Kyphosis (Greek – kyphos, a hump) also called “hunch back” or “hunchbackism” or “hunchbackedness”, in general terms, is a common condition of a curvature of the upper (thoracic) spine. It can be either the result of bad posture (slouching) or a structural, muscular abnormality in the spine.

In the sense of a deformity, it is the pathological curving of the spine, where parts of the spinal column lose some or all of their lordotic profile. This causes a bowing of the back, seen as a slouching back and breathing difficulties. Severe cases can cause great discomfort and even lead to death.

There are several kinds of kyphosis (ICD-10 codes are provided):

Body braces showed benefit in a randomized controlled trial.[7]

The Milwaukee brace is one particular body brace that is often used to treat kyphosis.

Surgical treatment can be used in severe cases. In patients with progressive kyphotic deformity due to vertebral collapse, a procedure called a kyphoplasty may arrest the deformity and relieve the pain. The procedure is serious and consists of fusion of the abnormal vertebrae[8].

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Kwashiorkor is a type of malnutrition with controversial causes, but it is commonly believed to be caused by insufficient protein consumption. It usually affects children aged 1–4 years, although it also occurs in older children and adults. Jamaican pediatrician Cicely D. Williams introduced the name into international scientific circles in her 1935 Lancet article[1][2]. When a child is nursing, it receives certain amino acids vital to growth from its mother’s milk. When the child is weaned, if the diet that replaces the milk is high in starches and carbohydrates, and deficient in protein (as is common in parts of the world where the bulk of the diet consists of starchy vegetables, or where famine has struck), the child may develop kwashiorkor.

The name is derived from one of the languages of coastal Ghana, translated literally “first-second”, and means “rejected one”, reflecting the development of the condition in the older child who has been weaned from the breast, often as the result of the birth of a sibling.

Symptoms of kwashiorkor include a swollen abdomen known as a pot belly, as well as alternating bands of pale and dark hair (flag sign) and weight loss. Common skin symptoms include dermatitis and depigmented skin.

The swollen abdomen is generally attributed to two causes: First, the appearance of ascites due to increased capillary permeability from the increased production of cysteinyl leukotrienes (LTC4 and LTE4) as a result of generalized intracellular deficiency of glutathione. Tolga is thought to be attributed to the effect of malnutrition on reducing plasma proteins (discussed below), resulting in a reduced oncotic pressure and therefore increased osmotic flux through the capillary wall. A second cause may be due to a grossly enlarged liver due to fatty liver. This fatty change occurs because of the lack of apolipoproteins which transport lipids(cholesterol) from the liver to tissues throughout the body.

Victims of kwashiorkor fail to produce antibodies following vaccination against diseases, including diphtheria and typhoid.[3] Generally, the disease can be treated by adding food energy and protein to the diet; however, it can have a long-term impact on a child’s physical and mental development, and in severe cases may lead to death. It also has been known to cause loss of teeth

There are various explanations for the development of kwashiorkor, and the topic remains controversial[4]. It is now accepted that protein deficiency, in combination with energy and micronutrient deficiency, is certainly important, but may not be the key factor[citation needed]. The condition is likely due to deficiency of one of several types of nutrients (e.g., iron, folic acid, iodine, selenium, vitamin C), particularly those involved with anti-oxidant protection. Important anti-oxidants in the body that are reduced in children with kwashiorkor include glutathione, albumin, vitamin E and polyunsaturated fatty acids. Therefore, if a child with reduced type one nutrients or anti-oxidants is exposed to stress (e.g. an infection or toxin) he/she is more liable to develop kwashiorkor.

Ignorance of nutrition can be a cause. Dr. Latham, director of the Program in International Nutrition at Cornell University cited a case where parents who fed their child cassava failed to recognize malnutrition because of the edema caused by the syndrome and insisted the child was well-nourished despite the lack of dietary protein.

One important factor in the development of kwashiorkor is aflatoxin poisoning. Aflatoxins are produced by molds and ingested with moldy foods. They are toxified by the cytochrome P450 system in the liver, the resulting epoxides damage liver DNA. Since many serum proteins, in particular albumin, are produced in the liver, the symptoms of kwashiorkor are easily explained. It is noteworthy that kwashiorkor occurs mostly in warm humid climates that encourage mold growth, in dry climates marasmus is the more frequent disease associated with malnutrition. This has important consequences for treatment of the patients: Protein should be supplied only for anabolic purposes, the catabolic needs should be satisfied with carbohydrate and fat. Protein catabolism involves the urea cycle, which is located in the liver and can easily overwhelm the capacity of an already damaged organ. The resulting liver failure can be fatal.

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Korsakoff’s syndrome (Korsakoff’s psychosis, amnesic-confabulatory syndrome; sometimes incorrectly spelled “Korsakov’s Syndrome”), is a brain disorder caused by the lack of thiamine (vitamin B1) in the brain. The syndrome is named after Sergei Korsakoff, the neuropsychiatrist who popularized the theory.

There are six major symptoms of Korsakoff’s syndrome:

These symptoms are caused by a deficiency of thiamine (vitamin B1), which is thought to cause damage to the medial thalamus and possibly to the mammillary bodies of the hypothalamus as well as generalized cerebral atrophy.[1]

When Wernicke’s encephalopathy accompanies Korsakoff’s syndrome, the combination is called the Wernicke-Korsakoff syndrome. Korsakoff’s is a continuum of Wernicke’s encephalopathy, though a recognised episode of Wernicke’s is not always obvious.

Korsakoff’s involves neuronal loss, that is, damage to neurons; gliosis which is a result of damage to supporting cells of the central nervous system; and hemorrhage or bleeding in mammillary bodies. Damage to the dorsomedial nucleus of the thalamus is also associated with this disorder.

It was once assumed that anyone suffering from Korsakoff’s syndrome would eventually need full time care. This is still often the case, but rehabilitation can help regaining some, often limited, level of independence.[2] [3] Treatment involves the replacement or supplementation of thiamine by intravenous (IV) or intramuscular (IM) injection, together with proper nutrition and hydration. However, the amnesia and brain damage caused by the disease does not always respond to thiamine replacement therapy. In some cases, drug therapy is recommended. If treatment is successful, improvement will become apparent within two years although recovery is slow and often incomplete.

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Köhler disease (also spelled “Kohler”) is a rare bone disorder of the foot found in children between six and nine years of age. It was first described in 1908 by Alban Köhler (1874-1947), a German radiologist. [1][2]

It is caused when the navicular bone temporarily loses its blood supply. As a result, tissue in the bone dies and the bone collapses. When treated, it causes no long term problems. As the navicular bone gets back to normal, symptoms typically abate.

Sufferers experience pain and swelling in the middle part of the foot and usually limp as a result. The disease typically affects boys, but it can also affect girls. Five is the age of boys most often affected and patients often complain of pain over the apex. X-ray of both feet is used to diagnose disease. The affected foot has dense flattened navicular bone.

Although no definitive cause has been found yet, the disease may be due to strain on a weak navicular bone.

The patient is often fit with a cast that stops below the knee. Moderate exercise is often beneficial.

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Klumpke’s paralysis or Klumpke’s palsy or Dejerine-Klumpke palsy is palsy of the brachial plexus.

A form of brachial plexus injury in which there is paralysis of the muscles of the forearm and hand due to a childbirth injury to the roots of eighth cervical C8 and first thoracic T1 nerves or the lower part of the brachial plexus, a network of spinal nerves that originates in the back of the neck, extends through the axilla (armpit), and gives rise to nerves to the upper limb.[1][2]

The risk is greater when the mother is small or when the infant is of large weight.

The most common aetiological mechanism is caused by a traumatic vaginal delivery, necessitated by shoulder dystocia.

Symptoms include paralysis of intrinsic hand muscles, and ulnar nerve distribution numbness. Involvement of T1 may result in Horner’s syndrome. It can be contrasted to Erb-Duchenne’s palsy, which affects C5 and C6.

Klumpke Palsy is listed as a ‘rare disease’ by the Office of Rare Diseases (ORD) of the National Institutes of Health (NIH). This means that Klumpke Palsy, or a subtype of Klumpke Palsy, affects fewer than 200,000 people in the US population.

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Klippel-Trénaunay-Weber Syndrome or KTS is a congenital medical condition in which blood vessels and/or lymph vessels fail to form properly.

There exists some controversy over the terminology.

Although the cause and processes surrounding Klippel-Trenaunay Syndrome (KTS) are poorly understood, the birth defect is diagnosed by the presence of a combination of these symptoms (often on approximately ¼th of the body, though some cases may present more of less affected tissue):

Note: In some cases, patients may present without port-wine stains. Such cases are very rare and may be classified as atypical Klippel-Trenaunay Syndrome.

Note that KTS can either affect blood vessels, lymph vessels, or both. The condition most commonly presents with a mixture of the two. Those with veinous involvements are subject to an overall harder lifestyle due to the increased pain and complications.

The birth defect affects men and women equally, and is not limited to any racial group. It not certain if it is genetic in nature, although testing is ongoing.[7] There is some evidence that it may be associated with a translocation at t(8;14)(q22.3;q13).[8] Some researchers have suggested VG5Q has an association.[9]

KTS is a complex syndrome, and no single treatment is applicable for everyone. Treatment is decided on a case-by-case basis with the individual’s doctors.

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Klippel-Feil syndrome is a rare disorder, initially reported in 1912 by Maurice Klippel and Andre Feil from France,[1] characterized by the congenital fusion of any 2 of the 7 cervical vertebrae.

[2] Autosomal dominant inheritance is especially associated with C2-C3 fusion. Autosomal recessive inheritance is especially associated with C5-C6 fusion

It is caused by a failure in the normal segmentation or division of the cervical vertebrae during the early weeks of fetal development.

The most common signs of the disorder are a short neck, low hairline at the back of the head, and restricted mobility of the upper spine.

Associated abnormalities may include:

The disorder also may be associated with abnormalities of:

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Klinefelter’s syndrome, 47,XXY or XXY syndrome is a condition caused by a chromosome aneuploidy. Affected individuals have at least two X chromosomes and at least one Y chromosome.[1] Klinefelter’s syndrome is the most common sex chromosome disorder.[2]:549

The principal effects are development of small testicles and reduced fertility. A variety of other physical and behavioral differences and problems are common, though severity varies and many boys and men with the condition have few detectable symptoms. Named after Dr. Harry Klinefelter, an endocrinologist at Massachusetts General Hospital, Boston, Massachusetts, who first described it in 1942[3], it is the second most common disease involving the presence of an extra chromosome. The condition exists in roughly 1 out of every 500 males.[4] Because of the extra chromosome, individuals with the condition are usually referred to as “XXY Males”, or “47, XXY Males”.[5]

Affected males are almost always effectively infertile although advanced reproductive assistance is sometimes possible.[6] Some degree of language learning impairment may be present,[7] and neuropsychological testing often reveals deficits in executive functions.[8] In adults, possible characteristics vary widely and include little to no signs of affectedness, a lanky, youthful build and facial appearance, or a rounded body type with some degree of gynecomastia (increased breast tissue).[9] Gynecomastia is present to some extent in about a third of affected individuals, a slightly higher percentage than in the XY population, but only about 10% of XXY males’ gynecomastia is noticeable enough to require surgery.[10]

The term “hypogonadism” in XXY symptoms is often misinterpreted to mean “small testicles” or “small penis”. In fact, it means decreased testicular hormone/endocrine function. Because of this hypogonadism, patients will often have a low serum testosterone level but high serum follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels.[11] Despite this misunderstanding of the term, however, it is true that XXY men often also have “microorchidism” (i.e. small testicles).[11]

The more severe end of the spectrum of symptom expression is also associated with an increased risk of germ cell tumors, breast cancer,[12] and osteoporosis,[4] risks shared to varying degrees[13] with females. Additionally, medical literature shows some individual case studies of Klinefelter’s syndrome coexisting with other disorders, such as pulmonary disease, varicose veins, diabetes mellitus, and rheumatoid arthritis, but possible correlations between Klinefelter’s and these other conditions are not well characterized or understood.[citation needed]

In contrast to these potentially increased risks, it is currently thought that rare X-linked recessive conditions occur even less frequently in XXY males than in normal XY males, since these conditions are transmitted by genes on the X chromosome, and people with two X chromosomes are typically only carriers rather than affected by these X-linked recessive conditions.

There are many variances within the XXY population, just as in the most common 46,XY population. While it is possible to characterise 47,XXY males with certain body types, that in itself should not be the method of identification as to whether or not someone has 47,XXY. The only reliable method of identification is karyotype testing.

A karyotype is used to confirm the diagnosis. In this procedure, a small blood sample is drawn. White blood cells are then separated from the sample, mixed with tissue culture medium, incubated, and checked for chromosomal abnormalities, such as an extra X chromosome.

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Kernicterus is damage to the brain centers of infants caused by increased levels of unconjugated-indirect bilirubin which is free (not bound to albumin). This may be due to several underlying pathologic processes. Newborn babies are often polycythemic, meaning they have too many red blood cells. When they break down the cells, one of the byproducts is bilirubin, which circulates in the blood and causes jaundice. Alternately, Rh incompatibility between mother and fetus may cause hemolysis of fetal red blood cells, thereby releasing unconjugated bilirubin into the fetal blood. Since the fetal blood brain barrier is not fully formed, some of this released bilirubin enters the brain and interferes with normal neuronal development. Kernicterus may also be found in infants as a symptom of Crigler-Najjar syndrome type I, a hereditary hyperbilirubinemia that is fatal within 18 months of life.

In adults and older children, jaundice is harmless in and of itself. However, the tissues protecting the brain (the blood-brain barrier) are immature in newborns. Bilirubin penetrates the brain and is deposited in the basal ganglia, causing irreversible damage. Depending on the level of exposure, the effects range from unnoticeable to severe brain damage.

Some medications, such as the antibiotic co-trimoxazole (a combination of trimethoprim/sulfamethoxazole) may induce this disorder in the baby, either when taken by the mother or given directly to the baby, due to displacement of bilirubin from binding sites on serum albumin. The bilirubin is then free to pass into the Central Nervous System, because the baby’s blood-brain barrier is not fully developed.

The word origantes from the German kern, nucleus, kernel, and the Greek ikterus, jaundice.[1]

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Keratosis pilaris (KP, also follicular keratosis) is a very common genetic follicular condition that is manifested by the appearance of rough bumps on the skin, hence referred to as chicken skin. It most often appears on the back and outer sides of the upper arms (though the lower arms can also be affected), and can also occur on the thighs and tops of legs, flanks, buttocks, or any body part except glabrous skin (like the palms or soles of feet).[1] Less commonly, lesions appear on the face, which may be mistaken for acne.[2]

There are several different types of keratosis pilaris, including keratosis pilaris rubra (red, inflamed bumps), alba (rough, bumpy skin with no irritation), rubra faciei (reddish rash on the cheeks), and related disorders.[3]

Keratosis pilaris occurs when the human body produces excess keratin, a natural protein in the skin. The excess keratin surrounds and entraps the hair follicles in the pore. This causes the formation of hard plugs (process known as hyperkeratinization). The painless bumps are skin-colored, although they can become red and inflamed at times. Usually many plugs form in an area, causing patches of rough, bumpy skin. This gives the skin a sandpaper or goose flesh appearance.[4] This may be more severe in the winter or times of low humidity, which causes the skin to become dry. It will eventually resolve on its own.[5]

Many KP bumps contain an ingrown hair that has coiled. This is a result of the keratinized skin’s “capping off” the hair follicle, preventing the hair from exiting. The hair, then, grows inside the follicle, often encapsulated. The hair can be removed, much like an ingrown hair, though removal can lead to scarring.[6]

Keratosis pilaris may be hereditary. It is present in babies and continues into adulthood, but is uncommon in elderly people. It is most obvious during the teenage years. KP is prevalent in those who have atopic dermatitis, ichthyosis, or descend from Celtic backgrounds. Keratosis pilaris occurs in otherwise healthy people.[7]

There is no cure for Keratosis pilaris, but treatment is available. One option is to use a loofa to remove the dead, dry skin. Another option is to use a dermotologist-prescribed cream or lotion that should be applied daily. The best lotions for this condition would have urea, 15% alphahydroxy acids, or Retin A in them. Over-the-counter lotions work as well and should be applied after showering, as well as several times a day.[8] The lotions are often soothing and can help improve the appearance of the skin. [9] Dermotologists also recommend mild peeling agents, or alpha hydroxy acids, that may open up the plugged follicles. Antibiotics may also help in some cases where the bumps are red and badly inflamed.[10] To temporarily reduce redness but not roughness, pulse dye laser treatment or intense pulsed light (IPL) can be done.[11]

Although it may clear up with treatment, reccurance of KP is very likely. Therefore, treatment should be continued regularly. It may take several months to years for the condition to completely clear up.

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