PCOD(Polycystic Ovarian Disease) & PCOS(polycystic ovary syndrome)
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Monday, 24 January 2022
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Homeopathy is safe and has no side effects
Homeopathy is safe and has no side effects
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Wednesday, 13 October 2021
Saethre- Chotzen Syndrome
Saethre- Chotzen Syndrome
Saether-Chotzen syndrome is a rare type of craniosynostosis- the early closing of one or more of the soft, fibrous seams(sutures) between the skull bone. When a suture closes too early, a baby skull cannot grow correctly.
Saethre-Chotzen syndrome is a genetic condition characterized by the premature fusion of certain skull bones. This early fusion prevents the skull from growing normally and affects the shape and symmetry of the head and face. Other features may include webbing of certain fingers or toes, small or unusually shaped ears, short stature, and abnormalities of the bones in the spine (the vertebrae). The signs and symptoms of Saethre- Chotzen syndrome vary from the TWIST1 gene cause most cases of Saethre- Chotzen syndrome. The condition is inherited in an autosomal dominant pattern. In some cases, an affected person inherits the mutation from one affected parent. Other cases may result from new mutations in the gene.
Treatment is aimed at addressing the symptoms found in each individual and may require the coordinated efforts of a team of specialists. Surgery is often needed to prevent or correct early closure of the cranial sutures and correct certain craniofacial abnormalities, syndactyly, and/or skeletal defects.
Causes:
Most cases of Saethre-Chotzen syndrome are caused by mutations in the TWIST1 gene. The TWIST1 gene provides instructions for making a protein that plays an important role in early development.
This protein is a transcription factor, which means that it attaches to a specific region of DNA and helps control the activity of particular genes. The TWIST1 protein is active in cells that give rise to bones, muscles, and other tissues in the head and face. It is also involved in the development of the limbs. Mutations in the TWIST1 gene prevent one copy of the gene in each cell from making any functional protein. A shortage of the TWIST1 protein affects the development and maturation of cells in the skull, face, and limbs. These abnormalities underline the signs and symptoms of Saethre- Chotzen syndrome, including the premature fusion of certain skull bones.
A small number of cases of Saethre-Chotzen syndrome have resulted from a structural chromosomal abnormality, such as a deletion or rearrangement of genetic material, in the region of chromosome 7 that contains the TWIST1 gene. When Saethre-Chotzen syndrome is caused by a chromosomal deletion instead of a mutation within the TWIST1 gene, affected children are much more likely to have intellectual disability, developmental delay, and learning difficulties.
Signs and Symptoms:
SCS presents in a variable fashion. The majority of individuals with SCS are moderately affected, with uneven facial features and a relatively flat face due to underdeveloped eye sockets, cheekbones, and lower jaw. In addition to the physical abnormality, people with SCS also experience growth delays, which results in relatively short stature. Although most individuals with SCS are of normal intelligence, some Individuals may have mild to moderate mental delays. More Severe Cases of SCS, with more serious facial deformities, occur when multiple cranial sutures close prematurely.
Cranial defects:
- Flat, asymmetric head and face
- Head is typically cone-shaped (acrocephaly) or flat (brachycephaly) but can also be long and narrow (Dolichocephaly).
- Head is short from front to back
- Lopsided face
- Low set hairline causing the forehead to appear tall and wide
Defects of the hands and feet:
- Webbing between the second and third finger and between the second and third toes
- Short fingers and toes
- Broad thumb and or a broad hallux with a valgus deformity.
- Hands have a single palmar flexion crease
Ocular defects:
- Unevenly positioned eyes that may be crossed(strabismus) or wide-set(hypertelorism)
- Vision problems due to abnormal facial anatomy, which causes mechanical disturbances of the extraocular muscles, resulting in strabismus(crossed eyes)
- Tear duct stenosis(narrowing of the tear duct)
- Drooping eyelids
- Downward slanting palpebral fissures(separation between upper and lower eyelids)
- Nearsightedness
- Epicanthal folds (skin folds of the upper eyelid covering the inner corner of the eye)
- Blepharophimosis(bilateral ptosis with reduced size of the eye)
- Optic atrophy
- Refractory errors
Ear, Nose, and mouth defects:
-Small, low-set ears that may be rotated somewhat backward and has a prominent(bulging) pinna.
- Beaked nose(slightly bent downward at the tip) that is slightly off-center and contains a deviated septum
- Malocclusion is associated with dental abnormalities including enamel hypoplasia(thin enamel due to incomplete formation), Hyperdontia (extra teeth), and peg teeth(small, abnormality shaped teeth)
- Cleft palate with a high arch
Less common defects:
- Short stature
- Vertebral fusion
- Congenital heart problems
- Speech problems
- Anal atresia (malformed rectum)
- Undescended testes (cryptorchidism)
- Renal kidney abnormality
- Personality disorders
Inheritance:
Saethre-Chptzen syndrome is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder. In some cases, an affected person inherited the mutation from one affected parent. Other cases may result from new mutations in the end. These cases occur in people with no history of the disorder in their families. Each child of an individual with Sarthre- Chotzen syndrome has a 50% chance of inheriting the mutation.
Diagnosis:
Making a diagnosis for a genetic or rare disease can often be challenging. Healthcare professionals typically look at t person's medical history, symptoms, physical exam, and laboratory test results in order to make a diagnosis. The following resources provide information relating to diagnosis and testing for this condition. If you have questions about getting a diagnosis, you should contact a healthcare professional.
Testing:
The genetic testing registry(GTR) provides information about the genetic tests for this condition. The intended audience for the GTR is health care providers and researchers. Patients and consumers with specific questions about a genetic test should contact a health care provider or a genetic professional.
Tuesday, 14 September 2021
Nipah Virus(Nipah Henipavirus)
Nipah Virus
Nipah virus, scientific name Nipah Henipavirus, is a bat-borne virus that causes Nipah Virus infection in humans and other animals, a disease with a high mortality rate. Numerous disease outbreaks caused by the Nipah virus have occurred in south and southeast Asia. Nipah Virus belongs to the genus Henipavirus along with the Hendra virus, which has also caused disease outbreaks.
Although the Nipah virus has caused only a few known outbreaks in Asia, it infects a wide range of animals and causes severe disease and death in people, making it a public health concern.
Transmission:
During the first recognized outbreak in Malaysia, which also affected Singapore, most human infections resulted from direct contact with sick pigs or their contaminated tissues. Transmission is thought to have occurred via unprotected exposure to secretions from the pigs, or unprotected contact with the tissue of a sick animal.
In subsequent outbreaks in Bangladesh and India, consumption of fruits or fruit products contaminated with urine or saliva from infected fruit bats was the most likely source of infection.
During the later outbreaks in Bangladesh a d India, Nipah virus spread directly from Human - to humans through close contact with people's secretions and excretions. Transmission of the virus was also reported within a healthcare setting, where 75% of cases occurred among hospital staff or visitors. Around half of reported cases in Bangladesh were die to the human-to-human transmission through providing care to infected patients.
Signs and symptoms:
Human infections range from asymptomatic infection to acute respiratory infection (mild, severe) and fatal encephalitis.
Infected people initially develop symptoms including fever, headaches, myalgia, vomiting, and sore throat. This can be followed by dizziness, drowsiness, altered consciousness, and neurological signs that indicate acute encephalitis. Some people can also experience atypical pneumonia and severe respiratory problems, including acute respiratory distress. Encephalitis and seizures occur in severe cases, progressing to coma within 24 to 48 hours.
The incubation period is believed to range from 4 to 14 days. However, an incubation period as long as 45 days have been reported.
Most people who survive acute encephalitis make a full recovery, but long-term neurological conditions have been reported in survivors. Approximately 20% of patients are left with residential neurological consequences such as seizure disorder and personality changes. A small number of people who recover subsequently relapse or develop delayed onset encephalitis.
The case fatality rate is estimated at 40% to 75%. This rate can vary by outbreak depending on local capabilities for epidemiological surveillance and clinical management.
- Fever
- Headache
- Muscle Pain(Myalgia)
- Vomiting
- Sore Throat
These symptoms can be followed by more serious conditions including:
- Dizziness
- Altered consciousness
- Acute encephalitis
- Atypical Pneumonia
- Severe Respiratory
- Seizures
Diagnosis:
Initial signs and symptoms of Nipah virus infection are nonspecific, and the diagnosis is often not suspected at the time of presentation. This can hinder accurate diagnosis and creates challenges in outbreak detection, effective and timely infection control measures, and outbreak response activities.
In addition, the quality, quantity, type, timing of clinical sample collection, and the time needed to transfer samples to the laboratory can affect the accuracy of laboratory results.
Nipah virus infection can be diagnosed with clinical history during the acute and convalescent phases of the disease. The main tests used are real-time polymerase chain reaction from bodily fluids and antibody detection via enzyme-linked immunosorbent assay (ELISA). Other tests used include polymerase chain reaction (PCR) assay and virus isolation by cell culture.
Treatment:
There are currently no drugs or vaccines specific for Nipah virus infection although WHO has identified Nipah as a priority disease for the WHO research and development Blueprint. Intensive supportive care is recommended to treat severe respiratory and neurological complications.
Saturday, 28 August 2021
Vitamin D
Vitamin D
Vitamin D is a group of fat-soluble secosteroids responsible for increasing intestinal absorption of calcium, magnesium, and phosphate, and many other biological effects. In humans, the most important compounds in this group are vitamin D3 and D2.
Vitamin D obtained from sun exposure, foods, and supplements are biologically inert and must undergo two hydroxylations in the body activation. The first hydroxylation, which occurs in the liver, converts vitamin D to 25- hydroxyvitamin D also known as "Calcidiol".
Vitamin D promotes calcium absorption in the gut and maintains adequate serum calcium and phosphate concentrations to enable normal bone mineralization and to prevent hypocalcemic tetany (involuntary contraction of muscles, leading to cramps and spasms). It is also needed for bone growth and bone remodeling by osteoblasts and osteoclasts, without sufficient vitamin D, bones can become thin, brittle, or misshapen. Vitamin D also helps protect older adults from osteoporosis.
Types:
Several forms (Vitamers) of vitamin D exist. The two major forms are vitamin D2 or ergocalciferol, and vitamin D3 or cholecalciferol. Vitamin D without a subscript refers to either D2 or D3, or both, and is known collectively as calciferol.
Vitamin D2 was chemically characterized in 1931. In 1935, the chemical structure of vitamin D3 was defined and shown to result from the ultraviolet irradiation of 7- dehydrocholesterol. A chemical nomenclature for vitamin D forms was recommended in 1981 but alternative names remain in common use.
Chemically, the various forms of vitamin D are secosteroids, that is steroids in which one of the bonds in the steroid rings is broken. the structural difference between vitamin D2 and vitamin D3 is in the side chain, which contains a double bond, between carbons 22 and 23, and a methyl group on carbon 24 in vitamin D2.
Vitamin D deficiency:
People can develop vitamin D deficiency when usual intakes are lower over time than recommended levels, exposure to sunlight is limited, the kidneys cannot 25(OH)D to its active form or absorption of vitamin D from the digestive tract is inadequate. Diets low in vitamin D are more common in people who have a milk allergy or lactose intolerance and those who consume a non-vegetarian or vegan diet.
In children, vitamin D deficiency is manifested as rickets, a disease characterized by a failure of bone tissue to become properly mineralized, resulting in soft bones and skeletal deformities. In addition to bone deformities and pain, severe rickets can cause failure to thrive, developmental delay, hypocalcemic seizures, tetanic spasm, cardiomyopathy, and dental abnormalities.
The incidence rate of rickets in children younger than 3 years in the decade beginning in 2000 was 24. 1per 100,000. Rickets occurred mainly in black children who were breastfed longer, were born with low birth weight, weighed less, and were shorter than other children. The incidence rate of rickets in infants and children are seen by 2325 pediatricians throughout Canada was 2.9 per 100,000, and almost all patients with rickets had been breastfed.
In adults and adolescents, vitamin D deficiency can lead to osteomalacia, in which existing bone is incompletely or effectively mineralized during the remodeling process, resulting in weak bones. Signs and symptoms of osteomalacia are familiar to those of rickets and include bone deformities and pain, hypocalcemic seizures, tetanic spasms, and dental abnormalities.
Screening for vitamin D status is becoming a more common part of the routine laboratory bloodwork ordered by primary-care physicians, irrespective of any indications for this practice. No studies have examined whether such screening for vitamin D deficiency results in improved health outcomes.
Symptoms:
Being sick it getting infections often:
One of vitamin D most important roles is keeping your immune system strong so you're able to fight off viruses and bacteria that cause illness. It directly interacts with the cells that are responsible for fighting infection. If you often become sick, especially with colds or the flu, low levels of vitamin D may be a contributing factor.
Fatigue and tiredness:
Feeling tired can have many causes, and vitamin D deficiency may be one of them. Unfortunately, it's often overlooked as a potential cause. case studies have shown that very low blood levels of vitamin D can cause fatigue that can have a severe negative effect on the quality of life.
Bone and back pain:
Vitamin D helps maintain bone health in a number of ways. for one, it improves your body's absorption of calcium. Bone pain and lower back pain may be signs of inadequate vitamin D levels in the blood. large observational studies have found a relationship between a deficiency and chronic lower back pain.
Bone Loss:
Vitamin D plays a crucial in calcium absorption and bone metabolism. Many older people who are diagnosed with bone loss believe they need to take more calcium. However, they may be deficient in vitamin D as well. Low bone mineral density is an indication that your bones have lost calcium and other minerals. This places older adults, especially women, at an increased risk for fractures.
Hair loss:
Hair loss is often attributed to stress, which is certainly a common cause. However, when hair loss is severe, it may be the result of disease or nutrient deficiency. Hair loss in women has been linked to low vitamin D levels, though there is very little research on this to date. In particular, research suggests that low vitamin D levels are linked to alopecia areata and may be a risk factor for developing the disease.
Muscle pain:
The causes of muscle pain are often difficult to pinpoint. There is some evidence that vitamin D deficiency may be a potential cause of muscle pain in children and adults. in one study, 71% of people with chronic pain were found to be deficient. The vitamin D receptor is present in nerve cells nociceptors, which sense pain.
Groups at risk of vitamin D inadequacy:
Obtaining sufficient vitamin D from natural food sources alone is difficult. For many people, consuming vitamin- D fortifies foods and exposing themselves to some sunlight are essential for maintaining a healthy vitamin D status.
Breastfeed Infants:
Consumption of human milk alone does not ordinarily enable infants to meet vitamin D requirements, because it provides less than 0.6 to 2.0 mcg/L. The vitamin D content of human milk is related to the mother's vitamin D status, studies suggest that the breastmilk of mothers who take daily supplements containing at least 50 mcg (2,000IU) vitamin D3 have higher levels of the nutrient.
Older Adults:
Older adults are at increased risk of developing vitamin D insufficiency, partly because the skin's ability to synthesize vitamin D decline with age. In addition, older adults are likely to spend more time than younger people indoors and might have an inadequate dietary intake of the vitamin.
People with limited sun exposure:
Homebound individuals, people who wear long robes, dresses, or head coverings for religious reasons, and people with occupations that limit sun exposure are among the groups that are unlikely to obtain adequate amounts of vitamin D from sunlight.
People with dark skin:
Greater amounts of the pigment melanin in the epidermal layer of the skin result in darker skin and reduce the skin's ability to produce vitamin D from sunlight. Black Americans, for example, typically have lower serum25(OH) D levels than white Americans. However, whether these lower levels in persons with dark skin have significant health consequences is not clear.
People with conditions that limit fat absorption:
Vitamin D is fat-soluble, its absorption depends on the Ability of dietary fat. Fat malabsorption is associated with medical conditions that include some forms of liver disease, cystic fibrosis, celiac disease, Crohn's disease, and ulcerative colitis. In addition to having an increased risk of vitamin D deficiency, people with these conditions might not eat certain foods, such as dairy products or eat only small amounts of these foods.
People who are obese or have undergone gastric bypass surgery:
Individuals with a body mass index(BMI) of 30 or more have lower serum 25(OH)D levels than nonobese individuals. Obesity does not affect the skin's capacity to synthesize vitamin D. Obese individuals who have undergone gastric bypass surgery can also become vitamin D deficient. In this procedure, part of the upper small intestine, where vitamin D is absorbed, is bypassed, and vitamin D that is mobilized into the bloodstream from fat stores might not rise 25(OH) D to adequate levels over time.
Other Conditions:
Diabetes:
A systematic review of 2014 concluded that the available studies show no evidence of vitamin D3 supplementation having an effect on glucose homeostasis or diabetes prevention. A review article of 201 reported that while there is increasing evidence that vitamin D deficiency may be a risk factor for diabetes, overall evidence regarding vitamin D levels and diabetes mellitus is contradictory, requiring future studies.
ADHD:
a meta-analysis of observational studies showed that children with ADHD have lower vitamin D levels and that there was a small association between low vitamin D levels at the time of birth and later development of ADHD. Several small randomized controlled trials of vitamin D supplementation indicated improved ADHD symptoms such as impulsivity and hyperactivity.
Depression:
Clinical trials of vitamin D supplementation for depressive symptoms have generally been of low quality and show no overall effect, although subgroup analysis showed supplementation for participants with clinically significant depressive symptoms or depressive disorder had a moderate effect.
Cognition and dementia:
A systematic review of clinical studies found an association between low vitamin D levels with cognitive impairment and a higher risk of developing Alzheimer's disease. However, lower vitamin D concentrations are also associated with poor nutrition and spending less time outdoors. Therefore, alternative explanations for the increase in cognitive impairment exist and hence the direct causal relationship between vitamin D levels and cognition could not be established.
Pregnancy:
Low levels of vitamin D in pregnancy are associated with gestational diabetes, pre-eclampsia, and small infants. Although taking vitamin D supplements during pregnancy raises blood levels of vitamin D in the mother at term, the full extent of benefits for the mother or baby is unclear.
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