Hypophysectomy, No ICD-10?

 

From Wikipedia, the free encyclopedia
Hypophysectomy
Intervention
ICD-9-CM 07.6
MeSH D007016

Hypophysectomy is the surgical removal of the hypophysis (pituitary gland). It is most commonly performed to treat tumors, especially craniopharyngioma tumors. [1] Sometimes it is used to treat Cushing’s syndrome due to pituitary adenoma. [2] It is also applied in neurosciences (in experiments with lab animals) to understand the functioning of hypophysis.

Medications that are given as hormone replacement therapy following a complete hypophysectomy (removal of the pituitary gland) are often glucocorticoids. Secondary Addison’s and hyperlipidemia can occur. Thyroid hormone is useful in controlling cholesterol metabolism that has been affected by pituitary deletion.[3]

Complications

Hypophysectomy performed at any age causes atrophy of the thyroid and adrenal glands as well as asthenia and cachexia. When the procedure is performed before sexual maturity, the reproductive tract remains undeveloped and non-functional. There is also a general lack of growth. If performed after sexual maturity, there will be a loss of reproductive function along with atrophy of gonads and accessory reproductive structures.

Your search for Hypophysectomy returned 15 results :
This code is a specific code that can be used to specify a diagnosis or procedure.

Postprocedural hypopituitarism
due to hypophysectomy E89.3 radiotherapy E89.3…
This code is a specific code that can be used to specify a diagnosis or procedure.

Constitutional tall stature
Constitutional gigantism · Gigantism (cerebral) (hypophyseal) (pituitary) E22.0 constitutional E34.4 Tall stature, constitutional E34.4…
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Malignant neoplasm of aryepiglottic fold, hypopharyngeal aspect
This code is a specific code that can be used to specify a diagnosis or procedure.

Acromegaly and pituitary gigantism
Gigantism (cerebral) (hypophyseal) (pituitary) E22.0 Hypersecretion hormone (s) growth E22.0 Hypophyseal, hypophysis – see also condition
This code is a specific code that can be used to specify a diagnosis or procedure.

Other disorders of pituitary gland
craniopharyngeal pouch E23.6 hypophysis, hypophyseal (duct) (recurrent) E23.6 cerebri…, infarction hypophysis (anterior lobe) E23.6 pituitary (gland) E23.6
This code is a non-specific code that cannot be used to specify a diagnosis or procedure. A child code underneath this code will provide greater detail.

Malignant neoplasm of hypopharynx
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Malignant neoplasm of hypopharynx, unspecified
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Benign neoplasm of hypopharynx
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Hypopituitarism
Hypogonadism hypogonadotropic E23.0 pituitary E23.0 Hypophyseal, hypophysis… R64 hypophyseal E23.0 hypopituitary E23.0 pituitary E23.0… pituitary E23.0 Dwarfism E34.3 hypophyseal E23.0 Lorain (-Levi… gland. It is also known as type i pituitary dwarfism. Human hypophysial dwarf is caused
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Occlusion and stenosis of other cerebral arteries
Occlusion and stenosis of perforating arteries · Anterior choroidal artery thrombosis · Pontine artery thrombosis · Thrombosis of anterior choroidal artery · Thrombosis of pontine artery · Thrombosis of posterior communicating artery · Thrombosis, anterior choroidal artery · Thrombosis, pontine artery · Thrombosis, posterior communicating artery · Embolism (multiple) (paradoxical) I74.9 meninges I66.8 artery I74.9 choroidal (anterior) I66.8 communicating posterior I66.8 hypophyseal I66.8 pontine I66.8 Occlusion, occluded artery – see also Embolism, artery I74.9 cerebral I66.9 specified NEC I66.8 Thrombosis, thrombotic (bland) (multiple) (progressive) (silent) (vessel) I82.90 meninges (brain) (arterial) I66.8
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Malignant neoplasm of posterior wall of hypopharynx
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Malignant neoplasm of overlapping sites of hypopharynx
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Congenital malformations of other endocrine glands
endocrine gland NEC Q89.2 hypophyseal Q89.2 parathyroid gland Q89.2… hypophyseal (congenital) Q89.2 parathyroid (gland) Q89.2 pituitary

Gout

Gout

From Wikipedia, the free encyclopedia
“Podagra” redirects here. For the moth genus, see Podagra (moth).
Gout
Classification and external resources
A small fierce creature with sharp teeth is biting into a swollen foot at the base of the big toe

The Gout (James Gillray, 1799) depicts the pain of the artist’s gout as a demon or dragon.[1][2]
ICD10 M10
ICD9 274.00 274.1 274.8 274.9
OMIM 138900 300323
DiseasesDB 29031
MedlinePlus 000422
eMedicine emerg/221 med/924 med/1112 oph/506 orthoped/124 radio/313
MeSH D006073

Gout (also known as podagra when it involves the big toe)[3] is a medical condition usually characterized by recurrent attacks of acute inflammatory arthritis—a red, tender, hot, swollen joint. The metatarsal-phalangeal joint at the base of the big toe is the most commonly affected (approximately 50% of cases). However, it may also present as tophi, kidney stones, or urate nephropathy. It is caused by elevated levels of uric acid in the blood. The uric acid crystallizes, and the crystals deposit in joints, tendons, and surrounding tissues.

Clinical diagnosis may be confirmed by seeing the characteristic crystals in joint fluid. Treatment with nonsteroidal anti-inflammatory drugs (NSAIDs), steroids, or colchicine improves symptoms. Once the acute attack subsides, levels of uric acid are usually lowered via lifestyle changes, and in those with frequent attacks, allopurinol or probenecid provide long-term prevention.

Gout has become more common in recent decades, affecting about 1–2% of the Western population at some point in their lives. The increase is believed due to increasing risk factors in the population, such as metabolic syndrome, longer life expectancy and changes in diet. Gout was historically known as “the disease of kings” or “rich man’s disease.”

Signs and symptoms

side view of a foot showing a red patch of skin over the joint at the base of the big toe

Gout presenting in the metatarsal-phalangeal joint of the big toe: Note the slight redness of the skin overlying the joint.

Gout can present in a number of ways, although the most usual is a recurrent attack of acute inflammatory arthritis (a red, tender, hot, swollen joint).[4] The metatarsal-phalangeal joint at the base of the big toe is affected most often, accounting for half of cases.[5] Other joints, such as the heels, knees, wrists and fingers, may also be affected.[5] Joint pain usually begins over 2–4 hours and during the night.[5] The reason for onset at night is due to the lower body temperature then.[3] Other symptoms may rarely occur along with the joint pain, including fatigue and a high fever.[3][5]

Long-standing elevated uric acid levels (hyperuricemia) may result in other symptomatology, including hard, painless deposits of uric acid crystals known as tophi. Extensive tophi may lead to chronic arthritis due to bone erosion.[6] Elevated levels of uric acid may also lead to crystals precipitating in the kidneys, resulting in stone formation and subsequent urate nephropathy.[7]

Cause

High levels of uric acid in the blood (hyperuricemia) is the underlying cause of gout. This can occur for a number of reasons, including diet, genetic predisposition, or underexcretion of urate, the salts of uric acid.[4] Underexcretion of uric acid by the kidney is the primary cause of hyperuricemia in about 90% of cases, while overproduction is the cause in less than 10%.[8] About 10% of people with hyperuricemia develop gout at some point in their lifetimes.[9] The risk, however, varies depending on the degree of hyperuricemia. When levels are between 415 and 530 μmol/l (7 and 8.9 mg/dl), the risk is 0.5% per year, while in those with a level greater than 535 μmol/l (9 mg/dL), the risk is 4.5% per year.[3]

Lifestyle

Dietary causes account for about 12% of gout,[4] and include a strong association with the consumption of alcohol, fructose-sweetened drinks, meat, and seafood.[6][10] Other triggers include physical trauma and surgery.[8] Studies in the early 2000s have found that other dietary factors once believed associated are, in fact, not, including the intake of purine-rich vegetables (e.g., beans, peas, lentils, and spinach) and total protein.[11][12] With respect to risks related to alcohol, beer and spirits appear to have a greater risk than wine.[13]

The consumption of coffee, vitamin C and dairy products, as well as physical fitness, appear to decrease the risk.[14][15][16] This is believed partly due to their effect in reducing insulin resistance.[16]

Genetics

The occurrence of gout is partly genetic, contributing to about 60% of variability in uric acid level.[8] Three genes called SLC2A9, SLC22A12 and ABCG2 have been found commonly to be associated with gout, and variations in them can approximately double the risk.[17][18] Loss-of-function mutations in SLC2A9 and SLC22A12 cause hereditary hypouricaemia by reducing urate absorption and unopposed urate secretion.[18] A few rare genetic disorders, including familial juvenile hyperuricemic nephropathy, medullary cystic kidney disease, phosphoribosylpyrophosphate synthetase superactivity, and hypoxanthine-guanine phosphoribosyltransferase deficiency as seen in Lesch-Nyhan syndrome, are complicated by gout.[8]

Medical conditions

Gout frequently occurs in combination with other medical problems. Metabolic syndrome, a combination of abdominal obesity, hypertension, insulin resistance and abnormal lipid levels, occurs in nearly 75% of cases.[5] Other conditions commonly complicated by gout include: polycythemia, lead poisoning, renal failure, hemolytic anemia, psoriasis, and solid organ transplants.[8][19] A body mass index greater than or equal to 35 increases a male’s risk of gout threefold.[12] Chronic lead exposure and lead-contaminated alcohol are risk factors for gout due to the harmful effect of lead on kidney function.[20] Lesch-Nyhan syndrome is often associated with gouty arthritis.

Medication

Diuretics have been associated with attacks of gout. However, a low dose of hydrochlorothiazide does not seem to increase the risk.[21] Other medicines that increase the risk include niacin and aspirin (acetylsalicylic acid).[6] The immunosuppressive drugs ciclosporin and tacrolimus are also associated with gout,[8] the former more so when used in combination with hydrochlorothiazide.[22]

Pathophysiology

Gout is a disorder of purine metabolism,[8] and occurs when its final metabolite, uric acid, crystallizes in the form of monosodium urate, precipitating in joints, on tendons, and in the surrounding tissues.[6] These crystals then trigger a local immune-mediated inflammatory reaction,[6] with one of the key proteins in the inflammatory cascade being interleukin 1β.[8] An evolutionary loss of uricase, which breaks down uric acid, in humans and higher primates has made this condition common.[8]

The triggers for precipitation of uric acid are not well understood. While it may crystallize at normal levels, it is more likely to do so as levels increase.[6][23] Other factors believed important in triggering an acute episode of arthritis include cool temperatures, rapid changes in uric acid levels, acidosis,[24][25] articular hydration, and extracellular matrix proteins, such as proteoglycans, collagens, and chondroitin sulfate.[8] The increased precipitation at low temperatures partly explains why the joints in the feet are most commonly affected.[4] Rapid changes in uric acid may occur due to a number of factors, including trauma, surgery, chemotherapy, diuretics, and stopping or starting allopurinol.[3] Calcium channel blockers and losartan are associated with a lower risk of gout as compared to other medications for hypertension.[26]

Diagnosis

Gout on X-rays of a left foot. The typical location is the big toe joint. Note also the soft tissue swelling at the lateral border of the foot.

numerous multi-colored needle-shaped crystals against a purple background

Spiked rods of uric acid crystals from a synovial fluid sample photographed under a microscope with polarized light. Formation of uric acid crystals in the joints is associated with gout.

Gout may be diagnosed and treated without further investigations in someone with hyperuricemia and the classic podagra. Synovial fluid analysis should be done, however, if the diagnosis is in doubt.[3] X-rays, while useful for identifying chronic gout, have little utility in acute attacks.[8]

Synovial fluid

A definitive diagnosis of gout is based upon the identification of monosodium urate crystals in synovial fluid or a tophus.[5] All synovial fluid samples obtained from undiagnosed inflamed joints should be examined for these crystals.[8] Under polarized light microscopy, they have a needle-like morphology and strong negative birefringence. This test is difficult to perform, and often requires a trained observer.[27] The fluid must also be examined relatively quickly after aspiration, as temperature and pH affect their solubility.[8]

Blood tests

Hyperuricemia is a classic feature of gout, but it occurs nearly half of the time without hyperuricemia, and most people with raised uric acid levels never develop gout.[5][28] Thus, the diagnostic utility of measuring uric acid level is limited.[5] Hyperuricemia is defined as a plasma urate level greater than 420 μmol/l (7.0 mg/dl) in males and 360 μmol/l (6.0 mg/dl) in females.[29] Other blood tests commonly performed are white blood cell count, electrolytes, renal function, and erythrocyte sedimentation rate (ESR). However, both the white blood cells and ESR may be elevated due to gout in the absence of infection.[30][31] A white blood cell count as high as 40.0×109/l (40,000/mm3) has been documented.[3]

Differential diagnosis

The most important differential diagnosis in gout is septic arthritis.[5][8] This should be considered in those with signs of infection or those who do not improve with treatment.[5] To help with diagnosis, a synovial fluid Gram stain and culture may be performed.[5] Other conditions that look similar include pseudogout and rheumatoid arthritis.[5] Gouty tophi, in particular when not located in a joint, can be mistaken for basal cell carcinoma,[32] or other neoplasms.[33]

Prevention

Both lifestyle changes and medications can decrease uric acid levels. Dietary and lifestyle choices that are effective include reducing intake of food such as meat and seafood, consuming adequate vitamin C, limiting alcohol and fructose consumption, and avoiding obesity.[4] A low-calorie diet in obese men decreased uric acid levels by 100 µmol/l (1.7 mg/dl).[21] Vitamin C intake of 1,500 mg per day decreases the risk of gout by 45%.[34] Coffee, but not tea, consumption is associated with a lower risk of gout.[35] Gout may be secondary to sleep apnea via the release of purines from oxygen-starved cells. Treatment of apnea can lessen the occurrence of attacks.[36]

Treatment

The initial aim of treatment is to settle the symptoms of an acute attack.[37] Repeated attacks can be prevented by different drugs used to reduce the serum uric acid levels.[37] Ice applied for 20 to 30 minutes several times a day decreases pain.[4][38] Options for acute treatment include nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine and steroids,[4] while options for prevention include allopurinol, febuxostat and probenecid. Lowering uric acid levels can cure the disease.[8] Treatment of comorbidities is also important.[8]

NSAIDs

NSAIDs are the usual first-line treatment for gout, and no specific agent is significantly more or less effective than any other.[4] Improvement may be seen within four hours, and treatment is recommended for one to two weeks.[4][8] They are not recommended, however, in those with certain other health problems, such as gastrointestinal bleeding, renal failure, or heart failure.[39] While indomethacin has historically been the most commonly used NSAID, an alternative, such as ibuprofen, may be preferred due to its better side effect profile in the absence of superior effectiveness.[21] For those at risk of gastric side effects from NSAIDs, an additional proton pump inhibitor may be given.[40]

Colchicine

Colchicine is an alternative for those unable to tolerate NSAIDs.[4] Its side effects (primarily gastrointestinal upset) limit its usage.[41] Gastrointestinal upset, however, depends on the dose, and the risk can be decreased by using a smaller yet still effective dose.[21] Colchicine may interact with other commonly prescribed drugs, such as atorvastatin and erythromycin, among others.[41]

Steroids

Glucocorticoids have been found as effective as NSAIDs[42] and may be used if contraindications exist for NSAIDs.[4] They also lead to improvement when injected into the joint; a joint infection must be excluded, however, as steroids worsens this condition.[4]

Pegloticase

Pegloticase (Krystexxa) was approved in the USA to treat gout in 2010.[43] It is an option for the 3% of people who are intolerant to other medications.[43] Pegloticase is administered as an intravenous infusion every two weeks,[43] and has been found to reduce uric acid levels in this population.[44]

Prophylaxis

A number of medications are useful for preventing further episodes of gout, including xanthine oxidase inhibitor (including allopurinol and febuxostat) and uricosurics (including probenecid and sulfinpyrazone). They are not usually started until one to two weeks after an acute flare has resolved, due to theoretical concerns of worsening the attack,[4] and are often used in combination with either an NSAID or colchicine for the first three to six months.[8] They are not recommended until a person has had two attacks of gout,[4] unless destructive joint changes, tophi, or urate nephropathy exist,[7] as medications have not been found cost-effective until this point.[4] Urate-lowering measures should be increased until serum uric acid levels are below 300–360 µmol/l (5.0–6.0 mg/dl), and are continued indefinitely.[4][8] If these medications are being used chronically at the time of an attack, discontinuation is recommended.[5] If levels cannot be brought below 6.0 mg/dl and there are recurrent attacks, this is deemed treatment failure or refractory gout.[45] Overall, probenecid appears less effective than allopurinol.[4]

Uricosuric medications are typically preferred if undersecretion of uric acid, as indicated by a 24-hour collection of urine results in a uric acid amount of less than 800 mg, is found.[46] They are, however, not recommended if a person has a history of kidney stones.[46] In a 24-hour urine excretion of more than 800 mg, which indicates overproduction, a xanthine oxidase inhibitor is preferred.[46]

Xanthine oxidase inhibitors (including allopurinol and febuxostat) block uric acid production, and long-term therapy is safe and well tolerated, and can be used in people with renal impairment or urate stones, although allopurinol has caused hypersensitivity in a small number of individuals.[4] In such cases, the alternative drug, febuxostat, has been recommended.[47]

Prognosis

Without treatment, an acute attack of gout usually resolves in five to seven days; however, 60% of people have a second attack within one year.[3] Those with gout are at increased risk of hypertension, diabetes mellitus, metabolic syndrome, and renal and cardiovascular disease, and thus are at increased risk of death.[8][48] This may be partly due to its association with insulin resistance and obesity, but some of the increased risk appears to be independent.[48]

Without treatment, episodes of acute gout may develop into chronic gout with destruction of joint surfaces, joint deformity, and painless tophi.[8] These tophi occur in 30% of those who are untreated for five years, often in the helix of the ear, over the olecranon processes, or on the Achilles tendons.[8] With aggressive treatment, they may dissolve. Kidney stones also frequently complicate gout, affecting between 10 and 40% of people, and occur due to low urine pH promoting the precipitation of uric acid.[8] Other forms of chronic renal dysfunction may occur.[8]

Epidemiology

Gout affects around 1–2% of the Western population at some point in their lifetimes, and is becoming more common.[4][8] Rates of gout have approximately doubled between 1990 and 2010.[6] This rise is believed due to increasing life expectancy, changes in diet, and an increase in diseases associated with gout, such as metabolic syndrome and high blood pressure.[12] A number of factors have been found to influence rates of gout, including age, race, and the season of the year. In men over the age of 30 and women over the age of 50, prevalence is 2%.[39]

In the United States, gout is twice as likely in African American males as it is in European Americans.[49] Rates are high among the peoples of the Pacific Islands and the Māori of New Zealand, but rare in Australian aborigines, despite a higher mean concentration of serum uric acid in the latter group.[50] It has become common in China, Polynesia, and urban sub-Saharan Africa.[8] Some studies have found attacks of gout occur more frequently in the spring. This has been attributed to seasonal changes in diet, alcohol consumption, physical activity, and temperature.[51]

History

A man wearing a long, curly wig and a full robe is sitting, looking out. His left arm rests on a small table, with his left hand holding a box. Behind him is a globe.

Antonie van Leeuwenhoek described the microscopic appearance of uric acid crystals in 1679.[52]

The word “gout” was initially used by Randolphus of Bocking, around 1200 AD. It is derived from the Latin word gutta, meaning “a drop” (of liquid).[52] According to the Oxford English Dictionary, this is derived from humorism and “the notion of the ‘dropping’ of a morbid material from the blood in and around the joints”.[53]

Gout has, however, been known since antiquity. Historically, it has been referred to as “the king of diseases and the disease of kings”[8][54] or “rich man’s disease”.[55] The first documentation of the disease is from Egypt in 2,600 BC in a description of arthritis of the big toe. The Greek physician Hippocrates around 400 BC commented on it in his Aphorisms, noting its absence in eunuchs and premenopausal women.[52][56] Aulus Cornelius Celsus (30 AD) described the linkage with alcohol, later onset in women, and associated kidney problems:

Again thick urine, the sediment from which is white, indicates that pain and disease are to be apprehended in the region of joints or viscera… Joint troubles in the hands and feet are very frequent and persistent, such as occur in cases of podagra and cheiragra. These seldom attack eunuchs or boys before coition with a woman, or women except those in whom the menses have become suppressed… some have obtained lifelong security by refraining from wine, mead and venery.[57]

In 1683, Thomas Sydenham, an English physician, described its occurrence in the early hours of the morning, and its predilection for older males:

Gouty patients are, generally, either old men, or men who have so worn themselves out in youth as to have brought on a premature old age—of such dissolute habits none being more common than the premature and excessive indulgence in venery, and the like exhausting passions. The victim goes to bed and sleeps in good health. About two o’clock in the morning he is awakened by a severe pain in the great toe; more rarely in the heel, ankle or instep. The pain is like that of a dislocation, and yet parts feel as if cold water were poured over them. Then follows chills and shivers, and a little fever… The night is passed in torture, sleeplessness, turning the part affected, and perpetual change of posture; the tossing about of body being as incessant as the pain of the tortured joint, and being worse as the fit comes on.[58]

The Dutch scientist Antonie van Leeuwenhoek first described the microscopic appearance of urate crystals in 1679.[52] In 1848, English physician Alfred Baring Garrod realized this excess uric acid in the blood was the cause of gout.[59]

Other animals

Cystinosis

Cystinosis

From Wikipedia, the free encyclopedia
Cystinosis
Classification and external resources
Cystine-skeletal.png

Chemical structure of cystine formed from L-cysteine (under biological conditions)
ICD10 E72.0
ICD9 270.0
DiseasesDB 3382
eMedicine ped/538
MeSH D003554

Cystinosis is a lysosomal storage disease characterized by the abnormal accumulation of the amino acid cystine.[1] It is a genetic disorder that typically follows an autosomal recessive inheritance pattern. Cystinosis is the most common cause of Fanconi syndrome in the pediatric age group. Fanconi syndrome occurs when the function of cells in renal tubules are impaired, leading to abnormal amounts of carbohydrates and amino acids in the urine, excessive urination, and low blood levels of potassium and phosphates.

Cystinosis was the first documented genetic disease belonging to the group of lysosomal-transport-defect disorders.[2] It is a rare autosomal recessive disorder resulting from accumulation of free cystine in lysosomes, eventually leading to intracellular crystal formation throughout the body. Cystinosis is caused by mutations in the CTNS gene that codes for cystinosin, the lysosomal membrane-specific transporter for cystine. Intracellular metabolism of cystine, as it happens with all amino acids, requires its transport across the cell membrane. After degradation of endocytosed protein to cystine within lysosomes, it is normally transported to the cytosol. But if there is a defect in the carrier protein, cystine is accumulated in lysosomes. As cystine is highly insoluble, when its concentration in tissue lysosomes increase, its solubility is immediately exceeded and crystalline precipitates are formed in almost all organs and tissues.[3]

However, the progression of the disease is not related to the presence of crystals in target tissues. Although tissue damage might depend on cystine accumulation, the mechanisms of tissue damage are not fully understood. Increased intracellular cystine profoundly disturbs cellular oxidative metabolism and glutathione status,[4] leading to altered mitochondrial energy metabolism, autophagy, and apoptosis.[5]

Cystinosis is usually treated with cysteamine, which is prescribed to decrease intralysosomal cystine accumulation.[6] However, the recent discovery of new pathogenic mechanisms and the development of an animal model of the disease may open possibilities for the development of new treatment modalities to improve long-term prognosis.[2]

Diagnosis

Cystinosis is a rare genetic disorder[7] that causes an accumulation of the amino acid cystine within cells, forming crystals that can build up and damage the cells. These crystals negatively affect many systems in the body, especially the kidneys and eyes.[1]

The accumulation is caused by abnormal transport of cystine from lysosomes, resulting in a massive intra-lysosomal cystine accumulation in tissues. Via an as yet unknown mechanism, lysosomal cystine appears to amplify and alter apoptosis in such a way that cells die inappropriately, leading to loss of renal epithelial cells. This results in renal Fanconi syndrome,[8] and similar loss in other tissues can account for the short stature, retinopathy, and other features of the disease.

Definitive diagnosis and treatment monitoring are most often performed through measurement of white blood cell cystine level using tandem mass spectrometry.

Symptoms

There (are) three distinct types of cystinosis each with slightly different symptoms: nephropathic cystinosis, intermediate cystinosis, and non-nephropathic or ocular cystinosis. Infants affected by nephropathic cystinosis initially exhibit poor growth and particular kidney problems (sometimes called renal Fanconi syndrome). The kidney problems lead to the loss of important minerals, salts, fluids, and other nutrients. The loss of nutrients not only impairs growth, but may result in soft, bowed bones (hypophosphatemic rickets), especially in the legs. The nutrient imbalances in the body lead to increased urination, thirst, dehydration, and abnormally acidic blood (acidosis).

Slit-lamp photographs of three-year-old patient with nephropathic cystenosis before (left) and after (right) cysteamine eyedrop therapy. The drops dissolve the crystals in the cornea.

By about age two, cystine crystals may also be present in the cornea. The buildup of these crystals in the eye causes an increased sensitivity to light (photophobia). Without treatment, children with cystinosis are likely to experience complete kidney failure by about age ten. Other signs and symptoms that may occur in untreated patients include muscle deterioration, blindness, inability to swallow, impaired sweating, decreased hair and skin pigmentation, diabetes, and thyroid and nervous system problems.

The signs and symptoms of intermediate cystinosis are the same as nephropathic cystinosis, but they occur at a later age. Intermediate cystinosis typically begins to affect individuals around age twelve to fifteen. Malfunctioning kidneys and corneal crystals are the main initial features of this disorder. If intermediate cystinosis is left untreated, complete kidney failure will occur, but usually not until the late teens to mid twenties.

People with non-nephropathic or ocular cystinosis do not usually experience growth impairment or kidney malfunction. The only symptom is photophobia due to cystine crystals in the cornea.

Research into cystinosis is currently being conducted at the University of California San Diego, University of Michigan, Tulane University School of Medicine, and the National Institutes of Health in Bethesda, Maryland, as well as at Robert Gordon University in Aberdeen, Scotland, University of Sunderland, UK, University College Dublin, Ireland, University College Cork, Ireland and the Necker Hospital in Paris.

Crystal morphology and identification

Cystine crystals are hexagonal in shape and are colorless. They are not found often in alkaline urine due to their high solubility. The colorless crystals can be difficult to distinguish from uric acid crystals which are also hexagonal. Under polarized examination, the crystals are birefringent with a polarization color interference.[9]

Genetics

Cystinosis has an autosomal recessive pattern of inheritance.

Cystinosis occurs due to a mutation in the gene CTNS, located on chromosome 17, which codes for cystinosin, the lysosomal cystine transporter. Symptoms are first seen at about 3 to 18 months of age with profound polyuria (excessive urination), followed by poor growth, photophobia, and ultimately kidney failure by age 6 years in the nephropathic form.

All forms of cystinosis (nephropathic, juvenile and ocular) are autosomal recessive, which means that the trait is located on an autosomal gene, and an individual who inherits two copies of the gene – one from both parents – will have the disorder. There is a 25% risk of having a child with the disorder, when both parents are carriers of an autosomal recessive trait.

Cystinosis affects approximately 1 in 100,000 to 200,000 newborns.[10] and there are only around 2,000 known individuals with cystinosis in the world. The incidence is higher in the province of Brittany, France, where the disorder affects 1 in 26,000 individuals.[11]

Treatment

Cystinosis is normally treated with a drug called cysteamine (brand name Cystagon).[12] The administration of cysteamine can reduce the intracellular cystine content. Cysteamine concentrates inside the lysosomes and reacts with cystine to form both cysteine and a cysteine-cysteamine complex, which are able to leave the lysosomes. When administered regularly, cysteamine decreases the amount of cystine stored in lysosomes and correlates with conservation of renal function and improved growth.[12] Cysteamine eyedrops remove the cystine crystals in the cornea that can cause photophobia if left unchecked. Patients with cystinosis are also often given sodium citrate to treat the blood acidosis, as well as potassium and phosphorus supplements. If the kidneys become significantly impaired or fail, then treatment must be begun to ensure continued survival, up to and including renal transplantation.

Cystaran, (cysteamine ophthalmic solution) 0.44%, was approved by the FDA in 2013 for the treatment of corneal cystine crystal accumulation in patients with cystinosis. Procysbi, an extended-release formulation of cysteamine, was approved by the FDA in 2013.[13]

Types

Cystinotic

Bronchitis

Bronchitis Nursing Care Plan

Bronchitis is inflammation of the mucous membranes of the bronchi, the airways that carry airflow from the trachea into the lungs. Bronchitis can be divided into two categories, acute and chronic, each of which has two distinct etiologies, pathologies, and therapies.

Acute bronchitis is characterized by the development of a cough, with or without the production of sputum, mucus that is expectorated (coughed up) from the respiratory tract. Acute bronchitis often occurs during the course of an acute viral illness such as the common cold or influenza. Viruses cause about 90% of cases of acute bronchitis, whereas bacteria account for fewer than 10%.

Chronic bronchitis, a type of chronic obstructive pulmonary disease, is characterized by the presence of a productive cough that lasts for three months or more per year for at least two years. Chronic bronchitis most often develops due to recurrent injury to the airways caused by inhaled irritants. Cigarette smoking is the most common cause, followed by air pollution and occupational exposure to irritants.

9 Nursing Diagnosis For Bronchitis

1. Ineffective airway clearance
related to: increased production of secretions.

2. Acute pain
related to: the inflammation of the pleura.

3. Impaired gas exchange
related to: airway obstruction by secretions, spasm of the bronchus.

Nursing Diagnosis : Impaired Gas Exchange

Goal: Demonstrate improved ventilation and adequate oxygenation of tissues with blood gas analysis in the normal range and free of symptoms of respiratory distress.

Nursing Interventions – Impaired Gas Exchange related to Bronchitis:

a. Assess the frequency, depth of breathing. Note the use of accessory muscles, mouth breathing, inability to speak / talk.
R / useful in the evaluation of the degree of respiratory distress and / or chronic disease process.

b. Elevate head of bed, help patients to choose a position that is easy to breathe. Encourage deep breath or breathing lips slowly as needed / individual tolerance.
R / oxygen delivery can be improved by a high seating position and breathing exercises to reduce airway collapse, dyspnea, and breath work.

c. Provide appropriate bronchodilator required. Can be administered orally, IV, rectal, or inhaled. Give oral bronchodilators or IV at the time interspersed with the action nebulizer, metered dose inhalers to extend the effectiveness of the drug. Observation of side effects: tachycardia, dysrhythmias, CNS excitation, nausea and vomiting.
R / Bronchodilators dilate the airway and helps fight the bronchial mucosal edema and muscular spasm. Because side effects can occur in this action, carefully adjusted doses for each patient, according to tolerance and clinical response.

d. Evaluate the effectiveness of the actions nebulizer, metered dose inhalers. Assess decrease shortness of breath, wheezing or crackles drop, looseness secretion, decreased anxiety. Make sure that the action is given before meals to prevent nausea and to reduce the fatigue that accompanies feeding activity.
R / Combining medication with a nebulizer aerosolized bronchodilator commonly used to control bronchoconstriction. Providing appropriate actions will reduce its effectiveness. Aerolisation ease bronchial clearance, help control the inflammatory process, and improve the function of ventilation.

e. Instruct and encourage the patient on diaphragmatic breathing and effective coughing.
R / techniques improve ventilation by opening the airway and clearing the airway of sputum. Improvement of gas exchange.

f. Provide supplemental oxygen in accordance with the indications of blood gas analysis results and patient tolerance.
R / can fix / prevent worsening hypoxia.

4. Ineffective breathing pattern
related to: bronchoconstriction, mucus.

5. Imbalanced Nutrition, Less Than Body Requirements
related to: dyspnoea, anorexia, nausea, vomiting.

6. Risk for infection
related to: the settlement of secretions, chronic disease processes.

7. Activity intolerance
related to: insufficiency of ventilation and oxygenation.

8. Anxiety
related to: changes in health status.

9. Knowledge Deficit
related to: the lack of information about the disease process and treatment at home.

Sample NCP for Bronchitis

bladder cancer

Displaying 1-20:
This code is a specific code that can be used to specify a diagnosis or procedure.

Malignant neoplasm of trigone of bladder
Bladder cancer, trigone · Cancer of the urinary bladder, trigone · Primary malignant neoplasm of trigone of urinary bladder
This code is a specific code that can be used to specify a diagnosis or procedure.

Malignant neoplasm of dome of bladder
Bladder cancer, apex · Cancer of the urinary bladder, apex · Primary malignant neoplasm of apex of urinary bladder · The upper, convex surface of the bladder….
This code is a specific code that can be used to specify a diagnosis or procedure.

Malignant neoplasm of bladder neck
Malignant neoplasm of internal urethral orifice · Bladder cancer, bladder neck · Cancer of the urinarybladder, neck · Primary malignant neoplasm of urinary bladder neck…
This code is a specific code that can be used to specify a diagnosis or procedure.

Malignant neoplasm of lateral wall of bladder
Bladder cancer, lateral wall · Cancer of the urinary bladder, lateral wall · Primary malignant neoplasm of lateral wall of urinary bladder
This code is a specific code that can be used to specify a diagnosis or procedure.

Malignant neoplasm of anterior wall of bladder
Bladder cancer, anterior wall · Cancer of the urinary bladder, anterior wall · Primary malignant neoplasm of anterior wall of urinary bladder
This code is a specific code that can be used to specify a diagnosis or procedure.

Malignant neoplasm of posterior wall of bladder
Bladder cancer, posterior wall · Cancer of the urinary bladder, posterior wall · Primary malignant neoplasm of posterior wall of urinary bladder
This code is a specific code that can be used to specify a diagnosis or procedure.

Malignant neoplasm of overlapping sites of bladder
Bladder cancer, overlapping sites · Cancer of the bladder, contiguous or overlap sites · Malignant neoplasm, overlapping lesion of bladder
This code is a specific code that can be used to specify a diagnosis or procedure.

Encounter for screening for malignant neoplasm of bladder
Screening for cancer of urinary bladder done · Screening for cancer of urinary bladder done (situation) · Screening for urinary bladder cancer · Screening (for) Z13.9 neoplasm (malignant) (of) Z12.9 bladderZ12.6 genitourinary organs NEC Z12.79 bladder Z12.6…
This code is a specific code that can be used to specify a diagnosis or procedure.

Malignant neoplasm of bladder, unspecified
Adenocarcinoma of bladder · Adenocarcinoma, bladder · Bladder cancer · Cancer of the urinarybladder · Cancer of the urinary bladder, adenocarcinoma · Cancer of the urinary bladder, current, localized · Cancer of the urinary bladder, invasive · Cancer of the urinary bladder, spindle cell · Cancerof the urinary bladder, squamous cell · Cancer of the urinary bladder, superficial · Cancer of the urinary bladder, transitional cell · Carcinoma of urinary bladder cancer · Localized bladder cancer · Localized primary malignant neoplasm… bladder cancer · Transitional cell carcinoma of bladder · Transitional cell… cancer occurs in the lining of the bladder. It is the sixth most common type ofcancer… pain when you urinate low back pain risk factors for developing bladder cancer include
This code is a specific code that can be used to specify a diagnosis or procedure.

Secondary malignant neoplasm of bladder
The spread of cancer to the urinary bladder wall from an adjacent or distant anatomic site

benign prostatic hyperplasia

Benign endometrial hyperplasia
Endometrial hyperplasia (complex) (simple) without atypia · Complex endometrial hyperplasia · Complex endometrial hyperplasia without atypia · Complex endometrial hyperplasia wo atypia · Simple endometrial hyperplasia · Simple endometrial hyperplasia without atypia · Simple endometrial hyperplasia wo atypia · Hyperplasia, hyperplastic endometrium, endometrial (adenomatous) (benign) (cystic) (glandular) (glandular-cystic) (polypoid) N85.00 complex (without atypia) N85.01 simple (without atypia) N85.01…
This code is a specific code that can be used to specify a diagnosis or procedure.

Enlarged prostate without lower urinary tract symptoms
Enlarged prostate without LUTS · Enlarged prostate NOS · Benign localized hyperplasia of prostate · Benign localized prostatic hyperplasia (BPH) · Benign prostatic hyperplasia · Benign prostatic hyperplasia (BPH) · BPH (benign prostatic hypertrophy) · Enlarged prostate · Hyperplasia of prostate · Hyperplasia of prostate without urinary obstruction · Large prostate · Prostate hyperplasia · Enlargement, enlarged – see also Hypertrophy prostate N40.0 without lower urinary tract symtpoms (LUTS) N40.0 Hyperplasia, hyperplastic prostate (adenofibromatous) (nodular) N40.0 without lower urinary tract symtpoms (LUTS) N40.0…
This code is a non-specific code that cannot be used to specify a diagnosis or procedure. A child code underneath this code will provide greater detail.

Enlarged prostate
benign neoplasms of prostate (adenoma, benign) (fibroadenoma) (fibroma) (myoma) (D29.1) · malignant neoplasm of prostate (C61) · adenofibromatous hypertrophy of prostate · benign hypertrophy of the prostate · benign prostatic hyperplasia · benign prostatic hypertrophy · BPH · nodular prostate · polyp of prostate · A benign (noncancerous) condition in which an overgrowth of prostate tissue pushes against the urethra and the bladder, blocking the flow of urine. · Increase in constituent cells in the prostate, leading to enlargement of the organ (hypertrophy) and adverse impact on the lower urinary tract function. This can be caused by increased rate of cell proliferation, reduced rate of cell death, or both….

This code is a specific code that can be used to specify a diagnosis or procedure.

Enlarged prostate with lower urinary tract symptoms
) · Benign prostatic hyperplasia w/ urinary symptoms · Benign prostatic hypertrophy (enlarged prostate) · Benign prostatic hypertrophy with outflow obstruction…; BPH w weak urinary stream · Incomplete emptying of bladder due to benign prostatic hypertrophy · Lower urinary tract symptoms due to benign prostatic hypertrophy · Nocturia due to benign prostatic hypertrophy · Straining on urination due to benign prostatic hypertrophy · Urinary frequency due to benign prostatic hypertrophy · Urinary hesitancy due to benign prostatic hypertrophy · Urinary incontinence due to benign prostatic hypertrophy · Urinary retention due to benign prostatic hypertrophy · Urinary urgency due to benign prostatic hypertrophy · Weak urinary stream due to benign prostatic hypertrophy · Enlargement, enlarged – see

Basal cell carcinoma of skin, unspecified

Basal cell carcinoma of skin, unspecified
Basal cell carcinoma of skin · Basal cell carcinoma, skin · Cancer of the skin, basal cell · Carcinoma (malignant) – see also Neoplasm, by site, malignant basal cell (pigmented) (see also Neoplasm, skin, malignant) C44.91…
This code is a specific code that can be used to specify a diagnosis or procedure.

Basal cell carcinoma of anal skin
Basal cell carcinoma of anal margin · Basal cell carcinoma of perianal skin · A basal cell carcinoma arising from the perianal skin. Local excision is the treatment of choice. Metastases are extremely rare….
This code is a non-specific code that cannot be used to specify a diagnosis or procedure. A child code underneath this code will provide greater detail.

Basal cell carcinoma of skin of other and unspecified parts of face
Basal cell carcinoma of ala nasi · Basal cell carcinoma of bridge of nose · Basal cell carcinoma of nose · Basal cell carcinoma of tip of nose · Basal cell carcinoma, bridge of nose · Basal cell carcinoma, nasal alar · Basal cell carcinoma, nose · Basal cell carcinoma, tip of nose · Cancer of the bridge of nose, basal cell · Cancer of the bridge of nose, squamous cell · Cancer of the nasal alar, basal cell · Cancer of the nasal alar, squamous cell · Cancer of the nose, basal cell · Cancer of the tip of nose, basal cell · Cancer of the tip of nose, squamous cell · Primary malignant neoplasm of skin of nose… cell carcinoma of ala nasi · Squamous cell carcinoma of bridge of nose · Squamous cell carcinoma of tip of nose · Squamous cell carcinoma, bridge of nose
This code is a specific code that can be used to specify a diagnosis or procedure.

Merkel cell carcinoma, unspecified
Merkel cell carcinoma of unspecified site · Merkel cell carcinoma NOS · Cancer, merkel tumor · Merkel cell carcinoma · A carcinoma arising from merkel cells located in the basal layer of the epidermis and occurring most commonly as a primary neuroendocrine carcinoma of the skin. Merkel cells are tactile cells of neuroectodermal origin and histologically show neurosecretory granules. The skin of the head and neck are a common site of merkel cell carcinoma, occurring generally in elderly patients. (holland et al., cancer medicine, 3d ed, p1245) · A rare malignant cutaneous tumor seen… Merkel cell C4A.9 · … is composed of small round cells with scanty cytoplasm arranged in a trabecular pattern, or in ill-defined nodules or in a diffuse pattern. The tumor cells contain cytoplasmic membrane

This code is a non-specific code that cannot be used to specify a diagnosis or procedure. A child code underneath this code will provide greater detail.

Merkel cell carcinoma
A carcinoma arising from merkel cells located in the basal layer of the epidermis and occurring most commonly as a primary neuroendocrine carcinoma of the skin. Merkel cells are tactile cells of neuroectodermal origin and histologically show neurosecretory granules. The skin of the head and neck are a common site of merkel cell carcinoma, occurring generally in elderly patients. (holland et al., cancer medicine, 3d ed, p1245) · A rare malignant cutaneous tumor seen in elderly patients. Its usual location is on the head, neck and extremities. The tumor is composed of small round cells with scanty cytoplasm arranged in a trabecular pattern, or in ill-defined nodules or in a diffuse pattern. The tumor cells contain cytoplasmic membrane-bound dense core granules resembling neurosecretory granules. · A rare type of cancer that forms on or just beneath the skin, usually in parts

Atelectasis

Atelectasis
newborn atelectasis · tuberculous atelectasis (current disease) (A15) · A disorder characterized by the collapse of part or the entire lung. · Absence of air in the entire or part of a lung, such as an incompletely inflated neonate lung or a collapsed adult lung. Pulmonary atelectasis can be caused by airway obstruction, lung compression, fibrotic contraction, or other factors. · Collapse of all or part of a lung due to bronchial plugging or the chest cavity being opened to atomspheric pressure. · Failure of the lung to expand (inflate) completely. This may be caused by a blocked airway, a tumor, general anesthesia, pneumonia or other lung infections, lung disease, or long-term bedrest with shallow breathing. Sometimes called a collapsed lung. ·… anesthesia. · Atelectasis (massive) (partial) (pressure) (pulmonary) J98.11
This code is a specific code that can be used to specify a diagnosis or procedure.

Other atelectasis of newborn
Partial atelectasis of newborn · Secondary atelectasis of newborn · Atelectasis (massive) (partial) (pressure) (pulmonary) J98.11 newborn P28.10 partial P28.19 secondary P28.19…
This code is a specific code that can be used to specify a diagnosis or procedure.

Unspecified atelectasis of newborn
Atelectasis of newborn NOS · Atelectasis (massive) (partial) (pressure) (pulmonary) J98.11 newborn P28.10…
This code is a specific code that can be used to specify a diagnosis or procedure.

Resorption atelectasis without respiratory distress syndrome
resorption atelectasis with respiratory distress syndrome (P22.0) · Atelectasis (massive) (partial) (pressure) (pulmonary) J98.11 newborn P28.10 due to resorption P28.11…
This code is a specific code that can be used to specify a diagnosis or procedure.

Primary atelectasis of newborn
Primary failure to expand terminal respiratory units · Pulmonary hypoplasia associated with short gestation · Pulmonary immaturity NOS · Apneumatosis, newborn P28.0 Atelectasis (massive) (partial) (pressure) (pulmonary) J98.11 primary (newborn) P28.0 newborn P28.10 primary P28.0 Failure, failed expansion terminal respiratory units (newborn) (primary) P28.0 Fetus, fetal – see also condition lung tissue P28.0 Hypoplasia, hypoplastic lung (lobe) (not associated with short gestation) Q33.6 associated with immaturity, low birth weight, prematurity, or short gestation P28.0 pulmonary (not associated with short gestation) Q33.6 associated with short gestation P28.0 Immaturity (less than 37 completed weeks) – see also Preterm, newborn lung, newborn
This code is a non-specific code that cannot be used to specify a diagnosis or procedure. A child code underneath this code will provide greater detail.

Other and unspecified atelectasis of newborn
This code is a specific code that can be used to specify a diagnosis or procedure.

Other pulmonary collapse
Brock’s syndrome (atelectasis due to enlarged lymph nodes) J98.19 Collapse R55 lung (massive) – see also Atelectasis J98.19 pulmonary – see also Atelectasis J98.19 Middle lobe (right) J98.19 Syndrome – see also Disease Hamman’s J98.19 middle lobe (lung) J98.19…

This code is a specific code that can be used to specify a diagnosis or procedure.

Other pulmonary complications of anesthesia during the puerperium
Obstetric anesthesia with pulmonary complications with postnatal problem · Pulmonary complication of anesthesia after childbirth · Pulmonary complication of OB anesthesia, postpartum · Collapse R55 lung (massive) – see also Atelectasis J98.19 pressure due to anesthesia (general) (local) T88.2 postpartum, puerperal O89.09 Complication (s) (from) (of) anesthesia, anesthetic – see also Anesthesia, complication T88.59 pulmonary postpartum, puerperal O89.09..

arterial occlusive disease

Hepatic veno-occlusive disease
Budd-Chiari syndrome (I82.0) · Veno-occlusive disease of the liver · A condition in which some of the veins in the liver are blocked. It is sometimes a complication of high-dose chemotherapy given before a bone marrow transplant and is marked by increases in weight, liver size, and blood levels of bilirubin. · A disorder characterized by damage of the hepatic sinusoidal endothelial cells of the hepatic venules that leads to venular occlusion and hepatocellular necrosis. It is usually the side effect of high dose chemotherapy in preparation for stem cell transplantation. Less frequently it may… leading to venous outflow occlusion and sinusoidal obstruction. · Disease, diseased – see also Syndrome liver (chronic) (organic) K76.9 veno-occlusive… hyperbilirubinemia, hepatomegaly, and fluid retention. · Liver disease that is caused by injuries
This code is a specific code that can be used to specify a diagnosis or procedure.

Combined arterial insufficiency and corporo-venous occlusive erectile dysfunction
Combined arterial insuff and corporo venous occlusive · Combined arterial insuff and corporo venous occlusive erectile dysfunction · Male erectile disorder due to arterial insufficiency and corporovenous occlusion · Dysfunction sexual (due to) R37 male N53.9 erectile N52.9 vasculogenic arterial insufficiency N52.01 with corporo-venous occlusive N52.03 corporo-venous occlusive N52.02 with arterial insufficiency N52.03…
This code is a specific code that can be used to specify a diagnosis or procedure.

Peripheral vascular disease, unspecified
· Pain at rest due to peripheral vascular disease · Peripheral arterial insufficiency · Peripheral arterial occlusive disease · Peripheral artery… I73.9 vasospastic I73.9 peripheral arterial I73.9 vascular NOS I73.9 vascular I99.9 peripheral (occlusive) I73.9 obliterative… Dilatation vasomotor I73.9 Disease, diseased – see also Syndrome… · atherosclerosis of the extremities (I70.2–I70.7-) · Arterial insufficiency, posterial tibial · Claudication due to peripheral vascular disease ·… to arterial stenosis; muscle ischemia; and accumulation of lactate. · Any disorder… angiospastic I73.9 Insufficiency, insufficient peripheral vascular (arterial) I73.9 arterial I77.1 peripheral I73.9 vascular I99.8

This code is a specific code that can be used to specify a diagnosis or procedure.

Disorder of arteries and arterioles, unspecified
Disorder of artery · Unspecified disease of artery · Arteriopathy I77.9 Disease, diseased – see also Syndrome aorta (nonsyphilitic) I77.9 arterial I77.9 arteriolar (generalized) (obliterative) I77.9 artery I77.9 Occlusion, occluded artery – see also Embolism, artery I74.9 peripheral I77.9..

Cardiac arrhythmia

Cardiac arrhythmia, unspecified
arrhythmias. Symptoms of arrhythmias include fast or slow heart beat skipping beats… or myocardial contraction. Cardiac arrhythmias can be classified by the abnormalities…Arrhythmia (cardiac) NOS · Atrial arrhythmia · Cardiac arrhythmia · Cardiac arrythmia complicating childbirth · Cardiac arrythmia in childbirth ·… · Conduction disorder of the heart postpartum · Neonatal (newborn) arrhythmia · Neonatal arrhythmia · Neonatal dysrhythmia · Postpartum (after… arrhythmia · Ventricular arrhythmia (heart beat disorder) · An arrhythmia… common type of arrhythmia is atrial fibrillation, which causes an irregular and fast heart… run tests to find out if you have an arrhythmia. Treatment to restore a normal heart… irregular I49.9 Arrhythmia (auricle)(cardiac)(juvenile)(nodal) (reflex)(sinus
This code is a non-specific code that cannot be used to specify a diagnosis or procedure. A child code underneath this code will provide greater detail.

Other cardiac arrhythmias
cardiac arrhythmia complicating: · abortion or ectopic or molar pregnancy (O00-O07, O08.8) · obstetric surgery and procedures (O75.4) · bradycardia NOS (R00.1) · neonatal dysrhythmia (P29.1-) · sinoatrial bradycardia (R00.1) · sinus bradycardia (R00.1) · vagal bradycardia (R00.1)…
This code is a specific code that can be used to specify a diagnosis or procedure.

Other specified cardiac arrhythmias
of a stressor. It may be associated with bradycardia-tachycardia syndrome. · An arrhythmia originating from within the atrioventricular node. · Arrhythmia (auricle)(cardiac… I49.8 nodal I49.8 Sinus – see also Fistula arrhythmia I49.8
This code is a specific code that can be used to specify a diagnosis or procedure.

Re-entry ventricular arrhythmia
Arrhythmia (auricle)(cardiac)(juvenile)(nodal) (reflex)(sinus)(supraventricular)(transitory)(ventricle) I49.9 ventricular re-entry I47.0…
This code is a non-specific code that cannot be used to specify a diagnosis or procedure. A child code underneath this code will provide greater detail.

Abnormalities of heart beat
abnormalities originating in the perinatal period (P29.1-) · specified arrhythmias (I47-I49)…
This code is a specific code that can be used to specify a diagnosis or procedure.

Other premature depolarization
Ectopic beats · Extrasystoles · Extrasystolic arrhythmias · Premature contractions · A group of cardiac arrhythmias in which the cardiac contractions are not initiated at the sinoatrial node. They include both atrial and ventricular premature beats, and are also known as extra or ectopic heartbeats. Their frequency is increased in heart diseases. · Arrhythmia (auricle)(cardiac)(juvenile)(nodal) (reflex)(sinus)(supraventricular)(transitory)(ventricle) I49.9 extrasystolic I49.49 Beat (s) ectopic I49.49 escaped, heart I49.49 Contraction (s) premature auriculoventricular I49.49 heart I49.49 Depolarization, premature I49.40 specified NEC I49.49 Ectopic, ectopia (congenital) beats I49.49 Extrasystoles (supraventricular) I49.49 Premature – see
This code is a specific code that can be used to specify a diagnosis or procedure.

Ventricular premature depolarization
Ventricular premature beats · A type of cardiac arrhythmia with premature contractions of the heart ventricles. It is characterized by the premature qrs complex on ecg that is of abnormal shape and great duration (generally >129 msec). It is the most common form of all cardiac arrhythmias. Premature ventricular complexes have no clinical significance except in concurrence with heart diseases. · Ectopic impulses originating in the ventricles. · Premature ventricular beats, the most common of all arrhythmias; in the absence of heart disease, they are not of great clinical significance, but in patients with coronary disease, they represent a constant danger of ventricular tachycardia or fibrillation and sudden death. · Contraction (s) premature ventricular I49.3 Depolarization, premature I49.40 ventricular I49.3

This code is a specific code that can be used to specify a diagnosis or procedure.

Long QT syndrome
Prolonged qt interval syndrome · A condition that is characterized by episodes of fainting (syncope) and varying degree of ventricular arrhythmia as indicated by the prolonged qt interval. The inherited forms are caused by mutation of genes encoding cardiac ion channel proteins. The two major forms are romano-ward syndrome and jervell-lange nielsen syndrome. · A ventricular arrhythmia characterized by syncopal episodes and a long qt interval, sometimes leading to sudden death due to paroxysmal ventricular arrhythmia. This arrhythmia is associated with a prolongation of repolarization following depolarization of the cardiac ventricles. The prolongation of the q-t interval combined with torsades de… may lead to serious arrhythmia and sudden cardiac death. · Prolongation of q-t… be acquired or congenital; may lead to serious arrhythmia and sudden cardiac death. ·