Common Diseases Beginning with Letter “M”

Written by on March 22, 2011 in Diseases & Issues, Health -
Common diseases beginning with letter M

Here is the list of most common diseases and conditions that start with letter “M“:


Macroglobulinemia is the presence of increased levels of macroglobulins in the circulating blood. A plasma cell dyscrasia resembling leukemia with cells of lymphocytic, plasmacytic, or intermediate morphology, which secrete an immunoglobulin M monoclonal component. There is diffuse infiltration of bone marrow and also, in many cases, of the spleen, liver, or lymph nodes. The circulating macroglobulin produces symptoms of hyperviscosity syndrome: weakness, fatigue, bleeding disorders, and visual disturbances. Peak incidence is in the sixth and seventh decades.

Macroglossia is the medical term for unusual enlargement (hypertrophy) of the tongue. Severe enlargement of the tongue can cause cosmetic and functional difficulties including in speaking, eating, swallowing and sleeping. Among the causes of this issue are: amyloid disorders (an accumulation of insoluble proteins in tissues that impedes normal function); hypothyroid macroglossia (a clinical feature in Hypothyroid disorders which include congenital hypothyroidism, young Simpson syndrome, Zadik Barak Levin syndrome); overgrowth disorders; chromosomal disorders.

Macular degeneration is a medical condition which usually affects older adults that results in a loss of vision in the center of the visual field (the macula) because of damage to the retina. It occurs in “dry” and “wet” forms. It is a major cause of visual impairment in older adults (>50 years). Macular degeneration can make it difficult or impossible to read or recognize faces, although enough peripheral vision remains to allow other activities of daily life. The inner layer of the eye is the retina, which contains nerves that communicate sight; behind the retina is the choroid, which contains the blood supply to the macula (the central part of the retina). In the dry (nonexudative) form, cellular debris called drusen accumulate between the retina and the choroid, and the retina can become detached. In the wet (exudative) form, which is more severe, blood vessels grow up from the choroid behind the retina, and the retina can also become detached. It can be treated with laser coagulation, and with medication that stops and sometimes reverses the growth of blood vessels. Although some macular dystrophies affecting younger individuals are sometimes referred to as macular degeneration, the term generally refers to age-related macular degeneration (AMD or ARMD).
Age-related macular degeneration begins with characteristic yellow deposits in the macula (central area of the retina, which provides detailed central vision) called drusen between the retinal pigment epithelium and the underlying choroid. Most people with these early changes (referred to as age-related maculopathy) have good vision. People with drusen can go on to develop advanced AMD. The risk is considerably higher when the drusen are large and numerous and associated with disturbance in the pigmented cell layer under the macula. Recent research suggests that large and soft drusen are related to elevated cholesterol deposits and may respond to cholesterol-lowering agents.

Mad cow disease, is a fatal neurodegenerative disease in cattle that causes a spongy degeneration in the brain and spinal cord. BSE has a long incubation period, about 30 months to 8 years, usually affecting adult cattle at a peak age onset of four to five years, all breeds being equally susceptible. In the United Kingdom, the country worst affected, more than 179,000 cattle have been infected and 4.4 million slaughtered during the eradication program. The disease may be most easily transmitted to human beings by eating food contaminated with the brain or spinal cord or digestive tract of infected carcasses. However, it should also be noted that the infectious agent, although most highly concentrated in nervous tissue, can be found in virtually all tissues throughout the body, including blood. In humans, it is known as new variant Creutzfeldt–Jakob disease (vCJD or nvCJD), and by October 2009, it had killed 166 people in Britain (the most recent being of a different genotype than other sufferers), and 44 elsewhere with the number expected to rise because of the disease’s long incubation period. Between 460,000 and 482,000 BSE-infected animals had entered the human food chain before controls on high-risk offal were introduced in 1989. A British inquiry into BSE concluded that the epizootic was caused by cattle, who are normally herbivores, being fed the remains of other cattle in the form of meat and bone meal (MBM), which caused the infectious agent to spread. There are studies indicating that the cause of BSE may be from the contamination of MBM from sheep with scrapie that were processed in the same slaughterhouse. The epidemic was probably accelerated by the recycling of infected bovine tissues prior to the recognition of BSE. The origin of the disease itself remains unknown. The infectious agent is distinctive for the high temperatures at which it remains viable; this contributed to the spread of the disease in Britain, which had reduced the temperatures used during its rendering process. Another contributory factor was the feeding of infected protein supplements to very young calves.
This first reported case in North America was in May 2003 from Alberta, Canada. The first known U.S. occurrence came in December of the same year. Canada announced two additional cases of BSE from Alberta in early 2005.

Maffucci syndrome is a sporadic disease characterized by the presence of multiple enchondromas associated with multiple hemangiomas. Also lymphangiomas may be apparent. Patients are normal at birth and the syndrome manifests during childhood and puberty. The enchondromas affect the extremities and their distribution is asymmetrical. Disfigurations of the extremities are a result. Pathological fractures can arise in affected metaphyses and diaphyses of the long bones and are common (26%). The risk for sarcomatous degeneration of enchondromas, hemangiomas, or lymphangiomas is 15-30% in the setting of Maffucci syndrome. Management entails careful examination and monitoring for malignant degenerations. Surgical interventions can correct or minimize deformities.

Malaria is a mosquito-borne infectious disease of humans caused by eukaryotic protists of the genus Plasmodium. It is widespread in tropical and subtropical regions, including much of Sub-Saharan Africa, Asia and the Americas. The disease results from the multiplication of malaria parasites within red blood cells, causing symptoms that typically include fever and headache, in severe cases progressing to coma, and death. Four species of Plasmodium can infect and be transmitted by humans. Severe disease is largely caused by Plasmodium falciparum. Malaria caused by Plasmodium vivax, Plasmodium ovale and Plasmodium malariae is generally a milder disease that is rarely fatal. A fifth species, Plasmodium knowlesi, is a zoonosis that causes malaria in macaques but can also infect humans. Malaria transmission can be reduced by preventing mosquito bites by distribution of inexpensive mosquito nets and insect repellents, or by mosquito-control measures such as spraying insecticides inside houses and draining standing water where mosquitoes lay their eggs. Although many are under development, the challenge of producing a widely available vaccine that provides a high level of protection for a sustained period is still to be met. Two drugs are also available to prevent malaria in travellers to malaria-endemic countries (prophylaxis).
A variety of antimalarial medications are available. In the last 5 years, treatment of P. falciparum infections in endemic countries has been transformed by the use of combinations of drugs containing an artemisinin derivative. Severe malaria is treated with intravenous or intramuscular quinine or, increasingly, the artemisinin derivative artesunate which is superior to quinine in both children and adults. Resistance has developed to several antimalarial drugs, most notably chloroquine.
Each year, there are more than 225 million cases of malaria, killing around 781,000 people each year according to the latest WHO Report. The majority of deaths are of young children in sub-Saharan Africa. Ninety percent of malaria-related deaths occur in sub-Saharan Africa.

Mallory–Weiss syndrome or gastro-esophageal laceration syndrome refers to bleeding from tears (a Mallory-Weiss tear) in the mucosa at the junction of the stomach and esophagus, usually caused by severe retching, coughing, or vomiting. It is often associated with alcoholism and eating disorders and there is some evidence that presence of a hiatal hernia is a predisposing condition. Mallory–Weiss syndrome often presents as an episode of vomiting up blood (hematemesis) after violent retching or vomiting, but may also be noticed as old blood in the stool (melena), and a history of retching may be absent. In most cases, the bleeding stops spontaneously after 24–48 hours, but endoscopic or surgical treatment is sometimes required and rarely the condition is fatal.
Treatment is usually supportive as persistent bleeding is uncommon. However cauterization or injection of epinephrine to stop the bleeding may be undertaken during the index endoscopy procedure.

Malouf syndrome (also known as “congestive cardiomyopathy-hypergonadotropic hypogonadism syndrome”) is a congenital disorder that causes one or more of the following symptoms: mental retardation, ovarian dysgenesis, congestive cardiomyopathy, broad nasal base, blepharoptosis, and bone abnormalities, and occasionally marfanoid habitus (tall stature with long and thin limbs, little subcutaneous fat, arachnodactyly, joint hyperextensibility, narrow face, small chin, large testes, and hypotonia).
This disease is named for Jean Malouf, a popular 19th century sideshow performer born in Montreal. His memoirs, I Am Jean Malouf, were published in 1904 in serial form (highly edited from the original, which proved nearly illegible) by The Columbian Monthly Miscellany.

Marburg virus or simply Marburg is the common name for the genus of viruses Marburgvirus, which contains one species, Lake Victoria marburgvirus. The virus causes the disease Marburg Hemorrhagic Fever (MHF), also referred to as Marburg Virus Disease, and previously also known as green monkey disease due to its primate origin. Marburg originated in Central and East Africa, and infects both human and nonhuman primates. The Marburg Virus is in the same taxonomic family as Ebola, and both are identical structurally although they elicit different antibodies.
There is no specific antiviral therapy indicated for treating Marburg, and hospital care is usually supportive in nature. Hypotension and shock may require early administration of vasopressors and haemodynamic monitoring with attention to fluid and electrolyte balance, circulatory volume, and blood pressure. Viral haemorrhagic fever (VHF) patients tend to respond poorly to fluid infusions and may develop pulmonary edema.

Marfan syndrome (also called Marfan’s syndrome) is a genetic disorder of the connective tissue. People with Marfan’s tend to be unusually tall, with long limbs and long, thin fingers. It is sometimes inherited as a dominant trait. It is carried by a gene called FBN1, which encodes a connective protein called fibrillin-1. People have a pair of FBN1 genes. Because it is dominant, people who have inherited one affected FBN1 gene from either parent will have Marfan’s. This syndrome has a range of expressions, from mild to severe. The most serious complications are defects of the heart valves and aorta. It may also affect the lungs, eyes, the dural sac surrounding the spinal cord, skeleton and the hard palate.
In addition to being a connective protein that forms the structural support for tissues outside the cell, the normal fibrillin-1 protein binds to another protein, transforming growth factor beta (TGF-β). TGF-β has deleterious effects on vascular smooth muscle development and the integrity of the extracellular matrix. Researchers now believe that secondary to mutated fibrillin there is excessive TGF-β at the lungs, heart valves, and aorta, and this weakens the tissues and causes the features of Marfan syndrome. Since angiotensin II receptor blockers (ARBs) also reduce TGF-β, they have tested this by giving ARBs (losartan, etc.) to a small sample of young, severely affected Marfan syndrome patients. In some patients, the growth of the aorta was indeed reduced.

Marshall-Smith syndrome, discovered in 1971 (Marshall, Graham, Scott, Boner, & Smith), is characterized by unusual accelerated skeletal maturation (usually starting before birth) and symptoms like conspicuous physical characteristics, respiratory difficulties, and mental retardation. Cases described in the literature show a clinical variabililty regarding related symptoms. For instance, respiratory difficulties are ranging from absent to severe difficulties.

McCune–Albright syndrome, described in 1937 by Donovan James McCune and Fuller Albright, is a genetic disorder of bones, skin pigmentation and hormonal problems along with premature puberty. It is suspected when two of the three following features are present:  (autonomous) endocrine hyperfunction such as precocious puberty; polyostotic fibrous dysplasia; unilateral Café-au-lait spots. Within the syndrome there are bone fractures and deformity of the legs, arms and skull, different pigment patches on the skin, and early puberty with increased rate of growth.
Polyostotic fibrous dysplasia has different levels of severity. For example one child may be entirely healthy with no outward evidence of bone or endocrine problems, enter puberty at close to the normal age and have no unusual skin pigmentation. The complete opposite of that would be children who are diagnosed in early infancy with the obvious bone disease and obvious increased endocrine secretions from several glands. Approximately 20-30% of fibrous dysplasias are polyostotic and two thirds of patients are polyostotic before the age of ten. Polyostotic fibrous dysplasia is usually caused by mosaicism for a mutation in a gene called GNAS1 (Guanine Nucleotide binding protein, Alpha Stimulating activity polypeptide 1).
The syndrome shows a broad spectrum of severity. The disease frequently involves the skull and facial bones, pelvis, spine and shoulder girdle. The sites of involvement are the femur (91%), tibia (81%), pelvis (78%), ribs, skull and facial bones (50%), upper extremities, lumbar spine, clavicle, and cervical spine, in decreasing order of frequency. The craniofacial pattern of the disease occurs in 50% of patients with the polyostotic form of fibrous dysplasia.

Measles, also known as rubeola or morbilli, is an infection of the respiratory system caused by a virus, specifically a paramyxovirus of the genus Morbillivirus. Morbilliviruses, like other paramyxoviruses, are enveloped, single-stranded, negative-sense RNA viruses. Symptoms include fever, cough, runny nose, red eyes and a generalized, maculopapular, erythematous rash.
Measles (sometimes known as English Measles) is spread through respiration (contact with fluids from an infected person’s nose and mouth, either directly or through aerosol transmission), and is highly contagious—90% of people without immunity sharing living space with an infected person will catch it. The infection has an average incubation period of 14 days (range 6–19 days) and infectivity lasts from 2–4 days prior, until 2–5 days following the onset of the rash (i.e. 4–9 days infectivity in total). An alternative name for measles in English-speaking countries is rubeola, which is sometimes confused with rubella (German measles); the diseases are unrelated.
Patients with the measles should be placed on respiratory precautions. It is believed that patients should always be isolated from populations until confirmed recovery, such as several days after disappearance of rash and symptoms of complications. Humans are the only known natural host of measles, although the virus can infect some non-human primate species.

Megaloblastic anemia is an anemia that results from inhibition of DNA synthesis in red blood cell production. When DNA synthesis is impaired, the cell cycle cannot progress from the G2 growth stage to the mitosis (M) stage. This leads to continuing cell growth without division, which presents as macrocytosis.
The defect in red cell DNA synthesis is most often due to hypovitaminosis, specifically a deficiency of vitamin B12 and/or folic acid. Vitamin B12 deficiency alone will not cause the syndrome in the presence of sufficient folate, for the mechanism is loss of B12 dependent folate recycling, followed by folate-deficiency loss of nucleic acid synthesis (specifically thymine), leading to defects in DNA synthesis. Folic acid supplementation in the absence of vitamin B12 prevents this type of anemia (although other vitamin B12-specific pathologies continue).
Megaloblastic anemia not due to hypovitaminosis may be caused by antimetabolites that poison DNA production directly, such as some chemotherapeutic or antimicrobial agents (for example azathioprine or trimethoprim).
The pathological state of megaloblastosis is characterized by many large immature and dysfunctional red blood cells (megaloblasts) in the bone marrow and also by hypersegmented or multisegmented neutrophils seen in the “peripheral blood” (i.e., a diagnostic smear of a blood-sample taken from the circulation).

Meige’s syndrome is a type of dystonia. It is also known as Brueghel’s syndrome and oral facial dystonia. It is actually a combination of two forms of dystonia, blepharospasm and oromandibular dystonia (OMD).When OMD is combined with Blepharospasm, it may be referred to as Meige’s Syndrome named after Henri Meige, the French neurologist who first described the symptoms in detail in 1910. The symptoms usually begin between the ages of 30 and 70 years old and appear to be more common in women than in men (2:1 ratio). The combination of upper and lower dystonia is sometimes called cranial-cervical dystonia.
There is no cure for Meige’s Syndrome, nor can it be prevented, except in cases where it is caused by medication. Although palliative treatments are available, such as Botox injections. In some instances, acupuncutre has been known to help. Even though it is a form of alternative medicine, there have been some reports of acupuncture minimizing the effects of Meige’s.

Melanoma is a malignant tumor of melanocytes. Melanocytes are cells that produce the dark pigment, melanin, which is responsible for the color of skin. They predominantly occur in skin, but are also found in other parts of the body, including the bowel and the eye (see uveal melanoma). Melanoma can occur in any part of the body that contains melanocytes.
Melanoma is less common than other skin cancers. However, it is much more dangerous and causes the majority (75%) of deaths related to skin cancer. Worldwide, doctors diagnose about 160,000 new cases of melanoma yearly. The diagnosis is more frequent in women than in men and is particularly common among Caucasians living in sunny climates, with high rates of incidence in Australia, New Zealand, North America, and northern Europe. According to a WHO report about 48,000 melanoma related deaths occur worldwide per year.
The treatment includes surgical removal of the tumor, adjuvant treatment, chemo- and immunotherapy, or radiation therapy. The chance of a cure is greatest when the tumor is discovered while it is still small and thin, and can be entirely removed surgically.
Melanoma happens when a UV photon strikes a chromophore in a skin cell. A chromophore is the part of a molecule which gives it color. This happens usually because the skin has been damaged in that location, or is otherwise unprotected by melanin. Melanin itself does not suffer this damage. When the chromophore is struck by the UV photon, a singlet oxygen (1O2) or hydroxyl (•OH) free radical is produced, which then travels about the body until it finds a home in a melanocyte, where it acts to mutate the DNA by oxidising it. The damaged melanocyte then becomes a malignant tumour, which is coloured brown to black by melanin. Not every such free radical results in a melanoma. Many of them act in unrelated body parts and are thus destroyed. The cancer does not always happen at the location of the strike, but can show up at places not usually exposed to sunlight.

Meningiomas are the second most common primary neoplasm of the central nervous system, arising from the arachnoid “cap” cells of the arachnoid villi in the meninges. These tumors are usually benign in nature. However, they can be malignant. Most cases are sporadic while some are familial. Persons who have undergone radiation to the scalp are more at risk for developing meningiomas.
The most frequent genetic mutations involved in meningiomas are inactivation mutations in the neurofibromatosis 2 gene (merlin) on chromosome 22q.

Meningitis is inflammation of the protective membranes covering the brain and spinal cord, known collectively as the meninges. The inflammation may be caused by infection with viruses, bacteria, or other microorganisms, and less commonly by certain drugs. Meningitis can be life-threatening because of the inflammation’s proximity to the brain and spinal cord; therefore the condition is classified as a medical emergency.
The most common symptoms of meningitis are headache and neck stiffness associated with fever, confusion or altered consciousness, vomiting, and an inability to tolerate light (photophobia) or loud noises (phonophobia). Sometimes, especially in small children, only nonspecific symptoms may be present, such as irritability and drowsiness. If a rash is present, it may indicate a particular cause of meningitis; for instance, meningitis caused by meningococcal bacteria may be accompanied by a characteristic rash.
A lumbar puncture may be used to diagnose or exclude meningitis. This involves inserting a needle into the spinal canal to extract a sample of cerebrospinal fluid (CSF), the fluid that envelops the brain and spinal cord. The CSF is then examined in a medical laboratory. The usual treatment for meningitis is the prompt application of antibiotics and sometimes antiviral drugs. In some situations, corticosteroid drugs can also be used to prevent complications from overactive inflammation. Meningitis can lead to serious long-term consequences such as deafness, epilepsy, hydrocephalus and cognitive deficits, especially if not treated quickly. Meningitis is usually caused by infection from viruses or micro-organisms. Most cases are due to infection with viruses, with bacteria, fungi, and parasites being the next most common causes. It may also result from various non-infectious causes.

Mental retardation is a generalized disorder appearing before adulthood, characterized by significantly impaired cognitive functioning and deficits in two or more adaptive behaviors. It has historically been defined as an Intelligence Quotient score under 70. Once focused almost entirely on cognition, the definition now includes both a component relating to mental functioning and one relating to individuals’ functional skills in their environment. As a result, a person with a below-average intelligence quotient (BAIQ) may not be considered mentally retarded. Syndromic mental retardation is intellectual deficits associated with other medical and behavioral signs and symptoms. Non-syndromic mental retardation refers to intellectual deficits that appear without other abnormalities.
Mental retardation is a subtype of intellectual disability, although that term is now preferred by most advocates in most English-speaking countries as a euphemism for MR. However, intellectual disability is a broader concept and includes intellectual deficits that are too mild to properly qualify as mental retardation, too specific (as in specific learning disability), or acquired later in life, through acquired brain injuries or neurodegenerative diseases like dementia. Intellectual disabilities may appear at any age.

Microcephaly is a neurodevelopmental disorder in which the circumference of the head is more than two standard deviations smaller than average for the person’s age and sex. Microcephaly may be congenital or it may develop in the first few years of life. The disorder may stem from a wide variety of conditions that cause abnormal growth of the brain, or from syndromes associated with chromosomal abnormalities. Two copies of a loss-of-function mutation in one of the microcephalin genes causes primary microcephaly.
In general, life expectancy for individuals with microcephaly is reduced and the prognosis for normal brain function is poor. The prognosis varies depending on the presence of associated abnormalities. A genetic factor may play a role in causing some cases of microcephaly. Relations have been found between autism, duplications of chromosomes and macrocephaly on one side. On the other side a relation has been found between schizophrenia, deletions of chromosomes and microcephaly.

Microcoria is a congenital disease in which the pupils of the subject are narrower than 2mm in diameter. Microcoria is associated with juvenile-onset glaucoma.
It is also part of the known manifestations of a born infant to a mother suffering from uncontrolled hyperglycemia. Other symptoms include transposition of great vessels, respiratory distress secondary to surfactant defect, sacral agensis, jitteriness, irritability, and lethargy due to rebound fetal hypoglycemia.

Migraine is a debilitating condition characterized by moderate to severe headaches, and nausea, about 3 times more common in women than in men. The typical migraine headache is unilateral pain (affecting one half of the head) and pulsating in nature, lasting from 4 to 72 hours; symptoms include nausea, vomiting, photophobia (increased sensitivity to light), phonophobia (increased sensitivity to sound); the symptoms are generally aggravated by routine activity. Approximately one-third of people who suffer from migraine headaches perceive an aura—unusual visual, olfactory, or other sensory experiences that are a sign that the migraine will soon occur.
Initial treatment is with analgesics for the headache, an antiemetic for the nausea, and the avoidance of triggering conditions. The cause of migraine headache is unknown; the most common theory is a disorder of the serotonergic control system. Studies of twins indicate a 60 to 65 percent genetic influence upon their propensity to develop migraine headache. Moreover, fluctuating hormone levels indicate a migraine relation: 75 percent of adult patients are women, although migraine affects approximately equal numbers of prepubescent boys and girls; propensity to migraine headache is known to disappear during pregnancy, although in some women migraines may become more frequent during pregnancy.

Moyamoya syndrome is a disease in which certain arteries in the brain are constricted. Blood flow is blocked by the constriction, and also by blood clots (thrombosis). The blood vessels develop collateral circulation around the blocked vessels to compensate for the blockage, but the collateral vessels are small, weak, and prone to hemorrhage, aneurysm and thrombosis. On X-rays, these collateral vessels have the appearance of a “puff of smoke” (“moyamoya” in Japanese).
The disease causes constrictions primarily in the internal carotid artery, which travels from the neck up inside the skull just under the brain in the cavernous sinus. At the Circle of Willis, the internal carotid artery flows into the middle cerebral artery, which continues into the brain, and the anterior cerebral artery, which is part of the Circle of Willis. Moyamoya disease often extends to the middle and anterior cerebral arteries.
When the internal carotid artery becomes completely blocked, the fine collateral circulation that it supplies is obliterated. Patients often survive on the collateral circulation from the back (posterior) of the Circle of Willis, from the basilar artery. Drugs such as antiplatelet agents (e.g., aspirin) are usually given to prevent clots, but surgery is usually recommended. Since moyamoya tends to affect only the internal carotid artery and nearby sections of the adjacent anterior and middle cerebral arteries, surgeons can direct other arteries, such as the external carotid artery or the superficial temporal artery to replace its circulation. The arteries are either sewn directly into the brain circulation, or placed on the surface of the brain to reestablish new circulation after a few weeks. Although there is a 4% risk of stroke soon (30 days) after surgery, there is a 96% probability of remaining stroke-free over the next 5 years.

Myeloperoxidase deficiency is a common genetic disorder featuring deficiency, either in quantity or function, of myeloperoxidase, an enzyme found in certain phagocytic immune cells, especially polymorphonuclear leukocytes. It can appear similar to chronic granulomatous disease on some screening tests. Although MPO deficiency classically presents with immune deficiency (especially candida albicans infections), the majority of individuals with MPO deficiency show no signs of immunodeficiency.
The lack of severe symptoms suggest that role of myeloperoxidase in the immune response must be redundant to other mechanisms of intracellular killing of phagocytosed bacteria. Patients with MPO deficiency have a respiratory burst with a normal NBT dye test because they still have NADPH oxidase activity, but do not form bleach due to their lack of myeloperoxidase activity. This is in contrast to chronic granulomatous disease in which the NBT test is negative due to the lack of NADPH oxidase activity.

Mucopolysaccharidoses are a group of metabolic disorders caused by the absence or malfunctioning of lysosomal enzymes needed to break down molecules called glycosaminoglycans – long chains of sugar carbohydrates in each of our cells that help build bone, cartilage, tendons, corneas, skin and connective tissue. Glycosaminoglycans (formerly called mucopolysaccharides) are also found in the fluid that lubricates our joints.
People with a mucopolysaccharidosis disease either do not produce enough of one of the 11 enzymes required to break down these sugar chains into simpler molecules, or they produce enzymes that do not work properly. Over time, these glycosaminoglycans collect in the cells, blood and connective tissues. The result is permanent, progressive cellular damage which affects appearance, physical abilities, organ and system functioning, and, in most cases, mental development.
The mucopolysaccharidoses are part of the lysosomal storage disease family, a group of more than 40 genetic disorders that result when a specific organelle in our body’s cells – the lysosome – malfunctions. The lysosome is commonly referred to as the cell’s recycling center because it processes unwanted material into substances that the cell can utilize. Lysosomes break down this unwanted matter via enzymes, highly specialized proteins essential for survival. Lysosomal disorders like mucopolysaccharidosis are triggered when a particular enzyme exists in too small an amount or is missing altogether.

Mucormycosis is the term used to describe fungal infections caused by fungi in the order Mucorales, and mucor, rhizopus, absidia, and cunninghamella species are most frequently implicated.
“Mucormycosis” and Zygomycosis are sometimes used interchangeably. However, zygomycota has been identified as polyphyletic, and is not included in modern fungal classification systems. Mucormycosis frequently involves the sinuses, brain, or lungs as the areas of infection. While oral or cerebral mucormycosis are the most common types of the disease, this infection can also manifest in the gastrointestinal tract, skin, and in other organ systems. In rare cases, the maxilla may be affected by mucormycosis. The rich vascularity of maxillofacial areas usually prevents fungal infections, although more prevalent fungi, such as those responsible for mucormycosis, can often overcome this difficulty.

Multiple sclerosis is an inflammatory disease in which the fatty myelin sheaths around the axons of the brain and spinal cord are damaged, leading to demyelination and scarring as well as a broad spectrum of signs and symptoms. Disease onset usually occurs in young adults, and it is more common in women. It has a prevalence that ranges between 2 and 150 per 100,000. MS was first described in 1868 by Jean-Martin Charcot. MS affects the ability of nerve cells in the brain and spinal cord to communicate with each other. Nerve cells communicate by sending electrical signals called action potentials down long fibers called axons, which are wrapped in an insulating substance called myelin. In MS, the body’s own immune system attacks and damages the myelin. When myelin is lost, the axons can no longer effectively conduct signals. The name multiple sclerosis refers to scars (scleroses—better known as plaques or lesions) particularly in the white matter of the brain and spinal cord, which is mainly composed of myelin. Although much is known about the mechanisms involved in the disease process, the cause remains unknown. Theories include genetics or infections. Different environmental risk factors have also been found.
Almost any neurological symptom can appear with the disease, and often progresses to physical and cognitive disability. MS takes several forms, with new symptoms occurring either in discrete attacks (relapsing forms) or slowly accumulating over time (progressive forms). Between attacks, symptoms may go away completely, but permanent neurological problems often occur, especially as the disease advances.
There is no known cure for multiple sclerosis. Treatments attempt to return function after an attack, prevent new attacks, and prevent disability. MS medications can have adverse effects or be poorly tolerated, and many patients pursue alternative treatments, despite the lack of supporting scientific study. The prognosis is difficult to predict; it depends on the subtype of the disease, the individual patient’s disease characteristics, the initial symptoms and the degree of disability the person experiences as time advances. Life expectancy of patients is 5 to 10 years lower than that of the unaffected population.

Mumps (epidemic parotitis) is a viral disease of the human species, caused by the mumps virus. Before the development of vaccination and the introduction of a vaccine, it was a common childhood disease worldwide. It is still a significant threat to health in the third world, and outbreaks still occur sporadically in developed countries.
Painful swelling of the salivary glands (classically the parotid gland) is the most typical presentation. Painful testicular swelling (orchitis) and rash may also occur. The symptoms are generally not severe in children. In teenage males and men, complications such as infertility or subfertility are more common, although still rare in absolute terms. The disease is generally self-limited, running its course before receding, with no specific treatment apart from controlling the symptoms with pain medication.

Muscular dystrophy (abbreviated MD) refers to a group of hereditary muscle diseases that weakens the muscles that move the human body. Muscular dystrophies are characterized by progressive skeletal muscle weakness, defects in muscle proteins, and the death of muscle cells and tissue. Nine diseases including Duchenne, Becker, limb girdle, congenital, facioscapulohumeral, myotonic, oculopharyngeal, distal, and Emery-Dreifuss are always classified as muscular dystrophy but there are more than 100 diseases in total with similarities to muscular dystrophy. Most types of MD are multi-system disorders with manifestations in body systems including the heart, gastrointestinal and nervous systems, endocrine glands, skin, eyes and even brain. The condition may also lead to mood swings and learning difficulties.
In the 1860s, descriptions of boys who grew progressively weaker, lost the ability to walk, and died at an early age became more prominent in medical journals. In the following decade, French neurologist Guillaume Duchenne gave a comprehensive account of 13 boys with the most common and severe form of the disease (which now carries his name — Duchenne muscular dystrophy). It soon became evident that the disease had more than one form, and that these diseases affected males of all ages.

Myocarditis is inflammation of heart muscle (myocardium). It resembles a heart attack but coronary arteries are not blocked. Myocarditis is most often due to infection by common viruses, such as parvovirus B19, less commonly non-viral pathogens such as Borrelia burgdorferi (Lyme disease) or Trypanosoma cruzi, or as a hypersensitivity response to drugs. The definition of myocarditis varies, but the central feature is an infection of the heart, with an inflammatory infiltrate, and damage to the heart muscle, without the blockage of coronary arteries that define a heart attack (myocardial infarction) or other common non-infectious causes. Myocarditis may or may not include death (necrosis) of heart tissue. It may include dilated cardiomyopathy.
It is often an autoimmune reaction. Streptococcal M protein and coxsackievirus B have regions (epitopes) that are immunologically similar to cardiac myosin. After the virus is gone, the immune system may attack cardiac myosin.
Because a definitive diagnosis requires a heart biopsy, which doctors are reluctant to do because they are invasive, statistics on the incidence of myocarditis vary widely. The consequences of myocarditis thus also vary widely. It can cause a mild disease without any symptoms that resolves itself, or it may cause chest pain, heart failure, or sudden death. An acute myocardial infarction-like syndrome with normal coronary arteries has a good prognosis. Heart failure, even with dilated left ventricle, may have a good prognosis. Ventricular arrhythmias and high-degree heart block have a poor prognosis. Loss of right ventricular function is a strong predictor of death.

Myopia is a refractive defect of the eye in which collimated light produces image focus in front of the retina when accommodation is relaxed. Eye care professionals most commonly correct myopia through the use of corrective lenses, such as glasses or contact lenses. It may also be corrected by refractive surgery, but this does have many risks and side effects. The corrective lenses have a negative optical power (i.e. are concave) which compensates for the excessive positive diopters of the myopic eye.
Myopia presents with blurry distance vision but generally gives good near vision. In High myopia, even near vision is affected and patients cannot read without their glasses for distance.
A diagnosis of myopia is typically confirmed during an eye examination by an ophthalmologist, optometrist or orthoptist. Frequently an autorefractor or retinoscope is used to give an initial objective assessment of the refractive status of each eye, then a phoropter is used to subjectively refine the patient’s eyeglass prescription.
The National Institutes of Health says that there is no known way of preventing myopia, and the use of glasses or contact lenses does not affect the progression of myopia. There is no universally accepted method of preventing myopia. Commonly attempted preventative methods include wearing reading glasses, eye drops and participating in more outdoor activities are described below. Some clinicians and researchers recommend plus power (convex) lenses in the form of reading glasses when engaged in close work or reading instead of using single focal concave lens glasses commonly prescribed. The reasoning behind a convex lens’s possible effectiveness in preventing myopia is simple to understand: Convex lenses’ refractive property of converging light are used in reading glasses to help reduce the accommodation needed when reading and doing close work. Although accommodation is irrelevant in Medina’s quantitative model of myopia, it reaches the same conclusion. The model teaches a very simple method to prevent myopia.

Myopathy is a muscular disease in which the muscle fibers do not function for any one of many reasons, resulting in muscular weakness. “Myopathy” simply means muscle disease. This meaning implies that the primary defect is within the muscle, as opposed to the nerves (“neuropathies” or “neurogenic” disorders) or elsewhere (e.g., the brain etc.). Muscle cramps, stiffness, and spasm can also be associated with myopathy. Muscular disease can be classified as neuromuscular or musculoskeletal in nature. Some conditions, such as myositis, can be considered both neuromuscular and musculoskeletal.

Myositis is a general term for inflammation of the muscles. Many such conditions are considered likely to be caused by autoimmune conditions, rather than directly due to infection (although autoimmune conditions can be activated or exacerbated by infections.) It is also a documented side effect of the lipid-lowering drugs statins and fibrates. Elevation of creatine kinase in blood is indicative of myositis.

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