The information below was pulled from different websites. Noted under each.

Dancing Doberman's Disease
This information was taken from
http://www.ask.com/bar?q=dancing+dobermans+disease&page=1&qsrc=0&ab=1&u=http%3A%2F%2Fbakaridobes.westhost.com%2Fpubliceducation%2FPECGeneticDDD.html

A Brief Explanation
Dancing Doberman Disease (DDD) can mimic many other conditions such as lumbosacral disc disease, cervical vertebral instability (CVI), inflammation of the spinal cord, spinal arthritis, cauda equina syndrome, some nervous system maladies, and spinal tumors. It is likely the condition is more prevalent than previously recognized because there is a general lack of awareness on the part of veterinarians and breeders, and therefore, the condition is often overlooked as a diagnosis.

The Textbook of Veterinary Internal Medicine, Ettinger and Feldman, 4th Edition, contains a description of this disease if you want to look it up at your library, or ask your veterinarian about it. A simple description would be that of a progressive disease, usually presenting with a holding up of one rear leg while standing. The age at onset can be anywhere from 4 months to 10 years. Both males and females are affected. Most affected dogs have normal findings on other tests, including blood counts, biochemistry, x-ray, and thyroid function. Over several months the condition progresses with a wasting of rear leg muscles, and a more constant shifting of weight on the rear legs to resemble a dog "dancing", hence the name "Dancing Doberman Disease". Frequently these dogs will knuckle over with their rear paws and ultimately prefer to sit or lie down rather than stand. The dogs show no sign of pain and are perfectly capable of running in the yard, chasing a ball or a squirrel, etc. Generally they live out their lives comfortably as pets although the condition is progressive, incurable, and at present, untreatable. It must be considered a genetic disease because it has never been reported in any mammal, let alone any dog breed other than the Doberman Pinscher.

Just because most breeders and many veterinarians are unaware of DDD doesn't mean it doesn't exist. Although it may not be wide-spread at this time, it represents a diagnostic conundrum because its symptoms are easily confused with other diseases stated above. Recognition that there is a condition known as DDD is important so that a proper diagnosis can be made. Accurate diagnosis of any disease is the key to treatment and prognosis and can only be made if there is an awareness of all possibilities.

Dr. Jan Steiss, in a grant funded by Auburn University College of Veterinary Medicine and the Doberman Pinscher Foundation of America, has completed the most recent research on DDD. She is preparing a manuscript for veterinary publication and, when available, information will be updated on the DPFA web site.
Dr. Jan Steiss is no longer with Auburn University. She may be
reached at 205-934-9229 or email
steisje@hotmail.com

Fanconi Syndrome
This information is taken from
http://www.ask.com/bar?q=Fanconi+Syndrome+in+Dogs&page=1&qsrc=6&ab=0&u=http%3A%2F%2Fwww.vet.uga.edu%2Fvpp%2Fclerk%2Fdavis%2Findex.php

Fanconi’s Syndrome in Dogs
Michael A. Davis, DVM; Perry J. Bain, DVM, PhD, Kenneth S. Latimer, DVM, PhD, and Bruce E. LeRoy, DVM, PhD.
Class of 2004 (Davis) and Department of Pathology (Bain, Latimer, LeRoy), College of Veterinary Medicine, The University of Georgia, Athens, GA 30602-7388

Fanconi’s Syndrome in Dogs
Fanconi's syndrome is an inherited disease that affects the proximal renal tubule and causes abnormalities in sodium, glucose, calcium, phosphate and amino acid retention, sometimes leading to fatal disturbances in acid-base balance.1,2,3 The disease can also be mimicked by certain toxins and drugs that affect the proximal renal tubule and interrupt normal functioning.4,5
Epidemiology
Fanconi's syndrome appears to have a hereditary predisposition for Basenjis as well as Norwegian Elkhounds. Other breeds that are predisposed (to a lesser degree) are Shetland sheepdogs and Schnauzers. The onset of the disease is not until later in life (3-11 yrs of age in Basenjis), and thus affected dogs may have been bred before diagnosis, passing on the genetic trait.6 Approximately 10% of adult Basenjis have Fanconi’s syndrome.6 The acquired form of Fanconi’s syndrome can be caused by heavy metal poisoning (lead, mercury, cadmium and uranium). Drugs such as a gentamicin,5 cephalosporins, outdated tetracycline, cisplatin, and streptozotocin can cause proximal renal tubule resorption abnormalities.4 Chemicals such as Lysol® and maleic acid also have been reported to cause the syndrome.4 Renal cystic disease and neoplasia,3 including multiple myeloma and monoclonal gammopathies, also have been found to cause acquired Fanconi’s syndrome.4
Etiology
The proximal renal tubule normally resorbs 100% of the glucose that is filtered through the glomerulus in normoglycemic conditions. Glucose resorption is coupled to sodium co-transport. Glucose enters the cell under secondary active transport driven by the sodium concentration gradient. This concentration gradient between extracellular fluid and intracellular fluid is maintained by sodium-potassium ATPase on the basolateral surface of the cell which pumps sodium out of the cell and into the interstitium. There are also similar co-transports between sodium and amino acids, inorganic phosphorous, and calcium. A sodium/hydrogen ion antiporter is present in the proximal renal tubule which shuttles sodium into the cell and hydrogen into the lumen of the tubule. This antiporter is also dependent upon the concentration gradient established by the sodium-potassium pump (Fig. 1).7
The defect in the proximal renal tubule is not known and may vary between the inherited and acquired forms of the syndrome. There are three proposed mechanisms for the failure to re-absorb the normal amount of solutes in Fanconi’s syndrome. The first is a defect in all of the transport systems which prevents them from working effectively (Fig 2).4 The second proposed mechanism is a defect in the metabolism of the cell that decreases the amount of available ATP.4,7 As a result, the concentration of sodium within the cell will increase and there will no longer be a sufficient concentration gradient (Fig 3). Finally, the third proposed mechanism is a defect in the cell membrane’s physical structure.8 The lack of either the concentration gradient or the defect in co-transports will leave sodium and other solutes in the tubular lumen, and these solutes are lost in the urine. The defects do not completely disable either the ATPase or the transport systems, but rather decrease their efficiency.
Gallery of Figures 1, 2 and 3 >>
Diagnosis of Fanconi's Syndrome
A dog suffering from Fanconi’s syndrome typically presents with polyuria and polydypsia, a history of weight loss, a poor hair coat and, sometimes weakness.1,4 The diagnosis of Fanconi's syndrome is strongly suggested by the detection of glucosuria in the face of normoglycemia.1,2,4,8 As stated previously, in normoglycemic conditions 100% of glucose should be resorbed in the proximal renal tubule. In the normal dog, the glucose co-transport system can tolerate glucose blood concentrations up to approximately 180 mg/dl before having glucose spill into the final renal filtrate.9 With all of the cotransporter and antiporter systems there is a maximum level at which the transports can work called the transport maximum (Tm). Once the transport maximum is exceeded, the remaining solute is not absorbed and is lost in the urine. In Fanconi’s syndrome, the Tm is reduced for the various solutes. The degree to which it is reduced varies between affected individuals and also varies according to the stage of the disease (Table 1).

Table 1. Differences in solute resorption in healthy dogs versus dogs with Fanconi syndrome.

	Percentage of solute resorbed in unaffected dogs	Percentage of solute resorbed in affected dogs
Glucose	100%	39-65%1
Amino Acids	97-100%	50 – 99%1
Phosphate	90%	47-79%1

*The above table assumes normal plasma levels for the solutes.

Other clinical findings in dogs with Fanconi syndrome may include a slight to mild proteinuria and a secretion-type metabolic acidosis (normal anion gap) with an alkaline urine (renal tubular acidosis).4
Consequences of Fanconi’s Syndrome
Fanconi’s syndrome is a progressive disease, which, if not treated, ultimately results in transport system failure to the point where solute losses are significant enough to overwhelm other compensatory mechanisms and the dog can no longer maintain homeostasis. The most significant of these is the loss of bicarbonate (HCO3-). Proximal renal tubular acidosis subsequently develops and, if left uncorrected, will ultimately lead to death. In an unaffected dog with a normal acid-base balance, most of bicarbonate ions in the urine are converted to carbonic acid (HCO3- + H+à H2CO3), which is then converted to H2O and CO2 with the aid of carbonic anhydrase found in the brush border of the renal tubular epithelial cell. The carbon dioxide formed readily diffuses across the luminal membrane of the renal tubular cell. In this way, bicarbonate is conserved.7 The hydrogen ion needed to form carbonic acid is supplied by the sodium-hydrogen ion antiporter, which has a high enough Tm to conserve the needed bicarbonate in an unaffected dog. In Fanconi’s syndrome, the Tm is reduced due to either the lack of a sufficient sodium concentration gradient or a defect in the transporter itself. As a result, fewer hydrogen ions are secreted and, thus, less bicarbonate is conserved. The loss of bicarbonate causes an acidemia and the plasma bicarbonate level decreases until it has reached a level which the impaired transport system can handle. Affected dogs can compensate somewhat for the acidemia through respiratory mechanisms (hyperventilation), shifts in intracellular potassium, and secreting hydrogen ions in the distal renal tubule.
Treatment
The treatment of Fanconi’s syndrome must be based on each individual as the severity of the disease is quite variable. The most important aspect of treatment is managing the metabolic acidosis.10 This can be very difficult due to the large quantities of bicarbonate being lost in the urine. The traditional treatment for Fanconi’s syndrome is administration of potassium citrate.2,4 Poor results from potassium citrate treatment alone, however, has lead to a more extensive treatment to compensate for renal bicarbonate losses, the “Gonto protocol.” For an extensive explanation of this treatment, see: http://www.zandebasenjis.com/protocol.htm In a recent study, Basenji dogs with Fanconi’s syndrome treated by this protocol were found to have lifespans similar to dogs without Fanconi’s syndrome.11 Bicarbonate concentration should be used to monitor the success of the alkali supplementation. Supplementation should be provided lifelong, as the affected dogs continuously lose bicarbonate into the urine. The increased amount of solutes in the urine causes an osmotic diuresis and an inability to concentrate urine. Therefore, it is important that affected dogs always have access to water.

Lupoid Onychopathy
This information was taken from
http://www.ask.com/bar?q=Lupoid+onychopathy&page=1&qsrc=2417&ab=0&u=http%3A%2F%2Fwww.vin.com%2Fproceedings%2FProceedings.plx%3FCID%3DWSAVA2005%26Category%3D1547%26PID%3D10980%26O%3DGeneric
The pathogenesis of this bizarre condition is unknown but hereditary and immune-mediated processes are suspected. There is onychomadesis and onychodystrophy (onychorrhexis, onychomalacia, onycholysis) often affecting ALL claws. Pain is variable, as is incidence of lameness.
Skin scrapings and cytology are non-diagnostic but histopathologic findings in the nail bed are consistent. It is also important to screen for underlying problems such as lupus, hypothyroidism, adverse food reactions and immune deficits. Successful management requires addressing any underlying problems, but treatment with marine oils, tetracycline and niacinamide, and pentoxifylline can all be successful.
For other Dermatology conditions copy and paste above link.

Narcolepsy
This information was taken from

http://www.ask.com/bar?q=Narcolepsy&page=1&qsrc=2417&ab=4&u=http%3A%2F%2Fwww.ninds.nih.gov%2Fdisorders%2Fnarcolepsy%2Fnarcolepsy.ht

What is Narcolepsy?

Narcolepsy is a chronic neurological disorder caused by the brain's inability to regulate sleep-wake cycles normally. At various times throughout the day, people with narcolepsy experience fleeting urges to sleep. If the urge becomes overwhelming, individuals will fall asleep for periods lasting from a few seconds to several minutes. In rare cases, some people may remain asleep for an hour or longer. In addition to excessive daytime sleepiness (EDS), three other major symptoms frequently characterize narcolepsy: cataplexy, or the sudden loss of voluntary muscle tone; vivid hallucinations during sleep onset or upon awakening; and brief episodes of total paralysis at the beginning or end of sleep. Narcolepsy is not definitively diagnosed in most patients until 10 to 15 years after the first symptoms appear. The cause of narcolepsy remains unknown. It is likely that narcolepsy involves multiple factors interacting to cause neurological dysfunction and sleep disturbances.

Is there any treatment?

What is the prognosis?

What research is being done?

More links to Dog Disease's can be found here
http://www.gopetsamerica.com/dog-health/doghealth.aspx

And here
Canine: Diseases

Diagnosing false pregnancy in Dogs
False pregnancy occurs most commonly in dogs that are not spayed. The symptoms are brought on when your dog goes through estrus (the period of the reproductive cycle known as "heat") and does not breed. The dog shows signs similar to pregnancy such as lactating, morning sickness, appetite fluctuations, weight gain, and nesting. She may also begin to "mother" toys or other items. These signs typically occur about a month of two after the estrus and can last up to three months.

Diagnosing False Pregnancy in Dogs

If there is a chance that your dog could have bred with another dog, your veterinarian will need to run tests to determine if your dog is pregnant or just experiencing a false pregnancy. First your veterinarian will ask for a history of your dog’s heat cycle for the past 2 to 3 months. She will also inquire about the symptoms your dog has been showing. A physical examination of your dog will be performed. Your veterinarian will palpate your dog’s abdomen to check for changes. She will also check for swelling in the mammary glands. Your veterinarian may choose to take X-rays or order an ultrasound. This can determine if problems with the uterus are causing these signs or if your dog is experiencing an actual pregnancy.

Prognosis

Most false pregnancies will resolve themselves. Only about 10% of false pregnancies will require treatment. Your veterinarian can determine if and what treatment is necessary.

How is Skin Irritation diagnosed in Dogs.
For many more wonderful articles on health issues for dogs visit
http://www.youpet.com/dog-health/?p=2



To help prevent some of the above problems I recommend putting your pet on NuVet Tabs or powder supplement.

1-800-474-7044 referral code 98794