idiopathic guttate hypomelanosis, characterised by numerous small areas
of depigmentation in areas of skin that have been exposed to the sun
5. Very rarely, phenylketonuria and hypopituitarism.
Oculocutaneous albinism
1. Albinism results from a range of genetic abnormalities leading to reduced
melanin biosynthesis in the skin and eyes; the number of melanocytes is
normal (in contrast to vitiligo).
2. There are a number of different forms of albinism, and considerable
variation even within one genetic type.
3. Albinism is usually inherited as an autosomal recessive trait.

15
a. Type 1 albinism is due to a defect in the tyrosinase gene, whose
product is rate-limiting in the production of melanin. Affected
individuals have an almost complete absence of pigment in the skin
and hair at birth, with resulting pale skin and white hair, and failure
of melanin production in the iris and retina. Patients have
photophobia, poor vision not correctable with refraction, rotatory
nystagmus, and an alternating strabismus associated with
abnormalities in the decussation of nerve fibres in the optic tract.
b. A second form of albinism is due to a defect in the P gene, which
encodes an ion channel protein in the melanosome. Patients may
have gross reduction of melanin in the skin and in the eyes, but
may be more mildly affected than type 1 albinos.
4. Establishing the subtype of albinism requires genetic analysis, as there is
considerable heterogeneity in the phenotype of the various subtypes.
5. Oculocutaneous albinos are at grossly increased risk of sunburn and skin
cancer. In equatorial regions, many die from squamous cell carcinoma or,
more rarely, melanoma in early adult life. They may, however, show
pigmented melanocytic naevi and may freckle in response to sun damage.
Management
1. Avoidance of sun exposure with protective clothing and hats is important,
as is a lifestyle that avoids the midday sun in particular, with indoor rather
than outdoor occupations. Sunblocks may be useful but can be expensive.
2. Early diagnosis and treatment of skin tumours is essential.
Vitiligo
1. Vitiligo is an acquired condition in which circumscribed depigmented
patches develop; it affects 1% of the population world-wide.
2. Unlike albinism, vitiligo involves focal areas of melanocyte loss.
3. There may be a positive family history of the disorder in those with
generalised vitiligo, and this type is associated with autoimmune diseases
such as diabetes, thyroid and adrenal disorders, and pernicious anaemia.
4. Trauma and sunburn may precipitate the appearance of vitiligo.
5. A number of hypotheses have been advanced to explain the pathogenesis,
including that the melanocytes are the target of a cellmediated
autoimmune attack, but why only focal areas are affected remains
unexplained.
Clinical assessment
1. Segmental vitiligo is restricted to one part of the body but not necessarily
a dermatome. Generalised vitiligo is often symmetrical and frequently
involves the hands, wrists, knees and neck, as well as the area around the
body orifices. The hair of the scalp and beard may also depigment.
2. The patches of depigmentation are sharply defined, and in Caucasians
may be surrounded by light brown caf au lait hyperpigmentation.
3. Some spotty perifollicular pigment may be seen within the depigmented
patches and is sometimes the first sign of repigmentation.
4. Sensation in the depigmented patches is normal (unlike in tuberculoid
leprosy). Examination with a Woods light enhances the contrast between
the pigmented and non-pigmented skin.
5. The course of vitiligo is unpredictable but most patches remain static or
enlarge; a few repigment spontaneously.
Management

16
1. This is unsatisfactory. Protecting the patches from excessive sun exposure
with clothing or sunscreen may be helpful in reducing episodes of burning
and potential skin cancer.
2. Camouflage cosmetics may also be helpful, particularly in those with dark
skin, as can potent topical corticosteroids.
3. Phototherapy with PUVA (psoralen + UVA) or more recently narrow band
UVB has been used but evidence is limited. PUVA therapy increases
pigmentation in normal skin, so the cosmetic effect (an increase in
contrast) may actually be worse than no treatment, except in very darkskinned individuals. When repigmentation occurs, it is frequently seen as
small foci of dark areas of skin surrounding hair follicles within the
vitiliginous area.
4. The absence of whiteness of the hairs in the area of vitiligo is a good
prognostic feature. Transplantation, using a range of techniques including
split-skin grafts and blister roof grafts, is occasionally used on to
dermabraded recipient skin.
5. The impact of vitiligo differs markedly between populations. In the Indian
subcontinent, the effects of vitiligo are more readily discernible than in
pale-skinned individuals in northern Europe.
6. Depigmentation is also seen in leprosy, which means that individuals with
vitiligo are often stigmatised. The use of more novel treatments, such as
grafting, is often pursued more extensively in such populations.
Other hypopigmented conditions:
1. Tinea versicolor:
Infection of the skin by Trichophyton
Manifests as patchy hypopigmentation and sometimes
hyperpigmentation
Commonly found on the trunk
2. Pityriasis alba
Related to eczema
Hypopigmented patches on the face
3.Postinflammatory hypopigmentation
May occur after any type of cutaneous inflammation
More obvious in dark-skinned individuals
Duration is weeks to months
4. Post-topical steroid hypopigmentation
Topical steroids, particularly fluorinated, may cause thinning, atrophy, and
hypopigmentation with prolonged use
More common on the face and perineum
5. Tuberous sclerosis (TS)
A neurocutaneous disorder affecting the brain, eyes, kidney, skin, and heart
Systemic symptoms are preceded by ash-leaf macules, which are usually
present in affected infants
Other skin findings are shagreen patches, adenoma sebaceum, periungual
fibromas
Mental retardation, seizures are common
6. P artial albinism (piebaldism) Eg> Waardenburg syndrome
White forelock, nonpigmentad patches on the face, trunk, elbows, and knees

17
Facial dysmorphism, a white forelock, and hypopigmentation
May be accompanied by hearing deficit

14. HIRSUTISM OCT 2003

Major points
1. Hirsutism is a condition of unwanted, male-pattern hair growth in women.
Hirsutism results in excessive amounts of coarse and pigmented hair on
body areas where men typically grow hair face, chest and back
2. Hair in masculine pattern in females on face,chest, upper back, abdomen
Signs of virilization may also include:
3. Deepening voice
4. Balding
5. Acne
6. Decreased breast size
7. Enlargement of the clitoris
Pathogenesis:
1. Abnormality of pituitary, adrenal glands or ovary with increase in male
hormones
Diagnosis
1. History
2. Physical examination
3. Women approaching menopause or in the early years of menopause may
develop coarse chin or other unwanted facial hair, but this isn't considered
hirsutism
4. Laboratory tests: serum testosterone and free testosterone,
dehydroepiandrosterone sulfate, cortisol levels, urinary 17-ketosteroids,
luteinizing hormone, follicle stimulating hormone, prolactin levels and
pelvic ultrasound examination
Differential diagnosis
1. polycystic ovary syndrome in teens
2. Genetic predisposition in some ethnic groups
3. Congenital adrenal hyperplasia
4. Cushing syndrome
5. Hyperprolactinemia
6. Ovarian and adrenal tumors
7.
Medications. Some medications can cause hirsutism. One such drug is
danazol, which is used to treat women with endometriosis .
Treatment
1. Removal of excess hair: shaving, epilation, chemical depilatories,
threading, waxing, electrolysis, laser hair removal
2. Oral contraceptives and weight reduction in PCOD
Prognosis
1. Depends upon etiology of hirsutism, usually permanent
2. Hirsutism can sometimes be emotionally distressing. Some women feel
self-conscious about having unwanted body hair. Also, although
hirsutism doesn't cause physical complications, the underlying cause of
a hormonal imbalance can.

18

15. CLUBBING - OCT 03

1. Hippocrates described the phenomenon in a patient with empyema
2. Digital clubbing, alternatively called Hippocratic fingers, watch-glass nails, or
drumstick fingers,2 can be an isolated finding or may occur as part of the
syndrome of hypertrophic osteoarthropathy (HOA).
3. HOA is characterized by periostosis of long bones,joint pain, and clubbing; it
may be primary, also known as pachydermoperiostosis, or secondary to a
variety of disease processes. Primary HOA is an autosomal dominant disorder
that presents in otherwise healthy children as clubbing, periostosis
4. Clubbing develops in five steps:
1. Fluctuation and softening of the nail bed (increased ballotability)
2. Loss of the normal <165 angle (Lovibond angle) between the nailbed and
the fold (cuticula)
3. Increased convexity of the nail fold
4. Thickening of the whole distal (end part of the) finger (resembling a
drumstick)
5. Shiny aspect and striation of the nail and skin
6. Unilateral clubbing is seen in hemiplegia and AV fistula in digit
5. Schamroth's test or Schamroth's window test (originally demonstrated
by South African cardiologist Dr Leo Schamroth on himself) is a popular test
for clubbing. When the distal phalanges (bones nearest the fingertips) of
corresponding fingers of opposite hands are directly apposed (place
fingernails of same finger on opposite hands against each other, nail to nail),
a small diamond-shaped "window" is normally apparent between the nail
beds. If this window is obliterated, the test is positive and clubbing is present.
6. Hypertrophic pulmonary osteoarthropathy (or Bamberger-Marie
disease) is a medical condition combining clubbing and periostitis of the
long bones of the upper and lower extremities. Distal expansion of the long
bones as well as painful, swollen joints and synovial villous proliferation are
often seen. The condition may be primary or secondary to diseases like lung
cancer.

Cuses:
1. Primary: autosomal dominant
2. Pulmonary

19
a. malignancy. Primary lung cancer, lymphoma, pleural mesothelioma,
and secondary pulmonary malignancies can all be accompanied by
clubbing.
b. Painful clubbing is more likely in patients with bronchogenic
carcinoma, lung abscess, and bronchiectasis.7
2. Chronic infection (or inflammation).
c. Digital clubbing has classically been associated with chronic
infections such as bronchiectasis, lung abscess, empyema,
pulmonary tuberculosis, and infective endocarditis.8 Both
inflammatory bowel disease (Crohn disease more than ulcerative
colitis) and chronic liver disease have been associated with
clubbing.
3. Clubbing has been seen with HIV and
4. Chronic parasitic infections with Trichuris trichiura (whipworm) and
schistosomal
5. Colonic polyposis.
3. Cyanotic congenital heart disease.
Pathogenesis:
1. Chronically elevated prostaglandin E2 levels plasma levels of vascular
endothelial growth factor (VEGF) are higher than in control subjects. VEGF
appears to be a promoter of angiogenesis
2. Resection of the vagus nerve can abate or abolish both clubbing and
pulmonary osteoarthropathy led to the theory that the vagus nerve may
be a key signalling pathway
3. In the pathogenesis of digital clubbing, local hypoxia, platelet activation,
release of signal proteins such as VEGF, and stimulation of angiogenesis
and other cellular activities are probably contributory.