Definition

Cherry angiomas are benign vascular skin lesions characterized by capillary proliferation within the dermis. Clinically known as Campbell de Morgan spots, these papular lesions are among the most common acquired cutaneous vascular proliferations. Though typically asymptomatic, their appearance can be cosmetically concerning. In rare instances, eruptive forms may be associated with systemic conditions.

Epidemiology

Cherry angiomas are extremely common, especially with increasing age. They usually start to appear in adulthood most often after the age of 30 and gradually become more numerous over time.

• By the age of 60, most people will have at least one.
• By 75 years old, around 75% of individuals are affected.

They occur equally in men and women, and affect all ethnic groups, although they tend to be more visible in lighter skin tones. There may also be a genetic tendency, as some people have a family history of similar lesions.

Rarely, sudden onset of numerous lesions (eruptive cherry angiomas) has been reported in association with internal malignancy or during pregnancy.

Etiology and Pathogenesis

Exact cause is not fully known, but several factors are linked:

1. Hormonal factors

– More common during pregnancy

– May shrink after delivery

– Linked to high prolactin levels in some cases

2. Genetic mutations

Changes in certain genes like GNAQ, GNA11, and GNA14, Also sometimes seen in HRAS and KRAS genes. These genes are involved in blood vessel growth.

3. Possibly minor trauma or skin irritation:

May trigger development in some cases.

4. Not caused by cancer, but may rarely appear alongside internal tumors or systemic diseases

Clinical Features

Cherry angiomas present as firm, dome-shaped papules ranging from red to blue or purple in color, typically measuring 1–10 mm in diameter. They are usually multiple and randomly distributed across the trunk and extremities, sparing mucous membranes, hands, and feet. The lesions are asymptomatic but may bleed if traumatized. In thrombosed angiomas, the surface may appear blackish, though dermoscopy can help reveal the underlying vascular hue.

Diagnosis

Diagnosis is primarily clinical, supported by characteristic dermoscopic features, such as red to purple lacunae in a lobular or “red clod” pattern. Histological evaluation, when necessary, reveals dilated venules within a thickened papillary dermis with intervening collagen bundles. Cherry angiomas should be distinguished from petechiae and glomeruloid hemangiomas, particularly when multiple lesions erupt suddenly or there is suspicion of systemic disease.

Management

Cherry angiomas are benign and generally require no treatment unless they are symptomatic, subject to recurrent trauma, or cosmetically undesirable. When removal is indicated, options include:

– Laser therapy (e.g., pulsed dye laser)

– Electrosurgery

– Cryotherapy

– Shave excision

Recurrence following treatment is uncommon, and procedures are typically well-tolerated.

Written by: 

Raneem Alahmadi, Medical Intern.

Revised by: 

 Naif Alshehri, Medical Intern

Resources:

Bolognia 5th edition

Dermnet

Definition and Epidemiology:

Basal cell carcinoma (BCC) is a common skin cancer arising from the basal layer of epidermis and its appendages. These tumors have been referred to as “epitheliomas” because of their low metastatic potential. However, the term carcinoma is appropriate, since they are locally invasive, aggressive, and destructive of skin and the surrounding structures including bone. Estimates of the incidence of BCC are imprecise since there is no cancer registry that collects data on BCC. The American Cancer society estimates that in 2012, 5.4 million cases of nonmelanoma skin cancers (NMSCs) were diagnosed in 3.3 million people, of which approximately 8 in 10 cases would have been BCC.

Risk factors:

• BCC is particularly common in Caucasians; it is very uncommon in darker-skinned populations.
• The incidence in men is 30 percent higher than in women, particularly with the superficial type.
• The incidence of BCC increases with age; persons aged 55 to 75 have about a 100-fold higher incidence of BCC than those younger than 20.
• Exposure to UV light.
• Chronic arsenic exposure
• Radiation therapy
• Long term immunosuppressive therapy
• Basal cell nevus syndrome.

Clinical features:

Approximately 70 percent of BCCs occur on the face, consistent with the etiologic role of solar radiation. Fifteen percent present on the trunk, and only rarely is BCC diagnosed on areas like the penis, vulva, or perianal skin.

The clinical presentation of BCC can be divided into three groups, based upon lesion histopathology: nodular, superficial, and morpheaform.

Nodular: Nodular BCCs, which represent about 60 percent of cases, typically present on the face as a pink or flesh-colored papule. The lesion usually has a pearly or translucent quality and a telangiectatic vessel is frequently seen within the papule. The papule may often be described as having a “rolled” border, where the periphery is more raised than the middle. Ulceration is frequent, and the term “rodent ulcer” refers to these ulcerated nodular BCCs.

Superficial: About 30 percent of BCCs are superficial BCCs. For unclear reasons, men have a higher incidence of superficial BCC than do women. 

Superficial BCCs most commonly occur on the trunk, and typically present as slightly scaly, non-firm macules, patches, or thin plaques light red to pink in color. The center of the lesion sometimes exhibits an atrophic appearance and the periphery may be rimmed with fine translucent papules. A shiny quality may be evident when a superficial BCC is illuminated. 

Morpheaform: Morpheaform or sclerosing BCCs constitute 5 to 10 percent of BCCs. These lesions are typically smooth, flesh-colored, or very lightly erythematous papules or plaques that are frequently atrophic; they usually have a firm or indurated quality with ill-defined borders.

Diagnosis:

Clinicians who are familiar with the clinical manifestations of BCC are often able to make the diagnosis based upon clinical examination. Even so, a skin biopsy is usually performed to provide histologic confirmation of the diagnosis.

Treatment:

The treatment for a BCC depends on its type, size and location, the number to be treated, patient factors, and the preference or expertise of the doctor. Most BCCs are treated surgically. Long-term follow-up is recommended to check for new lesions and recurrence; the latter may be unnecessary if histology has reported wide clear margins.

Treatment options include:

• Excision biopsy
• Mohs micrographically controlled surgery involves examining carefully marked excised tissue under the microscope, layer by layer, to ensure complete excision.
• Superficial skin surgery comprises shave, curettage, and electrocautery. It is a rapid technique using local anaesthesia and does not require sutures.
• Cryotherapy is the treatment of a superficial skin lesion by freezing it, usually with liquid nitrogen.
• Photodynamic therapy (PDT) refers to a technique in which BCC is treated with a photosensitising chemical, and exposed to light several hours later.
• Topical imiquimod
• Topical 5-Fluorouracil
• Radiotherapy

Written by: 

Bandar Alharbi, Medical Intern.

Revised by: 

Naif Alshehri, Medical Intern.

Resources:

UTD

Dermnet

Mayo clinic

Background

Ashy dermatosis, also known as erythema dyschromicum perstans (EDP), is a rare, chronic, idiopathic skin disorder characterized by the gradual appearance of bluish-gray to slate-colored macules and patches. It primarily affects individuals with darker skin phototypes (Fitzpatrick III–VI), particularly those from Latin America, Asia, and the Middle East. The condition is more commonly seen in young adults, but it can affect individuals of all ages. The term “ashy” refers to the gray color of the lesions, which gives the skin a dusky or dirty appearance.

Etiology

The exact cause of ashy dermatosis remains unknown, making it a diagnosis of exclusion. Several hypotheses have been proposed, including a delayed-type hypersensitivity reaction or cell-mediated immune response targeting basal keratinocytes. Histopathological findings often resemble a lichenoid tissue reaction, further supporting this theory.

There have been occasional associations with infections (e.g., hepatitis C), medications (e.g., proton pump inhibitors, antibiotics, and antiepileptics), and autoimmune conditions. However, these associations are not consistent and are often anecdotal.

Clinical Features

Ashy dermatosis typically begins with the insidious onset of slate-gray or bluish macules, which may be preceded by a faint erythematous border in early lesions. The patches are usually symmetrical, with a predilection for the trunk, neck, arms, and face. Lesions are non-scaly, non-itchy, and may gradually enlarge over time, coalescing into larger patches.The disease course is chronic and can persist for years.

Diagnosis

The diagnosis of ashy dermatosis is clinical, supported by histopathological examination when necessary to rule out mimickers. Skin biopsy typically shows interface dermatitis with basal cell vacuolization, melanin incontinence, and a perivascular lymphocytic infiltrate in the superficial dermis. However, these findings are not pathognomonic.

Dermoscopy may aid in identifying gray-blue dots and globules corresponding to dermal melanin. Differential diagnoses include lichen planus pigmentosus, post-inflammatory hyperpigmentation, macular amyloidosis, and drug-induced pigmentation. Careful clinical history and distribution of lesions help in differentiation.

Management

Treatment of ashy dermatosis is often challenging, as the condition tends to be resistant to therapy and cosmetically distressing for patients. There is no universally effective treatment, and management focuses on patient education, psychosocial support, and trial of medications with anecdotal or limited evidence.

Topical corticosteroids, calcineurin inhibitors (e.g., tacrolimus), and systemic agents such as clofazimine, dapsone, and isotretinoin have been tried with variable success. Some reports suggest that Q-switched lasers may provide pigment improvement, though recurrence is common. Sun protection is recommended as a general skincare measure, although sun exposure is not a known trigger.

Prognosis and Prevention

Ashy dermatosis is a benign condition without systemic involvement, but its chronicity and cosmetic impact can lead to psychological distress. Lesions may stabilize over time but often persist indefinitely. There is no established method for prevention, and recurrence after treatment is common.

Written by: 

Dr Renad AlKanaan

Revised by: 

Naif Alshehri, Medical Intern

References:

Dermnet

UpToDate

Bolognia 5th Edition

Picture Reference:

Bolognia 5th Edition

Introduction and Epidemiology:

Chickenpox is a highly contagious viral infection that causes an acute fever and blistered rash, mainly in children. Varicella virus is the etiologic agent of chickenpox. Varicella zoster virus has a worldwide distribution and 98% of the adult population is seropositive.  In  the  pre-vaccine  era,  90%  of  children  <10  years  of  age developed varicella and ~4 million cases occurred annually in the US, with large outbreaks during the winter and spring. Since the introduction of the varicella vaccine in 1995, the overall incidence of varicella has  decreased  by  ~85%,  with  evidence  of  herd  immunity.

Pathogenesis:

Airborne  droplets  are  the  usual  route  of  transmission  of  varicella, although direct contact with vesicular fluid is another mode of spread, and the incubation period is 11–20 days. Varicella is extremely contagious,  and  80–90%  of  susceptible  household  contacts  develop  a  clinically  evident  infection.  The  affected  individual  is  infectious  from  1–2 days before skin lesions appear until all the vesicles have crusted.

Clinical features:

A  prodrome  of  mild  fever,  malaise,  and  myalgia  may  occur,  especially in  adults.  This  is  followed  by  an  eruption  of  pruritic,  erythematous macules  and  papules,  which  starts  on  the  scalp  and  face,  and  then spreads to the trunk and extremities. Lesions rapidly evolve over 12 hours into 1–3 mm clear vesicles surrounded by narrow red halos (“dew drops on a rose petal”). The number of vesicles varies from only  a  few  to  several  hundred,  and  there  is  often  involvement  of  the oral mucosa. Sparing of the distal and lower extremities is common. Older vesicles evolve to form pustules and crusts, with individual lesions healing within 7–10 days. The presence of lesions in all stages of development is a hallmark of varicella. The  disease  course  is  usually  self-limited  and  benign  in  healthy children. Secondary  bacterial  infection  of  the  skin  with  subsequent  scarring  is the most common complication. CNS sequelae are uncommon ( <1 per 1000  cases)  and  may  include  encephalitis  and  acute  cerebellar  ataxia. Reye  syndrome  which  consists  of  encephalitis  plus  fatty  liver  is  now rare  due  to  avoidance  of  aspirin  in  children  with  varicella.  Varicella in  adolescents  and  adults  is  often  more  severe  than  in  children,  with an  increased  number  of  skin  lesions.

Diagnosis:

A clinical diagnosis can usually be made based upon the history, including previous varicella or vaccine administration, and physical examination.  A  Tzanck  smear,  PCR  or  DFA  can  assist  in  quickly  confirming the diagnosis.

Treatment:

Varicella in immunocompetent children can be treated symptomatically with  antipyretics  (e.g.  acetaminophen),  antihistamines,  calamine lotion,  and  tepid  baths.  If  started  within  24–72  hours  after  the  onset of  the  cutaneous  eruption,  acyclovir  has  been  shown  to  decrease  the duration and severity of varicella. Oral acyclovir and valacyclovir are FDA-approved for the treatment of varicella in children (2–17 years of age) while acyclovir is approved for adults. These antiviral  agents  are  recommended  for  varicella  in  healthy  adolescents  and adults  as  well  as  in  children  with  chronic  cutaneous  or  pulmonary disorders  and  in  those  receiving  chronic  salicylate  therapy,  inhaled corticosteroids,  or  intermittent  oral  corticosteroids.  However,  routine antiviral  therapy  is  not  recommended  for  otherwise  healthy  children with varicella due to the self-limited disease course and modest benefits of  treatment.

Written by: 

Bandar Alharbi, Medical Intern

Revised by: 

Naif Alshehri, Medical Intern

Resources:

Bolognia 5th edition

Dermnet

MOH 

Overview:

Impetigo is the most common bacterial skin infection in children. It is a highly contagious superficial infection primarily caused by the Staphylococcus aureus and, less commonly, Streptococcus pyogenes. The condition can present in two forms: non-bullous and bullous impetigo.

Epidemiology:

• Primarily affects children <6 years of age. 
• Highly contagious and spreads through direct contact with an infected individual or contaminated objects (fomites). 

Predisposing factors: 

Several factors increase the risk of developing impetigo, including:

• Environmental factors: Warm temperature and high humidity 
• Poor hygiene 
• Underlying skin conditions: Atopic dermatitis, scabies, and chicken pox.
• Skin trauma: Lacerations, insect bites, and burns.

Pathogenesis:

Infection occurs when bacteria enter through minor skin breaks, such as scratches, trauma, or other skin infections. Disruption of the skin barrier allows bacterial adherence and invasion, leading to infection.

Clinical features:

Non-Bullous Impetigo (Most common form):

Lesion characteristics:

• Commonly appears on the face (especially around the nose and mouth) and extremities.
• Initially presents as a single erythematous macule, which evolves into vesicle or pustule.
• Later develops into superficial erosions covered by characteristic honey-colored yellow crusts.
• Minimal or no surrounding erythema.

Bullous Impetigo:

Lesion characteristics:

• Affects the face, trunk, buttocks, axillae, and extremities.
• Begins as small vesicles that enlarge into superfecial Bullae.
• In late stages, bullae become flaccid and transparent, then ruptures to leave scale with no thick crust.
• More likely to be associated  with systemic symptoms.

Diagnosis:

• Impetigo is primarily a clinical diagnosis.
• A skin swab culture (from the exudate beneath crusts or fluid from an intact bullae) may be performed for confirmation.
• Approximately 50% of patients may have leukocytosis.

Treatment:

General Measures:

• Cleanse the affected area and remove crusts.
• Maintain proper hand hygiene.

Topical Antibiotics:

For healthy patients with few lesions and no systemic symptoms, the following topical treatments are recommended:

Mupirocin, retapamulin, or ozenoxacin.

Oral Antibiotics:

Systemic antibiotic therapy is required in the following situations: 

• Bullous impetigo 
• Widespread non-bullous impetigo 
• Failure to respond to topical treatment 
• High risk of complications 
• Presence of comorbidities 

First line oral antibiotic: flucloxacillin

Prevention:

• Avoid touching affected areas.
• Practice regular hand hygiene.
• Refrain from sharing personal items, such as towels and clothing.
• Change and wash clothing and bedding daily in hot water.
• Avoid close contact with others.

Done by:

Layan Alshehri, Medical Intern 

Revised by:

Naif Alshehri, Medical Intern

Resources:

Bolognia 5th Edition

DermNet

Overview:

Scabies is a contagious skin infestation caused by Sarcoptes scabiei var. hominis mite. It leads to severe pruritus and skin lesions due to the mite burrowing into the epidermis. 

Epidemiology:

Scabies is a widespread condition affecting individuals of all ages, ethnicities, and socioeconomic groups. Factors contribute to its spread:

• Overcrowded living conditions 
• Delayed diagnosis and treatment 
• Limited public awareness 
• Poor hygiene 

Transmission can be through direct skin to skin contact, and indirectly through contaminated objects (fomites). 

A severe form of scabies, crusted scabies (Norwegian scabies), occurs in immunocompromised individuals, and is highly contagious. 

Pathogenesis:

The Incubation period varies:

• First time infestation: symptoms appear within 2 to 6 weeks, 
• Reinfestation: symptoms develop faster,  within 24 to 48 hours. 

Scabies mites can survive outside the human body for up to 3 days. However, in crusted scabies, mites can survive up to 7 days. 

Clinical features:

Itching (pruritus):

• Often severe and worse at night or with hot showers. 
• It can be the first symptom before visible skin lesions appear.
  

Lesions distribution and appearance: 

• Lesions present as small erythematous papules with varying degree of excoriations. 
• Other possible lesions include nodules and vesicles.  
• Symmetrically affects interdigital web spaces of the hands, wrists, axillae, waist, ankles, feet, and buttocks. 
• The face and scalp are typically spared, except in infants, elderly, immunocompromised patients, and in crusted scabies cases.
• Burrows is a pathognomonic sign, representing the tunnels created by female mites as they lay eggs. Burrows appear as grayish-white, thread like lines, measuring 1 to 10 mm in length. 
• Crusted scabies has a widespread involvement of thick scaling and crusting.

Diagnosis:

Diagnosis is clinically, based on history and physical examination. Can be confirmed using diagnostic methods include:

• Dermoscopy allows visualization of mites and eggs. 
• Skin scraping and microscopy using mineral oil preparation. 

Treatment:

First line treatment: Topical Permethrin 5%

• Applied from head to toe in infants and elderly. In other age groups, face and scalp are excluded from treatment. Applied overnight for 8 to 12 hours on day 1 and 8. 

Environmental and Preventive Measures:

• Clothing, bedding, and towels should be washed in hot water and dried in high heat or sealed in a bag for 7 to 10 days. 
• All close contacts, even asymptomatic, must be treated in the same way. 

Post-Treatment: 

• After successful treatment, pruritus and skin lesions may persist for 2 to 4 weeks, this is called post scabetic pruritus. 

Oral ivermectin is an option for treatment failures, outbreaks, or non-adherence, with a repeat dose after two weeks. Other alternatives include 25% benzyl benzoate or 0.5% malathion lotion.

Done by:

Layan AlShehri, Medical Intern 

Revised by: 

Naif Alshehri, Medical Intern

Resources:

Bolognia 5th Edition. 

DermNet