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Pityriasis

Pityriasis (Tinea) Versicolor
  • A mild chronic infection of the skin caused by Malassezia yeasts, and characterized by discrete or confluent, scaly, discolored or hypopigmented areas mainly on the upper trunk. 
  • Caused by a lipophilic yeast species, Malassezia furfur, belonging to the genus Malassezia. 

Risk factors for the development of P. versicolor 

  • Hot, humid climate : The disease is more common in summers and in tropical countries.
  • Malnutrition states and in diseases like Cushing’s syndrome or in patients taking corticosteroids.
  • Pregnancy
  • Genetic predisposition

Pityriasis versicolor



Diagnosis of fungal infections 
  • Clinical features
  • KOH examination
Fungal hyphae in dermatophytes
“Spaghetti & meat ball” appearance in P.versicolor.
  • Fungal culture- SDA


Management of Pityriasis

May be treated with many therapeutic agents, but these regimens should be continued for several weeks to ensure cure. 
  • Topical: 
Selenium sulfide suspension.
Ketoconazole 2 % shampoo, for bath twice weekly.
Zinc pyrithione containing shampoos are also effective.
Topical antifungal and keratolytic creams/ointments.
  • Systemic: may be used in severe infections.
Oral Ketoconazole, 200 mg daily for 5 to 10 days OR 400 mg monthly for 4 to 15 months has a 90-95 % cure rate.
Oral Itraconazole, 200 mg daily for 5 to 7 days.
Oral Fluconazole, single dose of 400 mg may be used.
  • Preventive measures like keeping the skin dry and maintenance of hygiene aids in preventing recurrences

Pityriasis Rosea

Pityriasis denotes fine scales, and rosea is colored or pink.

  • Pityriasis rosea (PR) is a common benign papulosquamous disease that was originally described by Camille Melchior Gibert in 1860. 

  • PR can have a number of clinical variations. 

  • Its diagnosis is important because it may resemble secondary syphilis.

Pathophysiology

  • PR has often been considered to be a viral exanthem. 

  • Its clinical presentation supports this concept. 

  • PR has been linked to upper respiratory infections, it can cluster within families and close contacts, and it has an increased incidence in individuals who are immunocompromised. 

  • As with viral exanthems, the incidence may increase in the fall and the spring. 

  • A single outbreak tends to elicit lifelong immunity.

  • Immunologic data suggest a viral etiology. Increased amounts of CD4 T cells and Langhans cells are present in the dermis; this observation may indicate viral antigen processing and presentation. 

  • Also, anti-immunoglobulin M (IgM) to keratinocytes has been found in patients with PR; this finding may be associated with the exanthem phase of the presumed viral infection.

  • Despite these tendencies, no single virus has been proven to cause the disease. 

  • A number of viruses have been studied for a link to PR. 

  • Serology and polymerase chain reaction for viral DNA has been negative for Epstein-Barr virus, parvovirus B19, and cytomegalovirus in patients diagnosed with PR.

  • Human herpesvirus (HHV)–7 viral is demonstrated DNA in both the lesions and the plasma in patients with PR. 

  • In addition, a separate study found HHV-7 DNA in lymphocytes.

  • Polymerase chain reaction has shown both HHV-7 and HHV-6 DNA in a variety of tissues and secretions from patients with PR. 

  • In the same study, in situ hybridization of lesional lymphocytes showed both HHV-7 and HHV-6 mRNA. 

  • However, herpesvirus like particles were not seen via electron microscopy. Follow-up studies have not confirmed a herpes etiology, and because HHV-7 is frequently found in healthy individuals, its etiologic role is controversial

Causes

  • PR may represent a viral exanthem (and at times enanthem).

  • PR-like drug eruptions may be difficult to distinguish from non–drug-induced cases. Medication-induced eruptions have been reported with captopril, metronidazole, isotretinoin, penicillamine, levamisole, bismuth, gold, barbiturates, ketotifen, clonidine, aspirin, and omeprazole.
  • Certain vaccinations, such as the BCG vaccine or the diphtheria vaccine, have been reported to cause similar eruptions. 

  • Lesions are also thought to be increased in individuals with high stress levels.

Frequency

International

Worldwide, PR has been estimated to account for 2% of dermatologic outpatient visits. 
The disease is more common in the spring and the fall in temperate climate zones. 
However, it may be more frequent in the summer in some other regions, and it favors the hot, dry season in Australia, India, and Malaysia.

Mortality/Morbidity

PR is a benign self-limited disease associated with mild morbidity with rash and occasional pruritus.

Race
No racial predominance is reported. 
More intensely pigmented Africans tend to have more widespread disease. 
The lesions in African Americans may lack a rose color, and they may appear darker than the surrounding skin.

Sex
PR is more common in women than in men. 

Age
PR commonly develops in children and young adults, although any age group can be affected. 
Most patients are aged 10-35 years.

History

  • The history should include questions about close contacts with similar eruptions. 
  • This finding is uncommon because most cases of PR are sporadic, as PR is thought to reflect a weakly contagious disease. 
  • A history of medication intake should be obtained because several medications have been shown to cause a similar exanthem.

  • The disease typically begins with a solitary macule that heralds the eruption (called the herald spot/patch), which is usually a salmon-colored macule. 

  • This initial lesion enlarges over a few days to become a patch with a  collarette of fine scale just inside the well-demarcated border. 

  • Within the next 1-2 weeks, a generalized exanthem usually appears, although it may occur from hours to months after the herald patch.

  •  This secondary phase consists of bilateral and symmetric macules with a  collarette of scale oriented with their long axes along cleavage lines. 

  • This phase tends to resolve over the next 6 weeks, but variability is common. 

  • Pruritus is common, usually of mild-to-moderate severity, and it occurs in 75% of patients


Physical examination
  • The herald patch is usually a single pink patch, 2-10 cm in diameter, on the neck or the trunk with a fine collarette scale . It is observed in more than 50% of patients, and it may occur as multiple lesions or in atypical locations. 
  • About 1-2 weeks after the herald patch is seen, the generalized eruption appears, although it has been known to occur from hours to 3 months later. It consists of salmon-colored macules or patches, 0.5-1.5 cm in diameter, with a collarette scale, often described as having a cigarette paper–like appearance. The long axes of the lesions are oriented in a parallel fashion along cleavage lines, giving the classic Christmas tree pattern . These secondary lesions most commonly occur on the trunk, the abdomen, the back, and the proximal upper extremities. 
  • Pruritus occurs in 75% of patients and is severe in 25%. 
  • Lymphadenopathy is uncommon, but, when present, it is usually observed in African Americans

  • Atypical PR occurs in 20% of patients. 
These variations can be separated into changes in the lesions and/or their distribution. 
Photosensitivity may occur. Photoexacerbated and photoprotected forms have been documented, although photosensitivity is not a classic manifestation of the disease. 
Lesions may be localized to single areas, such as the abdomen, the groin, the axilla, the distal extremities, the palms, and the soles.
  • An inverse PR may be seen. This form manifests as lesions on the face and the distal extremities, and it is more common in children than in adults. The herald patch may be the only manifestation of the disease. 
  • A unilateral variant- lesions do not cross the midline. 
  • Drug-induced cases are frequently observed without the herald patch.

  • Variations in lesion morphology
Atypical, large patches tend to be fewer in number. They may coalesce to form a variant known as pityriasis circinata et marginata of Vidal. The primary lesions may be papules, vesicles, pustules, or urticarial or purpuric plaques. PR may first be evident with widespread, intensely pruritic papulovesicles in an unusual distribution, such as on the neck and the scalp. 

Papular PR tends to have scaling papules in the normal distribution; this form is more common in children than in adults. 

Erythema multiforme–like plaques may be evident. 

Purpuric PR is seen in both adults and children, and it follows the usual presentation of the disease


  • Oral involvement may occur as punctate hemorrhages, ulcers, papulovesicles, bullae, or erythematous plaques. 


Lab Studies

  • One must be careful to rule out syphilis. 
A screening rapid plasma reagin (RPR) test or a VDRL test should be ordered for appropriate individuals. 
One should be aware of the prozone phenomenon seen in secondary syphilis and request titration of the RPR test. 
An HIV test should also be considered in these patients.

  • Other laboratory tests are usually normal and, therefore, unhelpful. 

  • Changes in the white blood cell count and differential, as well as increases in erythrocyte sedimentation rate, total serum protein level, globulin level, and albumin level, are rarely reported

Histologic Findings

  • A biopsy specimen is helpful to confirm the diagnosis, especially in atypical cases. 

  • It shows superficial perivascular dermatitis . 

  • Focal parakeratosis in mounds, hyperplasia, and focal spongiosis are observed in the epidermis. 

  • The epidermis may show exocytosis of lymphocytes, variable spongiosis, mild acanthosis, and a thinned granular layer.

  • In the dermis, extravasated red blood cells are a helpful finding along with a perivascular infiltrate of lymphocytes, histiocytes, and eosinophils. A number of monocytes are also commonly present. 

  • The herald patch has similar features but has a deeper infiltrate and more acanthosis owing to its chronicity. 

  • Such variations as dyskeratotic cells in the epidermis, multinuclear giant cells, and focal acantholytic dysfunction have been observed. 

  • These features may closely resemble erythema annulare centrifugum, guttate psoriasis, superficial gyrate erythema, and small plaque parapsoriasis.


Medical Care

  • The most important part of treating patients with PR is reassurance that the rash will resolve.

  • Relief of pruritus is helpful and can be accomplished by using topical steroids, oral antihistamines, topical menthol-phenol lotions, and oatmeal baths. Systemic steroids are not recommended. Although they suppress pruritus, systemic steroids do not shorten the overall disease; in fact, they may prolong or exacerbate the disease. 

  • Ultraviolet B (UV-B) light therapy, starting at 80% of the minimum erythrogenic dose, may rapidly relieve pruritus in resistant cases. 

  • If itching is not controlled, the dose of UV-B light should be increased by 20% until symptoms decrease. 

  • Decreased lesion severity with UV-B light therapy. 

  • There is possibility of post inflammatory pigmentation with light therapy. 

  • For vesicular PR, 20 mg of dapsone twice a day. 
  • High-dose acyclovir (800 mg qid) may help shorten disease, especially if instituted early in the disease course




Further Outpatient Care


  • Generally, the disease resolves within 12 weeks. 



  • Most cases do not recur, but some patients may develop PR more than once. In cases where the diagnosis is in doubt or if the disease persists past this period, further evaluation is advised. 



  • Persistent PR of more than a 3-month duration is classified as pityriasis lichenoides chronica


LICHEN PLANUS

Synopsis :


Definition
History and epidemiology
Aetiopathogenesis
Clinical features
Classification
DD
Management
Prognosis



Introduction :


Papulosquamous inflammatory disorder characterized by

  • Distinctive color - Violacious
  • Morphology – Flat topped papule
  • Typical Location – Volar aspect of extremities
  • Characteristic pattern of evolution



Affect skin, mucous membrane, nail and hair


Prototype of lichenoid eruption




History :

Lichen = tree moss    Planus = flat

LP – name given by Erasmus Wilson in 1869

Whitish striae and punctation on flat LP lesion described by Wikham in 1895

Histological findings elaborated by Darier in 1909


Epidemiology :

Worldwide distribution

No racial predisposition

Less than 1% of general population affected

Age
Male – earlier
Female – late
Extremes of age – less common


Aetiopathogenesis :

Immunologically mediated disease in genetically susceptible individual

Other association –
Cutaneous LP - Hepatitis C, Anxiety and depression
Oral LP - Mercury and Gold sensitization



Clinical Features :

Shiny, violaceous, flat topped,     polygonal, pruritic papules with ‘wickham striae’ and koebnerization

Insidious onset and size ranges from pinpoint to centimeters



Koebnerization  

Wickhams striae  
Affect Volar aspect of wrists, ankles, lumbar region with bilateral symmetrical distribution

Oral mucous membrane and genitalia are additional site of involvement

Pruritus - mild irritation to intolerable

Pinkish papule change to violaceous then to brown macule as disease progress




Variant of LP


Configuration

  • Annular
  • Linear



Site of involvement

  • Palm and sole
  • Mucous membrane
  • Nail
  • Scalp



Morphology of lesion

  • Hypertrophic
  • Atrophic
  • Vesicobullous
  • Erosive and Ulcerative
  • Follicular
  • Actinic
  • Lichen Planus Pigmentosus
  • Others



Diagnosis

Clinical feature



Histology


Histology

Compact orthokeratosis
Wedge shaped hypergranulosis
Irregular acanthosis
Vacuolar alteration of the basal layer
Band like dermal lymphocytic infiltrates
Colloid bodies
Max –Joseph spaces


Management of LP

Challenging for both patient and physician

Only minor symptoms or considerable discomfort and disability

Many drugs lack conclusive evidence for efficacy


Oral LP


General measure


Good oral hygiene and regular professional dental care

Offending drugs or dental amalgam, gold- withdrawal and replacement

Topical lidocaine  gel or Diphenhydramine for pain relief



Topical steroids 

  • First line therapy in mucosal LP
  • Triamcinolone in orabase
  • Clobetasol propionate in ointment or paste
  • Corticosteroid lozenges
  • Betamethasone mouthwash
  • Fluticasone propionate spray

Intralesional injection

Chlorhexidine mouth wash and anticandidal  drug therapy

Hydrocortisone vaginal pessary



Systemic Glucocorticoids

For extensive, ulcerative/erosive lesion of oral and vulvovaginal LP

Used alone or in conjunction with topical therapy

Prednisolone 30-80mg/day tapered over 3-6 weeks

Relapse after dose reduction or discontinuation


Retinoids

Topical tretinoin gel for erosive and plaque like lesion – less attractive because of irritation

Isotretinoin gel for nonerosive oral lesion-improves in 2 months-recovers after discontinuation

In conjunction with topical steroid

Acitretin 30mg/day complete remission in 8 weeks


Cyclosporine
Oral – 3-10mg/kg/day in severe ulcerative disease
Topical – beneficial but not available commercially

Tacrolimus
Effective in erosive mucosal disease-rapid relief from pain and burning


Miscellaneous

Griseofulvin – used empirically
Fluconazole, itraconazole – for candidal overgrowth, concomitant use with systemic steroid
Hydroxychloroquine –  200-400mg/d for 6 months – complete healing of oral lesion
Azathioprine, cyclophosphamide
Laser therapy
Surgical excision of persistent ulcer


Cutaneous LP

Topical Glucocorticoids
For limited cutaneous disease
Potent creams is sufficient for  symptomatic relief for small area, larger area needs dilution

Intralesional trimcinolone acetonide
(5mg to 10mg/ml) every 4 week – lesion regress within 3-4 months
Hypertrophic LP:-10-20mg/ml
Monitor for atrophy or hypopigmentation

 Antihistamines for itching


Retinoids :

Acitretin : 30 mg / day for 8 weeks

Tretinoin : 10-30 mg/d

Etretinate : 10-20 mg/d


Photochemotherapy :

PUVA in generalized cutaneous LP

50 mg of Trioxsalen in 150 L  of water - 10 min of UVA bath

75 patients – 65% cured ; 15% improved



Immunosuppressive therapy 

Cyclosporine: 3-10 mg/kg/d

Azathioprine , mycophenolate mofetil

Ind : recalcitrant LP


Miscellaneous :

Dapsone : 200 mg/d

Hydroxychloroquine : 200-400 mg/d

IFN- α2b

Metronidazole : 500 mg b.d

Cyclophosphomide ,methotrexate


Prognosis :

Unpredictable ; 1-2 yrs

Duration  Î±  extent /site/ morphology

L planopilaris : most chronic

Generalised : rapid course

Gen < skin

Relapse : 15 -20 %

Melanocytic Disorders

Solar lentigo

  • Common finding in elderly individuals
  • Brown, macules located on sun-exposed areas ("liver spots“-on the back of the hands, and face)
  • Increased number of melanocytes which produce excessive melanin.
  • Not precancerous
  • No treatment is required



Freckles

  • Focal overproduction of melanin with normal number of melanocytes with increase in melasosomes.
  • Freckles are sharply demarcated light brown-ginger macules of upto 5mm in diameter due to over production of melanin.
  • Most prominent in sun exposed sites, and multiply and become darker with sun exposure



Vitiligo
  • Common in blacks
  • Autoimmune destruction of melanocytes
  • Causes extensive areas of skin depigmentation 
  • Often associated with other autoimmune conditions like diabetes, thyroid and adrenal disorders and pernicious anemia.



Clinical features

  • Segmental vitiligo- is restricted to one part of the body, but necessarily a dermatome.
  • Generalised vitiligo- is often symmetrical and involves the hands, wrists, knees, neck and area around the body orifices.
  • The hair of the scalp and beard may also depigment.
  • The patches of depigmentation are sharply defined.




Treatment
  • Protecting the patches from excessive sun exposure with clothing and sunscreen- helps in reducing episodes of burning and potentially of skin cancer.
  • Potent topical corticosteroids
  • Phototherapy with PUVA



Albinism

It occurs when the melanocytes are unable to synthsize melanin ( either by absence of tyrosinase activity or inability of cells to take up tyrosine)



Melasma

Macular, hyperpigmented lesions on the forehead and cheeks 
Female predominance; exacerbated (melanocytes produce more melanin) by:
a. Oral contraceptives (OCP)
b. Pregnancy ("pregnancy mask")
c. Sunlight
Treatment
Application of hydroquinone (bleaching agent) to skin




Heart Murmurs

Murmurs in valvular heart disease result when there is valvular insufficiency or regurgitation (the valves fail to close completely) or stenosis (narrowing of the valves). The aortic or mitral valves are most commonly involved in valvular disease.

For most of ventricular systole, the mitral valve should be closed and the aortic valve should be open, so that '' common systolic valvular defects '' include mitral insufficiency and aortic stenosis. For most of ventricular diastole, the mitral valve should be open and aortic valve should be closed , so that '' common diastolic valvular defects '' include mitral stenosis and aortic insufficiency.

A heart murmur is heard downstream from the valve. Thus, stenosis is orthograde direction from valve and insufficiency is retrograde direction from valve.

Auscultation sites for mitral and aortic murmurs are shown in figure 

Heart Murmurs

Acne vulgaris


Occurs mostly in teenagers.
Peak: late teenagers but may persist till third decade and beyond especially in females.
  • Etiology:

Elevated sebum excretion:
Sebum excretion is necessary for the development of acne but is not sufficient to cause acne on its own.
The main determinants of sebum excretion are hormonal, which accounts for the onset of acne in the teenagers. 
Androgens and  progestogens increase sebum excretion but estrogens reduce it.

Propionibacterium acnes
It colonises the pilosebaceous ducts and acts on lipids to produce a number of pro-inflammatory factors.

Occlusion or blockage of the pilosebaceous unit.

Clinical features

  • Site: usually limited to the face, shoulders, upper chest and back.
  • Greasy skin
  • Open comedones (blackheads) due to plugging by keratin and sebum of the pilosebaceous orifice, or closed comedones (whiteheads) due to accretions of sebum and keratin deeper in the pilosebaceous ducts are evident.
  • Inflammatory papules, nodules and cysts may occur with some lesion.
  • The lesion may be followed by scarring.
  • Mild form
Dominated by presence of comedones.
May be due to exogenous substances like oily cosmetics, chlorinated hydrocarbons, tars, etc
Pustular rash may also be seen in those treated with steroids, lithium, OCP and anticonvulsants.
  • Moderate or Severe form
May have systemic disorder. E.g- polycystic ovarian disease, Androgen secreting tumors




Blackheads & whiteheads

Clinical variants of Acne:

Conglobate acne: 
severe acne with many abscesses and cysts, marked scaring and sinus formation.

2.      Acne fulminans: 
severe acne accompanied by fever, joint pains and markers of systemic inflammation ( raised ESR)

2.      Acne excoriee: 
effect of scratching or pricking, mostly seen on the face of teenage girls with acne.

3.      Infantile acne: 
Rare. It is due to sebotropic effects of maternal hormones on the infant.

Investigation: Rarely reqd.

It is important to enquire about the details of previous treatments and their duration.

Treatment:

1.Fairly minor disease dominated by comedones:
      Topical benzoyl peroxide or tretinoin is used
2.Mild acne: require antibiotics therapy
                       Local antibiotics: Clindamycin or Erythromycin.
                       Oral antibiotics: Oxytetracycline 1.5g per day on empty stomach. If the response is inadequate: Minocycline ( both must be contiued till 3 mnths to see if the antibiotics have worked or not)
                       If little response after 3 mnths treatment: Erythromycin 1g/day.
In women, oestrogen containing OCP can be used as a adjunct in therapy. ( oral estrogen reduces sebum production)
3. If these systemic and topical agents fails to produce an adequate clinical response within 3-6 months;
 Systemic retinoids—isotretinoin (decreases follicular keratinization, Sebum production, bacterial count)

Physical measures
Cysts incised and drained under LA.
Stubborn cysts: intralesional triamcinolone



Rosacea

It is a chronic disorder affecting the facial convexities, characterized by frequent flushing, persistent erythema and telangiectasia, interspersed by episodes of inflammation during which swelling, papules and pustules are evident.






Clinical features

  • The areas characteristically affected are the central convex areas of the face (nose, forehead, cheeks and chin) . Occasionally, the scalp, upper chest, back and even the limbs may be involved. 
  • In cases of rosacea showing the classical pattern of progression, the onset is most often marked by vascular changes, notably episodic flushing usually unaccompanied by sweating.
  • Erythema, which is often accompanied by a burning sensation, gradually becomes more persistent, is easily triggered by minor irritants, and is associated with increasingly prominent telangiectasia.
  • More advanced cases show follicular and nonfollicular papules and pustules, without comedones, followed by persisting tissue thickening due to oedema, fibrosis and glandular hyperplasia, leading ultimately to a peau d’orange appearance and phymas.
  • Factors which trigger flushing include emotion and stress, hot drinks, alcohol and other vasodilating drugs, and spicy food. 
  • Aggravating factors include the use of topical steroids on those occasions when they are used (usually in error) to treat rosacea.
  • Sun exposure may worsen or improve rosacea.
  • Rhinophyma, with erythema, sebaceous gland hyperplasia  and overgrowth of the soft tissue of the nose, is sometimes associates.
  • There may be complications like blepharitis and conjunctivitis.


Treatment

Oral oxytetracycline can be used for the pustular component of rosacea.

Topical metronidazole can also be used.

Erythema and telangiectasia don’t respond to antibiotic therapy.