Treatment combo Sessions of Modern Medicine in Digital format

Treatment combo Sessions of Modern Medicine in Digital format - F

The frequencies used in these sessions are based upon Rife sets for resonant therapy devices masked in Algorithmic piano music.

More information regarding the items in the list is given below the list.

List of Treatment combo Sessions of Modern Medicine in Digital format for problems/products available at us for just Rs. 1,000/- for any 5 sessions from any one or multiple Treatment combo Sessions for 30 doses per session (2 times a day for 15 days) in max 15 days.

1) Facial Hemiatrophy
2) Facial Nerve Diseases
3) Facial Neuralgia
4) Familial Motor Neuron Disease
5) Fasciculation
6) Fasciitis
7) Fasciitis Necrotizing
8) Fatigue
9) Fatty Liver
10) Fatty-Acid Oxidation Disorders
11) Favism
12) Fecal Incontinence
13) Fetal Diseases-General
14) Fever
15) Fibrocystic Breast Disease
16) Fibrodysplasia O-P
17) Fibromuscular Dysplasia
18) Fibromyalgia
19) Fibrosis
20) Fibrous Dysplasia of Bone
21) Fibrous Dysplasia Polyostotic
22) Filarioidea Infections
23) Fisher Syndrome
24) Fistula
25) Floaters
26) Foot Deformities
27) Fournier Gangrene
28) Fragile-X Syndrome
29) Freeman-Sheldon Syndrome
30) Fucosidosis
31) Furunculosis

* Familial motor neuron disease (FMND) constitutes approximately 5%�10% of cases of motor neuron disease (MND). Whilst in most families the pattern of inheritance is consistent with an autosomal-dominant trait, with age-dependent penetrance, a few cases appear to show an autosomal-recessive mode of inheritance. Statistical analysis shows that the likelihood of chance aggregation is improbable because affected members span several generations, come from different environmental and geographical regions, and the condition does not develop in spouses. The familial and sporadic forms are clinically indistinguishable, so it is likely that a common abnormality may be present in both. A motor neuron disease (MND) is any of several neurological disorders that selectively affect motor neurons, the cells that control voluntary muscles of the body. They include amyotrophic lateral sclerosis (ALS), primary lateral sclerosis (PLS), progressive muscular atrophy (PMA), progressive bulbar palsy (PBP) and pseudobulbar palsy; spinal muscular atrophies are also sometimes included in the group. They are neurodegenerative in nature and cause increasing disability and eventually, death.

* Fanconi anemia (FA) is a rare genetic disease. Among those affected the majority develop cancer, most often acute myelogenous leukemia, and 90% develop bone marrow failure (the inability to produce blood cells) by age 40. About 60�75% of people have congenital defects, commonly short stature, abnormalities of the skin, arms, head, eyes, kidneys, and ears, and developmental disabilities. Around 75% of people have some form of endocrine problem, with varying degrees of severity. FA is the result of a genetic defect in a cluster of proteins responsible for DNA repair. During childhood, short stature and skin pigmentation, including caf� au lait spots, may become apparent. The first sign of a hematologic problem is usually petechiae and bruises, with later onset of pale appearance, feeling tired, and infections. Because macrocytosis usually precedes a low platelet count, patients with typical congenital anomalies associated with FA should be evaluated for an elevated red blood cell mean corpuscular volume. Clinically, hematological abnormalities are the most serious symptoms in FA. By the age of 40, 98% of FA patients will have developed some type of hematological abnormality. However, there are a few cases in which older patients have died without ever developing them. Symptoms appear progressively, and often lead to complete bone marrow failure. While at birth, blood count is usually normal, macrocytosis/megaloblastic anemia, defined as unusually large red blood cells, is the first detected abnormality, often within the first decade of life (median age of onset is 7 years). Within the next 10 years, over 50% of patients presenting haematological abnormalities will have developed pancytopenia, defined as abnormalities in two or more blood cell lineages.

* Fasciculation is simply a muscle twitch, or involuntary contraction of skeletal muscle fibers, that affects a small localized area. A fasciculation can occur anywhere in the body but are often most noticeable on the face. It can be caused by a number of common factors such as stress, vitamin deficiencies, or dehydration that have no long-term impact. It can also stem from some neurologic disorders, traumatic injuries, drug reactions, or poisoning. Extended periods of high stress can cause fasciculation, but usually these twitches don�t begin until the body starts to relax after the stress eases. A deficiency in magnesium or calcium can also lead to muscle twitches and is usually able to be corrected by changes in diet or the addition of supplements. A vitamin D deficiency can lead to twitches because of its tendency to cause low absorption of calcium. Dehydration may cause fasciculation because of the body�s tendency to lose both fluid and electrolytes at the same time; calcium and magnesium are some of the more common electrolytes needed for normal muscle function. Any muscle can experience these twitches, but they commonly occur in the eye area, in the tongue, and the larger muscles of the arms and legs.

* Fasciitis necrotizing, commonly known as flesh-eating disease or flesh-eating bacteria syndrome.

* Fasciitis, inflammation of the connective tissue that may be caused by streptococcal or other types of infection, an injury, or an autoimmune reaction.

* Fatty liver is a reversible condition wherein large vacuoles of triglyceride fat accumulate in liver cells via the process of steatosis (i.e., abnormal retention of lipids within a cell). Despite having multiple causes, fatty liver can be considered a single disease that occurs worldwide in those with excessive alcohol intake and the obese (with or without effects of insulin resistance). The condition is also associated with other diseases that influence fat metabolism. When this process of fat metabolism is disrupted, the fat can accumulate in the liver in excessive amounts, thus resulting in a fatty liver. It is difficult to distinguish alcoholic FLD from nonalcoholic FLD, and both show microvesicular and macrovesicular fatty changes at different stages. Accumulation of fat may also be accompanied by a progressive inflammation of the liver (hepatitis), called steatohepatitis. Liver disease with extensive inflammation and a high degree of steatosis often progresses to more severe forms of the disease. Hepatocyte ballooning and necrosis of varying degrees are often present at this stage. Liver cell death and inflammatory responses lead to the activation of hepatic stellate cells, which play a pivotal role in hepatic fibrosis. Defects in fatty acid metabolism are responsible for pathogenesis of FLD, which may be due to imbalance in energy consumption and its combustion, resulting in lipid storage, or can be a consequence of peripheral resistance to insulin, whereby the transport of fatty acids from adipose tissue to the liver is increased. Most individuals are asymptomatic and are usually discovered incidentally because of abnormal liver function tests or hepatomegaly noted in unrelated medical conditions. Elevated liver biochemistry is found in 50% of patients with simple steatosis. The serum alanine transaminase level usually is greater than the aspartate transaminase level in the nonalcoholic variant and the opposite in alcoholic FLD (AST:ALT more than 2:1).

* Fatty-acid oxidation disorders, such as hypertriglyceridemia, hyperlipidemia etc.

* Favism is a condition characterized by hemolytic anemia (breakup of red blood cells) after eating fava beans (broad beans) or being exposed to the pollen of the fava plant. This dangerous reaction occurs exclusively in people with a deficiency of the enzyme glucose-6-phosphate dehydrogenase (G6PD), an X-linked genetic trait. For someone with the severe form, exposure to even the pollen of fava beans can cause a reaction, as will consumption of the beans. The patient may feel tired, feverish, or experience a headache, and the condition can also cause abdominal pain, nausea, and vomiting. If left untreated, it can result in serious health problems, like a coma. Early warning signs include jaundice, dark urine, and a general sense of feeling run down and tired all the time.

* Fibrodysplasia ossificans progressiva, disorder in which muscle and connective tissue, such as tendons and ligaments, are gradually replaced by bone.

* Fibromuscular dysplasia (FMD) is the abnormal development or growth of cells in the walls of the body�s arteries. As a result of this growth, areas of the arteries can thicken, narrow and even enlarge, making it difficult for blood to flow through them. FMD most often affects the renal arteries, which supply the kidneys with blood, and carotid arteries, which bring blood to the brain. Less commonly, FMD develops in the arteries of the abdomen (mesenteric arteries) or the arteries of the arms and legs. In nearly one-third of people with FMD, more than one artery is affected. Depending on which arteries are affected, FMD can increase the risk of high blood pressure, impaired kidney function, aneurysm, stroke and other complications. FMD can increase risk of several conditions, including: High blood pressure: When the arteries become narrowed, blood pressure can increase. High blood pressure (hypertension) is the most common complication of FMD. Stroke: A stroke may occur if an aneurysm in one of the carotid arteries ruptures or if one of the carotid arteries dissects, disrupting the flow of blood to the brain. A tear in the artery (dissection): The lining of the artery wall may tear, causing blood to leak into the wall. Aneurysm: The pressure of blood flow through a narrowed artery can create a weakened area or bulge in the artery wall called an aneurysm. An aneurysm may rupture, resulting in a life-threatening situation. Pain or cramping in lower legs (intermittent claudication): FMD that affects the arteries in the legs can cause discomfort or pain when walking and exercising. Kidney dysfunction or failure: Reduced blood flow to the kidneys can impair kidney function and, in rare cases, lead to kidney failure.

* Fibromyalgia, disorder characterized by muscle pain, fatigue, joint stiffness, and depression or anxiety.

* Fibrosis, formation of excess fibrous connective tissue in an organ or tissue in a reparative or reactive process.

* Fibrous dysplasia of bone is a skeletal disorder in which bone-forming cells fail to mature and produce too much fibrous, or connective, tissue. Areas of healthy bone are replaced with this fibrous tissue. The replacement of normal bone in fibrous dysplasia can lead to pain, misshapen bones, and fracture, especially when it occurs in the long bones (arms and legs). When it occurs in the skull, there can also be a replacement of the normal bone with fibrous tissue, resulting in changes in the shape of the face or skull, pain, and, in rare circumstances, hearing or vision loss. Some people with fibrous dysplasia have only one bone involved (monostotic), whereas other people have more than one bone involved (polyostotic). The disease may occur alone, or as part of a condition known as the McCune-Albright syndrome. Fibrous dysplasia can affect any bone in the body. The most common sites are the bones in the skull and face, femur (thighbone), tibia (shinbone), humerus (upper arm), pelvis, and ribs. Although many bones can be affected at once�and affected bones are often found on one side of the body�the disease does not �spread� from one bone to another; that is, the pattern of which bones are involved is established very early in life and does not change with age.

* Fibrous dysplasia polyostotic, also known as McCune-Albright syndrome is a disorder that features the replacement of multiple areas of bone by fibrous tissue, which may cause fractures and deformity of the legs, arms, and skull. McCune-Albright's syndrome is a genetic disorder that is characterized by polyostotic fibrous dysplasia along with skin pigmentation and hormonal problems, with premature sexual development. The flat areas of increased skin pigment are called cafe au lait spots. The hormonal problems that can be related to polyostotic fibrous dysplasia include early puberty (with premature menstrual bleeding and development of breasts and pubic hair), thyroid abnormalities, and an increased rate of growth.

* Filarioidea infections cause disease conditions generically known as filariasis. Species within the Filarioidea superfamily are known as filarial worms or filariae (singular "filaria"). Filarioidea all are specialised parasites and the definitive host is always a vertebrate, a mammal, bird, reptile or amphibian, but not a fish. The intermediate host is always an Arthropod. Most of Filarioidea parasitise wild species, birds in particular, but some, especially in the family Onchocercidae, attack mammals, including humans and some domestic animals. Conditions that result from parasitism by Onchocercidae include some of the most troublesome diseases of the warmer regions, including river blindness and elephantiasis. Humankind is the definitive host of at least nine species of filariae in various families. Some of these mainly occupy lymph vessels and cause conditions such as adenolyrophangitis, elephantiasis, and filarial fever. Others may cause loiasis, streptocerciasis, cutaneous onchocerciasis, river blindness or other less serious pathogenic conditions.

* Fisher syndrome, also Miller-Fisher syndrome is a variant of Guillain-Barre syndrome, characterized by ophthalmoplegia, ataxia and areflexia. These clinical signs can overlap with other signs and symptoms of Guillain-Barre syndrome. Although it is assumed that Fisher syndrome is idiopathic, it was observed that this disease can develop after a recent viral, bacterial or mycoplasma infections and after vaccinations. Association with Campylobacter jejuni infection was also mentioned . Fisher syndrome occurs in both sexes, with a slight predominance in males. Clinically, symptomatic triad consisting of ophthalmoplegia, ataxia and areflexia is characteristic for this syndrome. Ophthalmoplegia tends to be complete, sometimes have been observed cases of internuclear ophthalmoplegia and Parinaud syndrome (a group of abnormalities of eye movement and pupil dysfunction). Palpebral ptosis is also present and may be unilateral or bilateral, symmetrical or asymmetrical, complete or incomplete. Pupillary disturbances occur in over 50% of cases of Fisher syndrome and are characterized by reduction of pupillary reaction to light, accommodation disorders and anisocoria (unequal size of the pupils). Ataxia is a result of peripheral non-myelinated spinocerebellar fibers conduction disturbances , being a truncal ataxia. Have been reported cases of Fisher syndrome associated with retrobulbar optic neuritis and accompanied by vision loss, with complete or incomplete vision recovery. Cranial nerve impairment occurs, especially of the facial nerve, causing facial paralysis which can be unilateral or bilateral. Other cranial nerves which can be affected are ophthalmic branch of cranial nerve V (trigeminal nerve) and cranial nerve VIII (acoustic). Cranial nerves II (optic) and III (oculomotor) are less affected in this disease. A characteristic of Fisher syndrome is the occurrence of migratory paresthesias, which are not usually accompanied by sensitive deficits. Sometimes, cases of sensitive ataxia have been reported. Neurological disorders in Fisher syndrome affects, in most cases, the peripheral nervous system. In some patients were reported impairments of central nervous system, accompanied by dysarthria, nystagmus, ataxic gait, ophthalmoparesis, pronounced tendon reflexes and positive Babinski sign). In some cases distinction between Fisher syndrome and brainstem encephalitis is very difficult.

* Fistula, abnormal connection between an organ, vessel, or intestine and another structure.

* Floaters, small particles in the fluid inside your eye.

* Fournier gangrene is a type of necrotizing fasciitis or gangrene affecting the perineum. It commonly occurs in elderly men, but it can also occur in women and children. It is more likely to occur in those with diabetes, alcoholics, or those who are immune compromised.

* Fragile X syndrome (FXS) is a genetic disorder. Symptoms often include mild to moderate intellectual disability. Physical features may include a long and narrow face, large ears, flexible fingers, and large testicles. About a third of people have features of autism such as problems with social interactions and delayed speech. Hyperactivity is common and seizures occur in about 10%. Males are usually more affected than females. Fragile X syndrome occurs in about 1 in 4,000 males and 1 in 8,000 females. Most young children do not show any physical signs of FXS. It is not until puberty that physical features of FXS begin to develop. Aside from intellectual disability, prominent characteristics of the syndrome may include an elongated face, large or protruding ears, flat feet, larger testes (macroorchidism), and low muscle tone. Recurrent otitis media (middle ear infection) and sinusitis is common during early childhood. Speech may be cluttered or nervous. Behavioral characteristics may include stereotypic movements (e.g., hand-flapping) and atypical social development, particularly shyness, limited eye contact, memory problems, and difficulty with face encoding. Some individuals with fragile X syndrome also meet the diagnostic criteria for autism. A 2013 review stated that life expectancy for FXS was 12 years lower than the general population and that the causes of death were similar to those found for the general population.

* Freeman-Sheldon syndrome is a condition that primarily affects the face, hands, and feet. People with this disorder have a distinctive facial appearance including a small mouth (microstomia) with pursed lips, giving the appearance of a "whistling face." People with Freeman-Sheldon syndrome may also have a prominent forehead and brow ridges, a sunken appearance of the middle of the face, a short nose, a long area between the nose and mouth, deep folds in the skin between the nose and lips, full cheeks, and a chin dimple shaped like an "H" or "V". Affected individuals may have a number of abnormalities that affect the eyes. Other facial features that may occur in Freeman-Sheldon syndrome include an unusually small tongue and jaw and a high arch in the roof of the mouth. People with this disorder may have difficulty swallowing, a failure to gain weight and grow at the expected rate, and respiratory complications that may be life-threatening. Speech problems are also common in this disorder. Some affected individuals have hearing loss. Freeman-Sheldon syndrome is also characterized by joint deformities that restrict movement. People with this disorder typically have multiple contractures in the hands and feet at birth. These contractures lead to permanently bent fingers and toes, and inward- and downward-turning feet. Affected individuals may also have a spine that curves to the side. People with Freeman-Sheldon syndrome also have an increased risk of developing a severe reaction to certain drugs used during surgery and other invasive procedures. This reaction is called malignant hyperthermia. Malignant hyperthermia occurs in response to some anesthetic gases, which are used to block the sensation of pain. If given these drugs, people at risk for malignant hyperthermia may experience muscle rigidity, breakdown of muscle fibers, a high fever, increased acid levels in the blood and other tissues, and a rapid heart rate. Intelligence is unaffected in most people with Freeman-Sheldon syndrome, but approximately one-third have some degree of intellectual disability.

* Fucosidosis is a rare lysosomal storage disorder in which the FUCA1 gene experiences mutations that severely reduce or stop the activity of the alpha-L-fucosidase enzyme. The result is a buildup of complex sugars in parts of the body, which leads to death. Brain cells are especially sensitive to this buildup. Other results are progressive neurological deterioration, skin abnormalities, growth retardation, skeletal disease, and coarsening of facial features. Fucosidosis is the consequence of faulty degradation of both sphingolipids and polysaccharides. Major accumulation of the H-antigen (a member of the ABO blood group antigens), a glycolipid, is seen primarily in the liver of fucosidosis patients. Fucosidosis is one of nine identified glycoprotein storage diseases. The disease has three different types. Type 1 and 2 are considered severe, and Type 3 being a mild disease. Symptoms are highly variable with mild cases being able to live to within the third or fourth decade. Type 1 and 2 are both linked with mental retardation. Severe cases can develop life-threatening complications early in childhood. Type 1 usually begins somewhere in the first three to 18 months of age and in considered the most severe of the three types. Symptoms include: Coarse facial features, Enlarged liver, spleen, and/or heart, Intellectual disability, Seizures, Abnormal bone formation of many bones, Progressive deterioration of brain and spinal cord, Increased or decreased perspiration. Patients have no vascular lesions, but have rapid psychomotor regression, severe and rapidly progressing neurologic signs, elevated sodium and chloride excretion in the sweat, and fatal outcome before the sixth year. Type 2 appears when a child is around 18 months of age and in considered milder than Type 1 but still severe. Symptoms are similar to Type 1 but milder and progress more slowly. Type 3 appears around 1�2 years of age and is considered mild.

* Furunculosis, boils.