pediagenosis: Integumentary
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Showing posts with label Integumentary. Show all posts
Showing posts with label Integumentary. Show all posts

Wednesday, April 28, 2021

ACNE

ACNE


ACNE
Acne is an almost universal finding in teenagers across the globe. Acne vulgaris is the most common form of acne; it affects almost every human at some point in their lifetime. Most cases are mild and do not cause any significant disease. Most acne vulgaris is seen in the postpubertal years. Many clinical variants exist, and excellent therapeutic modalities are available to treat this skin disease.
ACNE VULGARIS
ACNE VULGARIS

Clinical Findings: Acne vulgaris typically begins soon after puberty. It has no racial or gender preference, although males may develop more severe cases of the disease. The first signs of acne development are the formation of microcomedones, both open and closed. Open comedones, also known as blackheads, appear as small (0.5-1 mm), dilated skin pores that are filled with a dark material, oxidized keratin. This material can be easily expressed with lateral pressure or with the help of a comedone extractor. The closed comedone, also known as a whitehead, is a small (0.5-1 mm), whitish to skin-colored papule. Comedones are believed to be the precursor lesion to the other lesions of acne. As acne progresses, inflammatory red, slightly tender papules develop, along with a variable amount of pustules. The pustules are centered on the hair follicle. More severe cases of acne, such as nodulocystic acne, show inflammatory nodule formation as well as cyst formation. These nodules and cysts can become large (2-3 cm in diameter) and can cause considerable pain. They often heal with scarring of the skin.
ACNE KELOIDALIS NUCHAE

ACNE KELOIDALIS NUCHAE


ACNE KELOIDALIS NUCHAE
Acne keloidalis nuchae is a fairly common form of inflammatory, scarring alopecia that typically occurs on the posterior occipital scalp. There is a variable spectrum of disease, ranging from very mild cases to severe scarring alopecia. The condition has psychosocial implications and is difficult to treat effectively. It is diagnosed clinically, and biopsies are rarely needed.
ACNE KELOIDALIS NUCHAE

Clinical Findings: Acne keloidalis nuchae begins on the posterior scalp or nape of the neck as tiny, follicular, flesh-colored to red papules. The papules enlarge to form plaques, which coalesce into larger plaques. Ultimately in severe cases, the entire posterior scalp is involved. Early in the disease, no hair loss is appreciated. As the disease progresses, the hair follicles become scarred down and crowded out by the encroaching fibrosis, resulting in a variable amount of scarring alopecia.

Monday, April 12, 2021

ACUTE FEBRILE NEUTROPHILIC DERMATOSIS (SWEET’S SYNDROME)

ACUTE FEBRILE NEUTROPHILIC DERMATOSIS (SWEET’S SYNDROME)


ACUTE FEBRILE NEUTROPHILIC DERMATOSIS (SWEET’S SYNDROME)
Acute febrile neutrophilic dermatosis is an uncommon rash that most often is secondary to an underlying infection or malignancy. The diagnosis is made by fulfilling a constellation of criteria. Both clinical findings and pathology results are required to make the diagnosis in a patient with a consistent history.

ACUTE FEBRILE NEUTROPHILIC DERMATOSIS (SWEET’S SYNDROME)

Clinical Findings: Acute febrile neutrophilic dermatosis is often associated with a preceding infection. The infection can be located anywhere but most commonly is in the upper respiratory system. Females appear to be more likely to be afflicted, and there is no race predilection. Patients present with fever and the rapid onset of juicy papules and plaques. Because the papules can look as if they are fluid filled, they are given the descriptive term juicy papules. They can occur anywhere on the body and can be mistaken for a varicella infection. Patients also have neutrophilia and possibly arthritis and arthralgias. If this condition is associated with a preceding infection, it is usually self-limited and heals without scarring, unless the papules and plaques are excoriated or ulcerated by scratching. Variable amounts of pruritus and pain are associated with this skin disease. When one is evaluating a patient with this condition, a thorough history is required. A skin biopsy must be performed. A chest radiograph, throat culture, and urinalysis should be performed to assess for the possibility of bacterial infection.
ALLERGIC CONTACT DERMATITIS

ALLERGIC CONTACT DERMATITIS


ALLERGIC CONTACT DERMATITIS
Allergic contact dermatitis is one of the rashes most frequently encountered in the clinician’s office. It is responsible for a large proportion of occupationally induced skin disease. Urushiol from the sap of poison ivy, oak, or sumac plants is the most common cause of allergic contact dermatitis in the United States. The clinical morphology, the distribution of the rash, and results from skin patch testing are used to make the diagnosis. Patch testing is performed when the causative agent is unknown. Nickel has been the most frequent cause of positive patch testing in the world for years. Urushiol is not tested clinically, because almost 100% of the population reacts to this chemical.

MORPHOLOGY OF ALLERGIC CONTACT DERMATITIS
MORPHOLOGY OF ALLERGIC CONTACT DERMATITIS

Clinical Findings: Allergic contact dermatitis can manifest in a multitude of ways. The acute form may show linear streaks of juicy papules and vesicles. Variable amounts of surrounding edema can be seen. Edema is much more common in the loose skin around the eyelids and facial region. Chronic allergic contact dermatitis can manifest with red-pink patches and plaques with various amounts of lichenification. There are localized forms and generalized forms. One of the unique forms of allergic contact dermatitis is the scattered generalized form. Pruritus is an almost universal finding, and it can be so severe as to cause excoriations and small ulcerations.
ATOPIC DERMATITIS

ATOPIC DERMATITIS


ATOPIC DERMATITIS
Atopic dermatitis is one of the most common dermatoses of childhood. It typically manifests in early life and can have varying degrees of expression. It is commonly associated with asthma and allergies. Most children eventually outgrow the condition. Atopic dermatitis has been estimated to affect up to 10% of all children and 1% of adults, and its prevalence has been steadily increasing. Patients frequently have a family history of atopic dermatitis, asthma, or skin sensitivity.

INFANTS AND CHILDREN WITH ATOPIC DERMATITIS
INFANTS AND CHILDREN WITH ATOPIC DERMATITIS

Clinical Findings: Atopic dermatitis typically begins early in life. There is no racial predilection. The clinical course is often chronic, with a waxing and waning nature. Infants a few months old may initially present with pruritic, red, eczematous patches on the cheeks and extremities as well as the trunk. The itching is typically severe and causes the child to excoriate the skin, which can lead to secondary skin infections. The skin of atopics is abnormally dry and is sensitive to heat and sweating. These children have difficulty sleeping because of the severe pruritus associated with the rash. During flares of the dermatitis, patients may develop weeping patches and plaques that are extremely pruritic and occasionally painful. With time, the patches begin to localize to flexural regions, particularly the antecubital and popliteal fossae. Severely afflicted children may have widespread disease. Patients with atopic dermatitis are more prone to react to contact and systemic allergens. Sensitivity to contact allergens is likely a consequence of the frequent use of topical medicaments and the broken skin barrier. This combination leads to increased exposure to foreign antigens that are capable of inducing allergic contact dermatitis. One should suspect a coexisting contact dermatitis if a patient who is doing well experiences a flare for no apparent reason or if a patient continues to get worse despite aggressive topical or oral therapy. Laboratory testing commonly shows an eosinophilia and an elevated immunoglobulin E (IgE) level.
AUTOINFLAMMATORY SYNDROMES

AUTOINFLAMMATORY SYNDROMES


AUTOINFLAMMATORY SYNDROMES
The autoinflammatory syndromes are a rare group of diseases for which the specific causes have been determined. The diseases in this category include hyper-immunoglobulin D (hyper-IgD) syndrome (HIDS), the cryopyrinopathies, familial Mediterranean fever (FMF), and tumor necrosis factor (TNF) receptor associated periodic syndrome (TRAPS). The cryopyrinopathies are a group of conditions made up of Muckle-Wells syndrome, familial cold autoinflammatory syndrome (FCAS), neonatal-onset multisystem inflammatory disease (NOMID), and chronic infantile neurological cutaneous and articular syndrome (CINCA). These groupings were first proposed in the 1990s to bring together a collection of inflammatory disorders that are distinct in nature and pathophysiology from other forms of allergic, autoimmune, and immunodeficiency syndromes. Patients with these auto-inflammatory diseases lack the autoreactive immune cells (T and B cells) as well as autoantibodies. The identification of specific genes that are defective and the roles played by those genes in the development of these disorders has been critical in increasing understanding of these diverse diseases. The common link in these conditions is the fact that they all represent abnormalities of the innate immune system.

PATHOPHYSIOLOGY OF AUTOINFLAMMATORY SYNDROMES
PATHOPHYSIOLOGY OF AUTOINFLAMMATORY SYNDROMES

Clinical Findings: HIDS is inherited in an autosomal recessive fashion. Patients present with fever, arthralgias, abdominal pain, cervical adenopathy, and aphthous ulcers. Skin findings are consistent with a cutaneous vasculitis with palpable purpura and purpuric macules and nodules. Patients develop attacks of these symptoms with some evidence of periodicity. The attacks can last from 3 to 7 days, and typically the first attack occurs within the first year of life. As the child ages, the frequency and the severity of the attacks lessen. No reliable trigger has been found that initiates the attacks, and patients are completely normal between attack episodes.

Sunday, April 11, 2021

BUG BITES

BUG BITES


BUG BITES
Human skin is exposed to the environment on a constant basis and encounters multiple threats, including arthropods of many varieties. Each species of arthropod can inflict its own type of damage to the skin; some bites are mild and barely noticeable, and others can be life-threatening. The most common bites are those of mosquitoes, fleas, bedbugs, mites, ticks, and spiders. Not only can these bites cause direct damage to the skin, but these organisms may have the ability to transmit infectious diseases such as Lyme disease, leishmaniasis, and rickettsial diseases.
BUG BITES


Clinical Findings: Mosquitoes are prominent insects in the spring, summer, and early fall seasons. In warmer climates, they can be seen year round. Their bite is often not noticed until after the mosquito has gone. The recently bitten person is left with a pruritic urticarial papule that typically resolves by itself within an hour or so. Some individuals are prone to severe bite reactions and develop warm, red papules and nodules that can last for a week or two and can be associated with regional lymphadenopathy. Mosquitoes are essentially a nuisance for the most part, but in some areas of the world they are the major vectors for transmission of malaria and encephalitis viruses. Sand flies are similar, but they are the major vector for leishmaniasis.

Monday, March 8, 2021

SYPHILIS

SYPHILIS

SYPHILIS

Syphilis has been well described in the literature since the late 1400s. The history behind the discovery and treatment of the disease is a story of perseverance and the willpower of many scientists working separately and together to help treat one the most deadly diseases of their time. Philip Ricord, a French scientist, is given credit for describing the three stages of syphilis and differentiating it from other diseases such as gonorrhea. The infectious organism, Treponema pallidum, was described in 1905 by Fritz Schaudinn, a German zoologist, and Erich Hoffman, a German dermatologist. Soon after this discovery, the German scientist Paul Ehrlich developed the first specific therapy for syphilis. The oral medication he and his team discovered was initially called 606, because it was the 606th compound they had attempted to use to treat the disease. This organoarsenic molecule was soon renamed salvarsan. This medication is highly effective against T. pallidum.

ANDROGENIC ALOPECIA

ANDROGENIC ALOPECIA

ANDROGENIC ALOPECIA

Androgenic alopecia, also known as male pattern baldness or female pattern hair loss, is a major form of hair loss. The age at onset is variable and likely has a genetic determination. Some men lose their entire scalp hair, resulting in baldness. Baldness is rare in women, because their hair loss manifests as varying grades of thinning.

ALOPECIA AREATA

ALOPECIA AREATA

ALOPECIA AREATA

Alopecia areata is an autoimmune disease that causes discrete circular or oval areas of nonscarring alopecia. This form of alopecia has several clinical variants, including alopecia totalis, alopecia universalis, and an ophiasis pattern. Therapy is often difficult. The disease can have profound psychological impact, especially in young patients. It is critical to address this issue, because the effects on the patient’s psychological well-being are often more severe than the actual hair loss.

VERRUCAE (WARTS)

VERRUCAE (WARTS)

VERRUCAE (WARTS)

Verrucae are one of the most frequently encountered viral infections in humans. They are capable of causing disease in any individual, but severe infections seem to be more likely in those who are immunocompromised. Warts can affect any cutaneous surface, and unique wart subtypes are more prone to cause disease in different clinical locations. By far the most important aspect of infection with the human papillomavirus (HPV) is the ability of the virus to cause malignant transformation. This malignant potential is specific to certain subtypes and is especially a concern in women, who are at risk for cervical cancer. Most cases of cervical cancer can be traced to prior infection with certain HPV strains. In June 2006, the U.S. Food and Drug Administration approved the use of a prophylactic HPV vaccine in prepubertal girls. The vaccine is a recombinant quad-rivalent vaccine against HPV types 6, 11, 16, and 18. Types 16 and 18 are believed to have been responsible for up to 70% of cervical cancers.

HERPES ZOSTER (SHINGLES)

HERPES ZOSTER (SHINGLES)

HERPES ZOSTER (SHINGLES)

The varicella zoster virus (VZV) is responsible for causing varicella (chickenpox) as well as herpes zoster (shingles). Herpes zoster is caused by reactivation of dormant VZV. Only hosts who have previously been infected with VZV can develop herpes zoster. The incidence of herpes zoster is sure to decrease in the future, because the zoster vaccine has good efficacy in increasing immunity against the virus. The live attenuated vaccine is currently recommended for those individuals 60 years of age and older who fulfill the criteria for receiving a live vaccine. This age was chosen because the incidence of herpes zoster increases after age 60, possibly related to a waning immune response and anti-body titer remaining from the patient’s original VZV infection. Whether the VZV vaccine protects against herpes zoster will take years to determine. The United States introduced widespread childhood immunization against VZV in 1995, and none of these children have yet reached the age of 60. Whether future booster vaccinations or VZV revaccination will be required is yet to be determined.

VARICELLA

VARICELLA

VARICELLA

The varicella-zoster virus (VZV) causes two discrete clinical infections: chickenpox (varicella) and herpes zoster (shingles). Although chickenpox was once a universal infection of childhood, the incidence of this disease has plummeted since the advent of the chickenpox vaccine. VZV belongs to the herpesvirus family and is primarily a respiratory disease with skin manifestations.

Wednesday, February 17, 2021

STAPHYLOCOCCUS AUREUS SKIN INFECTIONS

STAPHYLOCOCCUS AUREUS SKIN INFECTIONS

STAPHYLOCOCCUS AUREUS SKIN INFECTIONS

Cutaneous infection with Staphylococcus aureus can manifest in many ways. With the emergence of methicillin-resistant S. aureus (MRSA), these cutaneous infections have once again been given the attention they deserve. Most cases of MRSA are community acquired, and they have entirely different sensitivity patterns than those of hospital-acquired MRSA infections. These cutaneous infections are increasing in incidence. They not only cause significant skin disease but have the potential to become systemic and cause septicemia, pneumonia, osteomyelitis, and other internal infections. S. aureus is a transient colonizer of the skin and nasopharynx. This bacteria has shown a remarkable ability to develop and acquire antibacterial resistance mechanisms. S. aureus and MRSA are major hospital-acquired S. aureus infections, and now community-acquired MRSA has become just as important. MRSA accounts for more than 50% of hospital-acquired S. aureus infections.

SPOROTRICHOSIS

SPOROTRICHOSIS

SPOROTRICHOSIS

Sporothrix schenckii is an environmental fungus that is capable of causing human disease after direct inoculation into the skin. Inoculation is the cause of cutaneous sporotrichosis, which is considered to be a subcutaneous mycosis. Unusual cases of inhalation sporotrichosis have been described in the literature, as have cases of central nervous system disease. These cases occur almost exclusively in immunosuppressed hosts. Sporotrichosis has classically been associated with inoculation after the prick from a rose plant. This is well reported; the fungus can be isolated from rose plants but is also found on many other plants and in soil environments. Clinical Findings: Gardeners, florists, and outdoor enthusiasts are at highest risk for infection from S. schenckii. These activities and occupations increase the likelihood of contact with the soil fungus. The fungus lives in the environment, and humans become infected by direct implantation of the fungus into the skin. Common methods of inoculation are the prick of a thorn or an injury contaminated with soil or plant mate- rial. Within a few days after entry into the skin, a papule and then a pustule form at the site of inoculation. Patients may initially be given an antibiotic in the belief that they have a bacterial infection. Often, it is not until the pustule ulcerates and develops into a larger plaque that the diagnosis is suspected or considered. Once this has occurred, the fungus enters the local lymphatics and proceeds to migrate proximally. As the fungus travels through the lymphatic system, it periodically causes draining sinus tracts to the surface, which appear as papules or nodules. This characteristic lymphangitic spread, also called sporotrichoid spread, is seen in most cases of cutaneous sporotrichosis.

PARACOCCIDIOIDOMYCOSIS

PARACOCCIDIOIDOMYCOSIS

PARACOCCIDIOIDOMYCOSIS

Paracoccidioidomycosis, also known as South American blastomycosis, is a disease that is seen almost exclusively in regions of Central and South America. It is caused by the dimorphic fungus, Paracoccidioides brasiliensis. Most infections are acquired by direct inhalation of the chlamydospores. The fungus is found in the environment in the mycelial or mold phase; it converts to the yeast phase at body temperature. Brazil has the highest incidence of paracoccidioidomycosis. Primary lung infection may lead to disseminated disease, with the skin being secondarily infected. Direct inoculation into the skin causes primary cutaneous disease.

SCABIES

SCABIES

SCABIES

Human infection with the parasite Sarcoptes scabiei var hominis causes scabies. Humans are the only known host, and the parasite is transferred from one person to another by close physical contact.

MOLLUSCUM CONTAGIOSUM

MOLLUSCUM CONTAGIOSUM

MOLLUSCUM CONTAGIOSUM

As its name implies, molluscum contagiosum is a highly contagious viral infection that has little morbidity. This infection is most commonly encountered in children. The diagnosis is made on clinical grounds after inspection of the characteristic skin findings. When seen in the genital region of adults, molluscum contagiosum is considered to be a sexually transmitted disease. This infection rarely occurs in immunocompetent adults outside sexual transmission. In adults with no clear evidence of transmission, an evaluation for an immunosuppressed state should be undertaken. Patients taking chronic immunosuppressive medications and those with the acquired immunodeficiency syndrome are more prone to infection with molluscum contagiosum.

Tuesday, February 16, 2021

MENINGOCOCCEMIA

MENINGOCOCCEMIA

MENINGOCOCCEMIA

Meningococcemia can cause a wide range of clinical diseases, of which neisserial meningitis is the most severe and life-threatening. The bacteria, Neisseria meningitidis, is capable of causing septicemia, pneumonia, and meningitis. These are all relentless diseases that are universally fatal if not promptly treated. The bacteria has been known to cause severe disseminated intravascular coagulation (DIC) and the Waterhouse-Friderichsen syndrome. The latter syndrome, also known as acute adrenocortical insufficiency, is directly caused by hemorrhagic destruction of both adrenal glands. This syndrome can result from a wide range of conditions, including infections, and N. meningitidis is one of the more frequent infectious causes.

Wednesday, February 10, 2021

LYMPHOGRANULOMA VENEREUM

LYMPHOGRANULOMA VENEREUM

LYMPHOGRANULOMA VENEREUM

Lymphogranuloma venereum (LGV) is a sexually transmitted disease (STD) that is produced by infection with Chlamydia trachomatis serotypes L1, L2, and L3. The disease progresses through three distinct phases of transmission. This bacterial disease was once limited to tropical regions, but with the ease of worldwide travel, it can now be seen globally. The skin manifestations are found predominantly in the groin and genital region. This disease is often seen in conjunction with other STDs, and screening for other STDs should be done routinely in patients diagnosed with LGV.

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