Tuesday, September 15, 2026
Thursday, September 10, 2026
Myxedema: Symptoms, Causes, Skin Findings, Diagnosis & Treatment
Tuesday, September 8, 2026
Dermatomyositis: Symptoms, Causes, Diagnosis, Histology & Treatment
Sunday, August 30, 2026
Glomus Tumor and Glomangioma: Symptoms, Histology, Causes and Treatment
Saturday, August 29, 2026
Becker’s Nevus: Symptoms, Causes, Diagnosis and Treatment
Acrochordon (Skin Tags): Causes, Clinical Features & Treatment
Monday, August 17, 2026
Nevus Lipomatosus Superficialis: Symptoms, Causes, Histology & Treatment
Sunday, August 16, 2026
Sporotrichosis: Causes, Symptoms, Diagnosis, Histology and Treatment
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| Plate 6-24 |
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.
Friday, August 7, 2026
Phenylketonuria (PKU): Symptoms, Causes, Diagnosis, Treatment & Low-Phenylalanine Diet Guide
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| NORMAL AND ABNORMAL METABOLISM OF PHENYLALANINE |
PHENYLKETONURIA
Phenylalanine is an essential amino acid that serves as a substrate for many different biochemical pathways. Two end products that use phenylalanine as their precursors are melanin and epinephrine. Under normal physiological and biochemical environments, any excess amount of phenylalanine is converted into tyrosine by the liver and used for a host of biochemical processes including protein synthesis. In patients with phenylketonuria, the enzyme in the liver that converts phenylalanine into tyrosine is completely absent. This inborn error of metabolism is one of the most thoroughly researched disease states. With early detection and therapy, the severe sequelae of phenylketonuria can be avoided. Screening is performed soon after birth for all children in the United States and in most of the world. Children born in regions with poor medical infrastructure and no testing are at risk for the disease. Once the disease symptoms have appeared, therapy usually cannot reverse the damage that has been done. Phenyl-ketonuria is inherited in an autosomal recessive manner, but many genotypes have been described, and many mutations in the responsible gene have been reported. The defect is located on the long arm of chromosome 12, where the PAH gene encodes the protein, phenylalanine hydroxylase.
Friday, July 31, 2026
Scurvy (Vitamin C Deficiency): Symptoms, Causes, Diagnosis, Treatment, and Prevention
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| DIETARY SOURCES OF VITAMIN C AND CLASSIC CUTANEOUS MANIFESTATIONS OF SCURVY |
SCURVY
Scurvy is a well-known nutritional disease that results from a lack of the water-soluble vitamin, ascorbic acid (vitamin C). Scurvy has a well-documented history. It was first recognized in the fourteenth century in sailors who spent long amounts of time at sea. The symptoms were recognized as being related to a lack of fresh foods, especially citrus products. In 1753, James Lind, a British surgeon aboard the HMS Salisbury, performed the first documented clinical trial proving that scurvy was caused by a lack of citrus fruit in the diet of sailors. After Lind’s discovery, citrus fruits were included in ships’ provisions, and the incidence of scurvy in sailors plummeted. It was not until 1928 that ascorbic acid was isolated by the Hungarian chemist, Albert von Szent-Grörgyi, who was eventually awarded the Nobel Prize for this discovery. Scurvy is still present in some areas of the world due to inadequate dietary intake of vitamin C. Scurvy is uncommon in North America but can be seen in individuals with abnormal diets.
Tuesday, July 21, 2026
Carney Complex: Symptoms, Causes, Diagnosis, Genetics, Treatment, and Long-Term Management
CARNEY COMPLEX
Carney complex, also known as NAME syndrome (nevi, atrial myxomas, myxoid neurofibromas, ephelides) or LAMB syndrome (lentigines, atrial myxomas, mucocutaneous myxomas, blue nevi), is an autosomal dominantly inherited disorder that affects the integumentary, endocrine, cardiovascular, and central nervous systems. This rare disorder is primarily caused by a genetic mutation in the tumor suppressor gene, PRKAR1A. Approximately 20% of patients have defects in an undescribed gene located at 2p16. Various genotypes and phenotypes exist, and the diagnosis is based on a complex list of major, supplemental, and minor criteria.
Cushing's Syndrome vs Cushing's Disease: Symptoms, Causes, Diagnosis & Treatment Guide
CUSHING’S SYNDROME AND CUSHING’S DISEASE
Cushing’s syndrome is caused by excessive secretion of endogenous glucocorticoids or, more frequently, by intake of excessive exogenous glucocorticoids. The latter type is typically iatrogenic in nature. The excessive glucocorticoid levels lead to the many cutaneous and systemic signs and symptoms of Cushing’s syndrome and Cushing’s disease. Endogenous glucocorticoids are made and secreted by the adrenal glands, and benign adrenal adenomas are the most frequently implicated adrenal tumors causing Cushing’s syndrome. Cushing’s disease is caused by excessive secretion from the anterior pituitary of adrenocorticotropic hormone (ACTH, corticotropin) as the result of a basophilic or chromophobe adenoma. The increased amount of ACTH causes the adrenal glands to hypertrophy and boost their production of cortisol, eventually leading to a state of hypercortisolism. Excessive release of corticotropin-releasing hormone (CRH) from the para- ventricular nucleus of the hypothalamus can also cause the syndrome. Any tumor that has the ability to produce ACTH also has the potential to cause Cushing’s syndrome. The most frequently reported such tumor is the small cell tumor of the lung, which is able to produce many neuroendocrine hormones including ACTH in large amounts.
Cushing's Syndrome Pathophysiology: Causes, Symptoms, Hormonal Mechanisms & Diagnosis
CUSHING’S SYNDROME: PATHOPHYSIOLOGY
Cushing’s syndrome is directly caused by excessive amounts of glucocorticoids and their effects on numerous organ systems. Cortisol is strikingly elevated in all cases of Cushing’s syndrome. In some cases, levels of 17-ketosteroids and aldosterone are slightly elevated, and this plays a role in the clinical manifestations of the disease. There are numerous disease states that can cause hypercortisolemia, including excessive secretion of adrenocorticotropic hormone (ACTH, corticotropin), adenoma and hyperplasia of the adrenal gland, carcinoma of the adrenal gland, primary pigmented nodular adrenocortical disease (PPNAD), and exogenous cortisol use. In all cases, it is the marked elevation of cortisol that ultimately is the cause of the disease.
Down Syndrome (Trisomy 21): Symptoms, Causes, Diagnosis, Skin Signs & Treatment Guide
DOWN SYNDROME
Down syndrome is a genetic disorder caused by trisomy of chromosome 21. Trisomy 21 occurs in approximately 1 of every 1000 births. Chromosome 21 is an acrocentric chromosome, and trisomy 21 is the most common form of chromosomal trisomy. Trisomy 21 most often occurs as the result of nondisjunction of meiosis, which leads to an extra copy of chromosome 21. Some patients with Down syndrome have a Robertsonian translocation to chromosome 14 or chromosome 22, which are two other acrocentric chromosomes. In these cases, the number of total chromosomes is normal at 46, but the extra chromosome 21 material is translocated to another chromosome. This, in effect, causes an extra chromosome 21. All or part of chromosome 21 may be trans-located, leading to variations in phenotype. Mosaicism is a rare cause of trisomy 21 in partial cell lines, and the clinical phenotype depends on how early the genetic defect occurred during embryogenesis.
Saturday, July 4, 2026
Ehlers-Danlos Syndrome (EDS): Symptoms, Causes, Types, Diagnosis & Treatment
EHLERS-DANLOS SYNDROME
Ehlers-Danlos syndrome is a heterogeneous disease of defective connective tissue production. There are many subtypes, most caused by defects in collagen formation or in the posttranslational modification of collagen. This grouping of diseases has been confusing because of the variable nature of the subtypes and the lack of a universally adopted classification system. Under the most recent system, there are 7 distinct subtypes; under the historical classification, there were 11 types. The new classification system has not been universally adopted, which contributes to the confusion. As the genetic defects behind each subtype are determined, researchers and clinicians will gain a better understanding of the syndrome.
Thursday, July 2, 2026
Neurofibromatosis (NF1 & NF2): Symptoms, Causes, Diagnosis, Treatment, and Long-Term Management
Tuberous Sclerosis (Bourneville Syndrome): Symptoms, Causes, Diagnosis, Treatment & Skin Signs
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| Genodermatoses and Syndromes |
Tuberous sclerosis (Bourneville’s syndrome) is a multisystem disease that often manifests with cutaneous findings. It is inherited in an autosomal dominant manner and is directly caused by a defect in one of two genes, TSC1 or TSC2, usually due to a spontaneous mutation. TSC1 has been shown to encode the hamartin protein, whereas TSC2 gene encodes the tuberin protein. The skin, central nervous system (CNS), cardiovascular, respiratory, visual, and musculoskeletal systems are affected. This genodermatosis has an extremely variable phenotype. At one extreme is the severely disabled and mentally delayed individual with severe seizure disorders; at the other end of the spectrum is the individual with mild skin disease and unappreciable CNS disease.
Saturday, June 13, 2026
Median Raphe Cyst: Causes, Symptoms, Diagnosis, and Treatment of a Rare Congenital Penile Cyst
Sunday, October 5, 2025
HERPES ZOSTER (SHINGLES)
HERPES ZOSTER (SHINGLES)
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| CLINICAL PRESENTATION OF HERPES ZOSTER |
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.



















