skin images

Skin Type: 4

  • Lentigines, Solar Lentigines

    Lentigines, Solar Lentigines

    Lentigines, Solar Lentigines

    Definition: Lentigines are clearly defined, pigmented, flat or slightly raised lesions. Lentigines do not fade in the winter months. Solar Lentigines (SL) are also known as “liver” or “wisdom- spots”, are harmless areas of hyperpigmentation on the skin due to ultraviolet (UV) radiation.

    Etiology:  Lentigines can occur due to exposure to ionizing radiation. Familial syndromes associated with widespread lentigines originate from mutations in Ras-MAP kinase, mTOR signaling and PTEN pathways. SLs occur due to exposure to ultraviolet radiation, as seen in sun damage/ sunburn, indoor tanning and phototherapy. Exposure causes local proliferation of melanocytes and the accumulation of melanin within keratinocytes.

    Epidemiology: Lentigines affect males and females equally, and may occur in all ages and races. Lentigines are common in individuals with fair- skin, and frequently arise in sun- exposed areas on individuals with darker skin. Lentigines are commonly seen in individuals over 40 years of age. 

    Signs: There are many classifications of lentigines depending on their appearance on the body, causative factors and likelihood of progressing to other diseases or conditions. These include lentigo simplex, ink spot lentigo, and tanning bed lentigo. SLs are flat, well- circumcised round, oval or irregularly shaped patches. They may be skin coloured, tan, dark- brown or black depending on skin tone. Sls range from a few millimeters to several centimeters in diameter. SLs may be scaly.

    Differentials: Actinic keratosis, Seboorhoeic keratosis, Melanoma, nMelasma

    Diagnosis: Lentigines are diagnosed clinically by their appearance. Examination using dermatoscopy may be used to differentiate lentigines from melanoma. A diagnostic excisional skin biopsy may be performed for histological examination. Histopathology will show a thickened epidermis, increased melanocytes along the basal layer of the epidermis and increased melanin pigment within the keratinocytes.

    Treatment: Most lentigines persist indefinitely. SPF 50+ broad-spectrum sunscreen or hydroquinone bleaching cream may be used to lighten the lesions. Bleaching agents, however, are not effective in SL. Individual lesions may be lightened using cryotherapy, intense pulsed light or pigment lasers. Preventative measures include minimizing sun exposure and using sunscreen early in life.

    References:

    Chan B. Solar lentigo | DermNet NZ. dermnetnz.org. Published 2014. https://dermnetnz.org/topics/solar-lentigo

    Brown spots, lentigines and freckles. DermNet®. Published October 26, 2023. Accessed September 25, 2024. https://dermnetnz.org/topics/brown-spots-and-freckles#:~:text=Lentigines%20are%20common%20in%20people

    Lentigo, lentigines | DermNet NZ. dermnetnz.org. https://dermnetnz.org/topics/lentigo

  • Kaposi Sarcoma

    Kaposi Sarcoma

    Kaposi Sarcoma

    Definition: Kaposi sarcoma (KS) is a rare disease of the endothelial cells of blood vessels and the lymphatic system. There are four types of Kaposi sarcoma: Classic KS, Human immunodeficiency virus (HIV)- associated KS, endemic or African KS and iatrogenic KS.

    Etiology: Kaposi sarcoma herpesvirus (KSHV) or Human herpesvirus-8- 8 (HHV-8) is present in all forms of KS. HHV-8 is a double-stranded enveloped DNA virus with 6 major subtypes (A-F). HHV-8 interferes with many normal cell functions and requires co-factors that result in the decrease in CD4 cells and the development of Kaposi sarcoma. HHV-8 may be found in men who have sex with men (MSM), and heterosexuals and may be transmitted through saliva or arthropod bites. Iatrogenic KS occurs as a result of drug treatment leading to immunosuppression.

    Epidemiology: Classic KS affects patients over 50 years old of Sub-Saharan African, Middle European and Mediterranean descent. It is associated with Diabetes Mellitus. The male-to-female ratio is 17:1. Prevalence in the United States is 1: 100,000, and mirrors the distribution of HHV-8. HIV- HIV-associated KS mainly affects MSM, and is the most common malignancy affecting children in Uganda and Zambia. HIV- positive MSM have a 5 to 10-fold increased risk of developing KS. Endemic KS arises in Africa and has a unique predilection for the pediatric population. The male-to-female ratio is 2:1. Iatrogenic KS has a male-to-female ratio of approximately 3:1. Over 5% of transplant patients who develop a de-novo malignancy have a 400- 500 fold increased risk of developing KS when compared to the general population.

    Signs: KS presents with erythematous to violaceous macules, papules and nodules on the skin or mucous membranes. KS lesions begin small and eventually ulcerate. Early KS lesions appear as flat patches with associated lymphedema. These eventually evolve into plaques, nodules or scaly tumors. Patients with HIV- HIV-associated KS may develop lesions at any time during the illness. The aggression of KS is directly related to the degree of immunosuppression a patient is experiencing.

    Symptoms: External KS lesions ulcerate and become painful. Internal KS lesions may be associated with bleeding, hematemesis, hematochezia, melena, shortness of breath, and peripheral edema.

    Differentials: Interstitial granuloma annulare, spindle cell hemangioma, gasiform hemangioendothelioma, cutaneous angiosarcoma, pyogenic granuloma

    Diagnosis: A biopsy shoring characteristic features of KS is required for a definitive diagnosis. Histologically, KS presents as a spindle cell vascular neoplasm with extravasated red blood cells and hyaline globules. Immunohistochemistry positivity for LANA-1 also differentiates KS from similar lesions.

    Treatment: Skin involvement of KS is treated by local excision, liquid nitrogen and vincristine infections. Chemotherapy is used to treat endemic and systemic forms. HIV- HIV-associated KS is treated with Highly active antiretroviral therapy (HAART) and is combined with chemotherapy in severe cases. Iatrogenic KS treatment requires a reduction in immunosuppression to reduce levels of tumor growth-promoting proteins.

    References:

    1.     Kaposi sarcoma | DermNet NZ. dermnetnz.org. https://dermnetnz.org/topics/kaposi-sarcoma

    2.     Bishop BN, Lynch DT. Kaposi Sarcoma. In: StatPearls. Treasure Island (FL): StatPearls Publishing; June 5, 2023.

    3.     Grabar S, Costagliola D. Epidemiology of Kaposi’s Sarcoma. Cancers (Basel). 2021;13(22):5692. Published 2021 Nov 14. doi:10.3390/cancers13225692

  • Bullous Pemphigoid

    Bullous Pemphigoid

    Bullous Pemphigoid

    Definition: Bullous Pemphigoid is a chronic autoimmune bullous disease that is characterized by tense bullae on normal or erythematous skin (1).

    Etiology: Bullous Pemphigoid is caused by autoantibodies against hemidesmosomal proteins BP180 (type XVII collagen) and BP230 that lead to the production of subepidermal blisters (1).

    Epidemiology: Bullous Pemphigoid is the most common autoimmune subepidermal blistering condition  and it commonly affects older adults usually above 70 years old(1,2).

    Signs: It is characterized by severe pruritus along with tense blisters over urticaria plaques typically seen in the limbs and trunks (1). It is not typically seen in mucosal areas (1). 

    Symptoms: Patients typically face intense pruritus and discomfort or pain at the site of active lesions (1,2).

    Differentials: Pemphigus foliaceus, pemphigus herpetiformis, bullous lupus erythematosus, eczema, urticaria, prurigo, impetigo, erythema multiforme, Sweet syndrome, toxic epidermal necrolysis, and autotoxic pruritus (1).

    Diagnosis: The diagnosis is based on three factors; histopathological evaluation showing eosinophilic spongiosis or a subepidermal detachment with eosinophils, use of direct or indirect immunofluorescence assays to detect IgG and/or C3 deposition at the basement membrane and ELISA measurement of circulating autoantibodies (1).

    Treatment: The treatment is based on the patient’s clinical status and disease severity  (1). Systemic and topical high potency steroids are the current treatment options (1).

    References: (AMA)

    1.      Miyamoto D, Santi CG, Aoki V, Maruta CW. Bullous pemphigoid. Anais Brasileiros de Dermatologia. 2019;94(2):133-146. doi:10.1590/abd1806-4841.20199007 

    1. Miyamoto D, Santi CG, Aoki V, Maruta CW. Bullous pemphigoid. Anais Brasileiros de Dermatologia. 2019;94(2):133-146. doi:10.1590/abd1806-4841.20199007 
  • Bites, Bullous Insect Bites

    Bites, Bullous Insect Bites

    Bites, Bullous Insect Bites

    Definition: Bullous insect bites are delayed hypersensitivity reactions that occur in people who are already sensitized (2). They are characterized by blisters packed with fluid that appear on the skin (1).

    Etiology: The bites arise from an immune response to toxins being released at the bite site (1). The most common bites come from spiders, fleas, bed bugs and mosquitos.

    Epidemiology: Bullous reactions can occur often in people with various hematological malignancies and chronic lymphocytic leukemia (2).

    Signs: Plaques or erythematous papules that develop into tight, fluid filled bullae (1,2). Lesions may be encircled by erythema or edema and frequently appear at the site of an insect attack (1).

    Symptoms: At the location of the blisters, patients may experience itching, burning, or pain (1,2). Scratching the blisters increases the risk of bacterial infection (1).

    Differentials: Bullous pemphigoid, dermatitis herpetiformis, contact dermatitis, insect sting hypersensitivity (1,3).

    Diagnosis: Diagnosis is clinical and based on the patient’s history of insect exposure and characteristics of the lesions. 

    Treatment: Due to the increased risk of bacterial infection, appropriate wound care is necessary using soap and water (1). Antihistamines and topical or oral corticosteroids can be used to relieve symptoms(2). The use of insect repellant and protective clothing is the best way to prevent bites.

    References: (AMA)

    1.      B Koyani B, D Pathak R, H Thacker D. Bullous arthropod bite reaction. International Journal of Case Reports and Images. 2022;13(2):164-167. doi:10.5348/101352z01bk2022cr 

    1. Collins P, Sepede J. Bullous arthropod bite reaction. BMJ Case Reports. 2018;11(1). doi:10.1136/bcr-2018-228079 
    2. Kim JE, Kim S-C. Insect bite-like reaction with bullous lesions mimicking bullous pemphigoid in a patient with chronic lymphocytic leukemia. Annals of Dermatology. 2018;30(4):468. doi:10.5021/ad.2018.30.4.468 
  • Porphyria Cutanea Tarda

    Porphyria Cutanea Tarda

    Porphyria Cutanea Tarda

    Condition Name: Porphyria Cutanea Tarda (PCT)

    Definition: PCT is a disorder characterized by blistering lesions on sun-exposed skin due to a deficiency of the enzyme uroporphyrinogen decarboxylase (UROD).

    Etiology: PCT can be inherited or acquired. Acquired PCT is often linked to liver disease, such as hepatitis C, alcohol abuse, or hemochromatosis, while familial PCT involves a genetic mutation in the UROD gene.

    Epidemiology: PCT is the most common type of porphyria, typically presenting in adults in their 40s or 50s. Familial cases tend to present earlier in life, while sporadic cases often appear in the fourth or fifth decades.

    Signs: Blistering, fragile skin on sun-exposed areas like the hands and face, with potential hyperpigmentation, scarring, and milia.

    Symptoms: Skin sensitivity to sunlight, pain and discomfort in affected areas, and dark urine due to elevated porphyrins.

    Differentials: Variegate porphyria, bullous pemphigoid, lupus erythematosus.

    Diagnosis: Confirmed through porphyrin level testing in blood, urine, and stool, with a Wood’s lamp examination revealing fluorescence in urine.

    Treatment: Therapeutic phlebotomy to reduce iron levels, low-dose antimalarials like hydroxychloroquine, and strict sun protection.

    References:

    1.     Singal AK. Porphyria cutanea tarda: Recent update. Mol Genet Metab. 2019;128(3):271-281. doi:10.1016/j.ymgme.2019.01.004

    2.     Frank J, Poblete-Gutiérrez P. Porphyria cutanea tarda–when skin meets liver. Best Pract Res Clin Gastroenterol. 2010;24(5):735-745. doi:10.1016/j.bpg.2010.07.002

  • Impetigo

    Impetigo

    Impetigo

    Definition: Impetigo is a common infection of the superficial layers of the epidermis that is very contagious and most often caused by gram-positive bacteria. This condition is characterized by pustules and honey-coloured crusted erosions. It can be classified into non-bullous and bullous impetigo. 

    Etiology: Impetigo is caused by Staphylococcus aureus and less commonly, Streptococcus pyogenes. Nonbullous impetigo can be caused by either bacteria or a conjoint infection. Disruption in skin integrity allows for the invasion and colonization of bacteria on the surface. Bullous impetigo is caused by Staphylococcus aureus, which produces exfoliative toxins that target intracellular adhesion molecules of the epidermal granular layer. This results in the dissociation of epidermal cells, leading to blister formation.

    Epidemiology: Impetigo accounts for approximately 10% of skin ailments in the pediatric population, most prevalent in children aged 2-5. The male-to-female ratio of incidence is approximately 1:1. Men are more commonly affected. Bullous impetigo is more common in children younger than two. Non-bullous impetigo caused by S. aureus accounts for approximately 80% of cases. Group A beta-hemolytic Strep (GABHS) accounts for 10% of cases. Methicillin-resistant S aureus (MRSA) has become more prevalent in hospitalized patients. 

    Signs: Non-bullous impetigo can occur on the face, extremities or other body parts. It begins with a single erythematous macule that evolves into a pustule. This may be erythematous on lighter skin tones, and violaceous or brown on deeper skin tones. When this pustule or vesicle ruptures, it releases serous contents which dry to leave a typical honey-coloured crust.

    Bullous impetigo is typically found on the face, trunk, extremities, buttocks and perianal regions. Autoinoculation may cause distal spread of lesions. Bullous impetigo appears as superficial small or large, thin-roofed bullae which spontaneously rupture to leave collarette.

    Ecthyma is a deep ulcerated infection that can develop as a complication of bullous impetigo.

    Symptoms: Individuals with non-bullous impetigo may experience some itching and regional lymphadenopathy. Individuals with bullous impetigo may experience systemic symptoms of fever, malaise and lymphadenopathy.

    Differentials: scabies, atopic dermatitis, contact dermatitis, candidiasis, herpes simplex

    Diagnosis: diagnosis of impetigo begins with a thorough history and physical examination. Bacterial cultures may be in the confirmation of diagnosis if MRSA is suspected or if there is an impetigo outbreak. Skin biopsy may be used in refractory cases. Human immunodeficiency virus testing should be considered when a previously healthy adult develops bullous impetigo.

    Treatment: Specific measures in treating impetigo include topical or oral antibiotics, proper hand hygiene and avoiding close contact with confirmed cases.

    References:

    1.     Nardi NM, Schaefer TJ. Impetigo. In: StatPearls. Treasure Island (FL): StatPearls Publishing; July 31, 2023.

    2.     Quirke K. Impetigo | DermNet NZ. dermnetnz.org. Published March 2022. https://dermnetnz.org/topics/impetigo

  • Impetigo

    Impetigo

    Impetigo

    Definition: Impetigo is a common infection of the superficial layers of the epidermis that is very contagious and most often caused by gram-positive bacteria. This condition is characterized by pustules and honey-coloured crusted erosions. It can be classified into non-bullous and bullous impetigo. 

    Etiology: Impetigo is caused by Staphylococcus aureus and less commonly, Streptococcus pyogenes. Nonbullous impetigo can be caused by either bacteria or a conjoint infection. Disruption in skin integrity allows for the invasion and colonization of bacteria on the surface. Bullous impetigo is caused by Staphylococcus aureus, which produces exfoliative toxins that target intracellular adhesion molecules of the epidermal granular layer. This results in the dissociation of epidermal cells, leading to blister formation.

    Epidemiology: Impetigo accounts for approximately 10% of skin ailments in the pediatric population, most prevalent in children aged 2-5. The male-to-female ratio of incidence is approximately 1:1. Men are more commonly affected. Bullous impetigo is more common in children younger than two. Non-bullous impetigo caused by S. aureus accounts for approximately 80% of cases. Group A beta-hemolytic Strep (GABHS) accounts for 10% of cases. Methicillin-resistant S aureus (MRSA) has become more prevalent in hospitalized patients. 

    Signs: Non-bullous impetigo can occur on the face, extremities or other body parts. It begins with a single erythematous macule that evolves into a pustule. This may be erythematous on lighter skin tones, and violaceous or brown on deeper skin tones. When this pustule or vesicle ruptures, it releases serous contents which dry to leave a typical honey-coloured crust.

    Bullous impetigo is typically found on the face, trunk, extremities, buttocks and perianal regions. Autoinoculation may cause distal spread of lesions. Bullous impetigo appears as superficial small or large, thin-roofed bullae which spontaneously rupture to leave collarette.

    Ecthyma is a deep ulcerated infection that can develop as a complication of bullous impetigo.

    Symptoms: Individuals with non-bullous impetigo may experience some itching and regional lymphadenopathy. Individuals with bullous impetigo may experience systemic symptoms of fever, malaise and lymphadenopathy.

    Differentials: scabies, atopic dermatitis, contact dermatitis, candidiasis, herpes simplex

    Diagnosis: diagnosis of impetigo begins with a thorough history and physical examination. Bacterial cultures may be in the confirmation of diagnosis if MRSA is suspected or if there is an impetigo outbreak. Skin biopsy may be used in refractory cases. Human immunodeficiency virus testing should be considered when a previously healthy adult develops bullous impetigo.

    Treatment: Specific measures in treating impetigo include topical or oral antibiotics, proper hand hygiene and avoiding close contact with confirmed cases.

    References:

    1.     Nardi NM, Schaefer TJ. Impetigo. In: StatPearls. Treasure Island (FL): StatPearls Publishing; July 31, 2023.

    2.     Quirke K. Impetigo | DermNet NZ. dermnetnz.org. Published March 2022. https://dermnetnz.org/topics/impetigo

  • Impetigo

    Impetigo

    Impetigo

    Definition: Impetigo is a common infection of the superficial layers of the epidermis that is very contagious and most often caused by gram-positive bacteria. This condition is characterized by pustules and honey-coloured crusted erosions. It can be classified into non-bullous and bullous impetigo. 

    Etiology: Impetigo is caused by Staphylococcus aureus and less commonly, Streptococcus pyogenes. Nonbullous impetigo can be caused by either bacteria or a conjoint infection. Disruption in skin integrity allows for the invasion and colonization of bacteria on the surface. Bullous impetigo is caused by Staphylococcus aureus, which produces exfoliative toxins that target intracellular adhesion molecules of the epidermal granular layer. This results in the dissociation of epidermal cells, leading to blister formation.

    Epidemiology: Impetigo accounts for approximately 10% of skin ailments in the pediatric population, most prevalent in children aged 2-5. The male-to-female ratio of incidence is approximately 1:1. Men are more commonly affected. Bullous impetigo is more common in children younger than two. Non-bullous impetigo caused by S. aureus accounts for approximately 80% of cases. Group A beta-hemolytic Strep (GABHS) accounts for 10% of cases. Methicillin-resistant S aureus (MRSA) has become more prevalent in hospitalized patients. 

    Signs: Non-bullous impetigo can occur on the face, extremities or other body parts. It begins with a single erythematous macule that evolves into a pustule. This may be erythematous on lighter skin tones, and violaceous or brown on deeper skin tones. When this pustule or vesicle ruptures, it releases serous contents which dry to leave a typical honey-coloured crust.

    Bullous impetigo is typically found on the face, trunk, extremities, buttocks and perianal regions. Autoinoculation may cause distal spread of lesions. Bullous impetigo appears as superficial small or large, thin-roofed bullae which spontaneously rupture to leave collarette.

    Ecthyma is a deep ulcerated infection that can develop as a complication of bullous impetigo.

    Symptoms: Individuals with non-bullous impetigo may experience some itching and regional lymphadenopathy. Individuals with bullous impetigo may experience systemic symptoms of fever, malaise and lymphadenopathy.

    Differentials: scabies, atopic dermatitis, contact dermatitis, candidiasis, herpes simplex

    Diagnosis: diagnosis of impetigo begins with a thorough history and physical examination. Bacterial cultures may be in the confirmation of diagnosis if MRSA is suspected or if there is an impetigo outbreak. Skin biopsy may be used in refractory cases. Human immunodeficiency virus testing should be considered when a previously healthy adult develops bullous impetigo.

    Treatment: Specific measures in treating impetigo include topical or oral antibiotics, proper hand hygiene and avoiding close contact with confirmed cases.

    References:

    1.     Nardi NM, Schaefer TJ. Impetigo. In: StatPearls. Treasure Island (FL): StatPearls Publishing; July 31, 2023.

    2.     Quirke K. Impetigo | DermNet NZ. dermnetnz.org. Published March 2022. https://dermnetnz.org/topics/impetigo

  • Granuloma Annulare

    Granuloma Annulare

    Granuloma annulare 

    Condition Name: Granuloma annulare

    Definition: Granuloma annulare is a benign, chronic skin condition characterized by the formation of annular plaques or papules.

    Etiology: The exact cause of granuloma annulare is unknown, though it is believed to involve an immune-mediated response.

    Epidemiology: Granuloma annulare affects individuals of all ages but is more commonly seen in children and young adults. It is slightly more prevalent in females than in males. The prevalence in the general population is relatively low, and the condition is not typically associated with significant morbidity.

    Signs: The appearance of small, firm, flesh-colored or erythematous papules that coalesce to form rings with a central depression. These lesions most commonly appear on the hands, feet, elbows, and knees but can occur on any part of the body.

    Symptoms: The lesions are usually asymptomatic but can occasionally cause mild itching.

    Differentials: Conditions such as tinea corporis, sarcoidosis, and necrobiosis lipoidica should be considered.

    Diagnosis: Diagnosis is primarily clinical, based on the characteristic appearance of the lesions. A skin biopsy can confirm the diagnosis by revealing necrobiotic collagen surrounded by histiocytes and multinucleated giant cells.

    Treatment: Treatment is often unnecessary as granuloma annulare can resolve spontaneously, particularly in localized cases. Treatment options for persistent or widespread cases include topical or intralesional corticosteroids, cryotherapy, or laser therapy. Systemic treatments, such as dapsone, isotretinoin, or hydroxychloroquine, may be considered for more severe cases.

    References:

    ●       Piette, E. W., & Rosenbach, M. (2016). Granuloma annulare: Pathogenesis, disease associations, and triggers, and therapeutic options. Journal of the American Academy of Dermatology, 75(3), 467-479. doi:10.1016/j.jaad.2016.02.1222

    ●       Marneros, A. G., & Bruckner, A. L. (2010). “Granuloma annulare.” Journal of the American Academy of Dermatology, 62(2), 207-222. doi:10.1016/j.jaad.2009.03.044

  • Basal Cell Carcinoma

    Basal Cell Carcinoma

    Basal Cell Carcinoma (BCC)

    Definition: BCC is a slow-growing nonmelanocytic skin cancer arising from basal cells in the epidermis that rarely metastasizes but can invade locally and be destructive (1,4,5).

    Etiology:  Ultraviolet exposure is a major risk factor and explains why BCC typically grows on sun-exposed areas of the skin (1). Other factors that influence the development of BCC include fairer skin colour, light-coloured eyes, Northern European ancestry, red hair and a history of sunburns (5). Pathobiologicallt, most BCCs are caused by activation of the Hedgehog signaling system, which is also a target for therapeutic intervention (5).

    Epidemiology: The incidence of BCC varies depending on geographic location and race (5). Australia is reported to have one of the highest incidences of 1000/100,000 (5). BCC is one of the most common skin cancers in fair-skinned individuals and is increasing in incidence globally (1). It is usually seen after the age of 50 with an incidence ratio of 2:1 in females and males respectively (1).

    Signs: BCC manifests as a translucent or pearly nodule accompanied by telangiectasia on sun-exposed regions such as the neck, ears, and face (2).

    Symptoms: Typically asymptomatic but with time may crust, bleed or develop ulcers (2,3).

    Differentials: Squamous cell carcinoma, adnexal tumors, seborrheic keratosis(1).

    Diagnosis: Diagnosis requires a biopsy and is recommended before undergoing surgery or systemic treatment (1). Diagnosis also involves historical examination and direct inspection of the lesion (5). 

    Treatment: The standard treatment for BCC is typically surgery (surgical excision, Mohs micrographic surgery and curettage and electrodesiccation) but non-surgical treatments options are also available including: freezing or light therapy, topical medications and radiation treatments (1).

    References: (AMA)

    1.      Basset-Seguin N, Herms F. Update in the management of basal cell carcinoma. Acta Dermato Venereologica. 2020;100(11). doi:10.2340/00015555-3495 

    2.     1. McDaniel B. Basal cell carcinoma. StatPearls [Internet]. March 13, 2024. Accessed August 18, 2024. https://www.ncbi.nlm.nih.gov/books/NBK482439/#:~:text=BCC%20typically%20presents%20as%20a,rolled%20or%20rodent%20ulcer%20appearance.

    3.     Oakley A. Basal cell carcinoma: Symptoms, causes, and treatment – dermnet. DermNet®. July 3, 2024. Accessed August 18, 2024. https://dermnetnz.org/topics/basal-cell-carcinoma. 

    4.     Robert S Bader M. Basal cell carcinoma. Practice Essentials, Background, Pathophysiology. April 3, 2024. Accessed August 18, 2024. https://emedicine.medscape.com/article/276624-overview?gad_source=1&gbraid=0AAAAADoSQiUCwFng3uMBdxWlXHVuNMVrw&gclid=Cj0KCQjwt4a2BhD6ARIsALgH7Dqhf-P79uzm848PdW5k8auVX_QjoRGo38V0m2dFrNN42l3MpFCbyS0aAm4_EALw_wcB&form=fpf#a2.

    5.     Tanese K. Diagnosis and management of basal cell carcinoma. Current Treatment Options in Oncology. 2019;20(2). doi:10.1007/s11864-019-0610-0