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• HEALTH •

BLOAT (​gastric dilatation-volvulus​)
Bloat is a dire medical emergency and one of the most rapidly life-threatening conditions that vets treat in dogs. It involves the stomach but can quickly lead to life-threatening shock if left untreated. It is not uncommon in deep-chested dogs such as the Weimaraner.

When bloat happens, the stomach fills with gas and often twists in a way that cuts off the blood supply to the gut and stops gas and food from leaving. It can also make the spleen twist and lose circulation and block vital veins in the back that transport blood to the heart.

Bloat is immensely painful for dogs, and it can kill in a matter of hours without veterinary intervention, so it’s crucial that Weimaraner owners know the signs. The condition is also known, more scientifically, as gastric dilatation-volvulus.

Symptoms can appear quickly and will usually include one or more of the following:
  • A swollen, hard belly
  • Retching but not able to vomit
  • Drooling
  • Pain in the abdomen when touched
  • Other signs of distress, such as panting and restlessness

If you even suspect bloat, take your dog to the vet immediately. Bloat is a veterinary emergency, and minutes can make a difference to your Weimaraner’s chances of survival.  It is better to take your dog to the vet and be proven wrong about it being bloat,  than it is to assume it's not bloat - with possible tragic consequences for waiting too long. 

Great article here:  veterinarypartner.vin.com/default.aspx?pid=19239&id=4951541
VACCINATION
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A percentage of Weimaraner puppies may manifest an autoimmune reaction following vaccination. When the immune system of susceptible individuals is challenged by the multiple antigens found in combination vaccines, it becomes hyper–reactive and responds in the same way it would respond to fight off an infection: fever, elevated white blood cells and inflammatory reaction of tissues and joints. Although many puppies can be vaccinated with no adverse reactions, there is no way at the present time to determine which puppies may react. Although controversial, some research has suggested that the distemper component of the combination vaccines may present the highest risk for immune mediated problems. Past research has documented that most vaccine reactions occur between 12 and 16 weeks of age.

Weimaraner Club of America  Policy On Vaccinating Weimaraners: www.weimaranerclubofamerica.org/puppy_protocol.php​

In an effort to reduce the incidence of serious vaccine reactions, an alternative to the traditional vaccination protocol may be considered, where the maximum level of protection is accomplished with the minimum number of vaccines. In view of this, the use of Recombinant Vaccine Technology and employing the following schedule of CORE vaccines is strongly recommended:
  • 8 weeks: Canine Distemper, Adenovirus Type 2, Parainfluenza– Parvovirus
  • 12 weeks: Canine Distemper, Adenovirus Type 2, Parainfluenza– Parvovirus
  • 15–16 weeks: An antibody titer is recommended to confirm immunity since a small proportion of puppies may still not be covered.
  • Puppies showing no evidence of antibody production in the titer should be re–inoculated.

The use of NON-CORE vaccines such as Corona, Leptospirosis, Bordetella, Lyme, etc., is not recommended unless these diseases are prevalent in the area; and should never be administered along with the CORE vaccines listed above, but rather separately and at a time when the pup’s immune system is mature. Rabies vaccinations should be given as required by law, but NOT coincident with any other vaccinations. As Rabies vaccinations should be given as required by law, it is strongly recommended that the puppy is older than 16 weeks of age. If a serious adverse immune response occurs, further vaccination prior to one year of age is NOT recommended. Options should be discussed with your veterinarian. Some states provide exemptions for Rabies in cases where an underlying medical condition is likely to result in a life-threatening condition in response to vaccination. While this protocol helps in preventing reactions, it does not prevent them in all susceptible individuals.

**
The recommendations expressed are those of the WCA and the WCA Health Committee. These recommendations are not a substitute for professional veterinary advice, diagnosis or treatment. The WCA recognizes that decisions about veterinary care are private matters which must remain within the purview of an individual dog’s owner(s) and veterinarian(s). It is the responsibility and ethical mandate of all WCA members to ensure that their dogs receive appropriate and timely veterinary care.
Hip Dysplasia
​ofa.org/diseases/hip-dysplasia/
​Canine Hip Dysplasia typically develops because of an abnormally developed hip joint, but can also be caused by cartilage damage from a traumatic fracture.With cartilage damage or a hip joint that isn’t formed properly, over time the existing cartilage will lose its thickness and elasticity. This breakdown of the cartilage will eventually result in pain with any joint movement.
No one can predict when or even if a dysplastic dog will start showing clinical signs of lameness due to pain. The severity of the disease can be affected by environmental factors, such as caloric intake or level of exercise. There are a number of dysplastic dogs with severe arthritis that run, jump, and play as if nothing is wrong and some dogs with barely any arthritic x-ray evidence that are severely lame.
Screenings for Hip Dysplasia are performed by a veterinarian with x-rays sent to OFA for grading and certification. 

The OFA classifies hips into seven different categories: Excellent, Good, Fair (all within Normal limits), Borderline, and then Mild, Moderate, or Severe (the last three considered Dysplastic).
  • Excellent: Superior conformation; there is a deep-seated ball (femoral head) that fits tightly into a well-formed socket(acetabulum) with minimal joint space.
  • Good: Slightly less than superior but a well-formed congruent hip joint is visualized. The ball fits well into the socket and good coverage is present.
  • Fair: Minor irregularities; the hip joint is wider than a good hip. The ball slips slightly out of the socket. The socket may also appear slightly shallow.
  • Borderline: Not clear. Usually more incongruency present than what occurs in a fair but there are no arthritic changes present that definitively diagnose the hip joint being dysplastic.
  • Mild: Significant subluxation present where the ball is partially out of the socket causing an increased joint space. The socket is usually shallow only partially covering the ball.
  • Moderate: The ball is barely seated into a shallow socket. There are secondary arthritic bone changes usually along the femoral neck and head (remodeling), acetabular rim changes (osteophytes or bone spurs) and various degrees of trabecular bone pattern changes (sclerosis).
  • Severe: Marked evidence that hip dysplasia exists. The ball is partly or completely out of a shallow socket. Significant arthritic bone changes along the femoral neck and head and acetabular rim changes.
  • The hip grades of excellent, good and fair are within normal limits and are given OFA numbers.
HOD (Hypertrophic Osteodystrophy)
Hypertrophic Osteodystrophy (HOD) is a canine autoinflammatory disease affecting young rapidly growing large breed dogs between eight weeks to eight months of age. Affected dogs exhibit swelling and pain in their legs with reluctance to stand or walk. In addition to orthopedic pain, there are variable systemic signs of which some or all may be present during an HOD episode. Systemic signs include fever, lethargy, depression, and loss of appetite.
A diagnosis of HOD is founded on radiographic evidence of bone involvement concurrent with hyperthermia and pain, and by ruling out infectious causes of the clinical signs. The cause of the disease is unknown and current treatments are focused on controlling the fever, alleviating the pain and treating the specific systemic signs present. Prognosis for severe cases is poor due to relapsing episodes and the low quality of life for the affected puppies that sometimes result in euthanasia. Currently, dog breeders have no means of selecting against HOD.
Several breeds of dogs, including the Weimaraner are at high risk for developing HOD. 
More information here: https://www.weimaranerclubofamerica.org/hod.php
​https://www.weimaranerclubofamerica.org/hod.php
lipomas (FATTY TUMORS)
Lipomas are tumors or fatty growths in dogs. They appear randomly, in different parts of the body, over time. They are soft, "mobile" growths that can be found directly under the skin. Lipomas can be very small or medium-sized. They are generally benign. These fatty tumors can appear in dogs of any age, but generally begin to manifest themselves with age.  They are particularly noticeable in short-haired Weimaraners. Lipomas can also be found in muscle and tissue, and can be tissue-bound. There's usually nothing to worry about, but fatty tumors can sometimes be malignant. That's why, when a dog has a growth, it's very important to have it examined by a veterinarian. 

Some breeds have lipomas more often than others, such as the Weimaraner and other large dogs, but all dogs can get them as they age. 
wobbler syndrome
Wobbler syndrome is the common term used for the spinal disease cervical vertebral instability, (CVI). The name comes from the weak, uncoordinated gait dogs with the condition have, giving the appearance of “wobbling” as they move.

Wobbler syndrome is primarily a disease of large and giant breed dogs, with Dobermans and Great Danes being the breeds most commonly affected. Other breeds of note include Rottweilers, Mastiffs, Weimaraners, German Shepherds, Bernese Mountain dogs, and Swiss Mountain dogs, but any large or giant breed dog can have the disease.

Wobbler syndrome affects the neck and spine in dogs. Dogs with CVI experience compression of the spinal cord and the spinal nerve roots, causing either neck or back pain or both, and gait problems. A narrowing, or stenosis, of the spinal canal and spinal nerve passages in the neck may occur.

While the first signs of wobblers are often an abnormal gait, symptoms include neck pain and stiffness, lameness or stiffness in the dog’s front legs or shoulders, and difficulty standing or laying down. Your dog can have weakness in the front or hind legs and not want to move, leading eventually to muscle weakness and deterioration. The disease can become so severe as to cause partial or complete paralysis in all four legs.

Approximately 40-54% of dogs with CVI that don’t require surgery improve. With surgery, about 80% of dogs improve. 
Von Willebrand Disease
​Von Willebrand Disease closely resembles hemophilia in humans. It's a hereditary bleeding disorder caused by low levels or a lack of the protein known as the von Willebrand factor, which regulates the first step in clot formation.

It's the most common disease inherited by dogs and is typically seen in the following dog breeds:
Weimaraners
Doberman Pinschers
German Shepherds
Golden Retrievers
Miniature Schnauzers
Pembroke Welsh
Gorgis
Shetland Sheepdogs
Basset Hounds
Scottish Terriers
Standard Poodles
Standard Manchester Terriers

The first signs of this bleeding disorder in your Weimaraner may be a minor cut or scrape that bleeds excessively, or more bleeding than expected after a vaccination or surgery.

​A DNA test is available for a few breeds. The Weimaraner is one of them. The test is accurate, and your vet can do it.
Hypomyelination (​HYM)
Hypomyelination in Weimaraners (HYM)
Hypomyelination in Weimaraners leads to tremors during puppyhood that often resolve by 3-4 months of age.
Phenotype: Hypomyelination leads to tremors during puppyhood. Affected puppies have tremors when awake as early as 2 weeks of age. Clinical signs resolve in most cases by 3-4 months of age, though some of the dogs may have a mild persistent tremor of the hind legs.

​Mode of Inheritance: Autosomal recessive
Alleles: N = Normal, HYM = Hypomyelination

Results Reported As:
Test Result    Hypomyelination
N/N    No copies of hypomyelination mutation. Dog is normal.
N/HYM    1 copy of hypomyelination mutation. Dog is normal but is a carrier.
HYM/HYM    2 copies of hypomyelination mutation. Dog is affected.

Explanation of Results:
Dogs with N/N genotype will not have hypomyelination and cannot transmit this variant to their offspring.
Dogs with N/HYM genotype will not be affected by hypomyelination, but are carriers. They will transmit this variant to 50% of their offspring. Matings between two carriers are predicted to produce 25% hypomyelination-affected puppies.
Dogs with HYM/HYM genotype will have hypomyelination and will transmit this variant to all of their offspring.

Researchers from the University of Wisconsin, Madison, lead by Dr. Ian Duncan, in collaboration with researchers from Dr. Patel’s Laboratory at University of Southern California and Dr. Bannasch’s Laboratory at University of California, Davis have identified the genetic basis for hypomyelination (HYM) in the Weimaraner. This condition leads to tremors during puppyhood. The disease is inherited as a simple autosomal recessive disorder and the carrier frequency has been estimated to be 4.29% within the breed. Hypomyelination is also called "tremors" and "shaking puppies" by dog breeders based on the fact that affected puppies have tremors when awake as early as 2 weeks of age. Clinical signs resolve in most cases by 3-4 months of age. Some of the dogs may have a mild persistent tremor of the hind legs.

Testing for hypomyelination assists owners and breeders in identifying affected and carrier dogs. Breeders can use results from the test as a tool for selection of mating pairs to avoid producing affected dogs.

Dogs that have only one mutant copy of HYM (N/HYM genotype) are normal but they are carriers of the disease. When two carriers are bred to each other the resulting puppies can be affected. At the time that this test was released, approximately 4.3% of Weimaraners were carriers of HYM; however, the number of carriers can change with each generation. Dogs that are carriers of HYM are completely normal and they can be safely bred to dogs that are non-carriers of HYM (N/N) in order to maintain diversity within the breed and to select for other positive attributes in carrier dogs.

https://vgl.ucdavis.edu/test/hypomyelination-weimaraner
Hyperuricosuria (HUU)
​Hyperuricosuria is an inherited disorder characterized by elevated levels of uric acid in the urine that can lead to the formation of bladder/kidney stones.
Phenotype: Hyperuricosuria is characterized by elevated levels of uric acid in the urine and can lead to the formation of bladder/kidney stones.
Mode of Inheritance: Autosomal recessive
Alleles: N = Normal/Unaffected, HU = Hyperuricosuria
Results Reported As:
Test Result    Hyperuricosuria
N/N    No copies of hyperuricosuria mutation detected. Dog is normal.
N/HU    1 copy of hyperuricosuria mutation is detected. Dog is a carrier and unaffected. If bred to another carrier, 25% of offspring are predicted to be affected.
HU/HU    2 copies of hyperuricosuria mutation detected. Dog is affected and susceptible to develop bladder/kidney stones.

Explanation of Results:
Dogs with N/N genotype will not have hyperuricosuria and will not transmit this hyperuricosuria variant to their offspring.
Dogs with N/HU genotype will not have hyperuricosuria, but are carriers. They will transmit this variant to 50% of their offspring. Matings between two carriers are predicted to produce 25% hyperuricosuria-affected puppies.
Dogs with HU/HU genotype will be affected and are susceptible to develop bladder/kidney stones. They will transmit this hyperuricosuria variant to all of their offspring.

Hyperuricosuria (HUU) means elevated levels of uric acid in the urine. This trait predisposes dogs to form stones in their bladders or sometimes kidneys. These stones often must be removed surgically and can be difficult to treat. HUU is inherited as a simple autosomal recessive defect. A mutation in exon 5 of the gene Solute carrier family 2, member 9 (SLC2A9) has been found to be associated with hyperuricosuria in dogs. HUU can occur in any breed but is most commonly found in the Dalmatian, Bulldog, and Black Russian Terrier. 

A DNA test for the SLC2A9 mutation can determine the genetic status of dogs for HUU. Dogs that carry two copies of the mutation will be affected and susceptible to develop bladder/kidney stones. However, the SCL2A9 mutation is not the sole cause of urate bladder stones in dogs. Other factors, in addition to genetic test results, such as liver disease and diet need also be considered in clinical evaluation.  

https://vgl.ucdavis.edu/test/hyperuricosuria
Spinal Dysraphism (SD)
Spinal dysraphism (SD)  is a genetic disorder present at birth that results from faulty embryonic development, leading to an abnormal gait as well as weakness and lack of coordination in the rear legs.
Phenotype: Affected Weimaraners have a defective spinal canal, which leads to neurological abnormalities. Puppies born with SD may have difficulties starting to walk due to weakness of their rear legs. Adults with SD show a typical abnormal gait that includes simultaneous movement of the hind legs or “bunny hopping” in the rear. Additional characteristics include weakness and lack of coordination in the rear, together with normal front end coordination and strength. Rarely a “bunny hopping” gait is observed in the front. The condition is not painful, and it does not progress during the life of an affected dog.

​Mode of Inheritance:
Autosomal recessive
Alleles: N = Normal, SD = Spinal dysraphism
Results Reported As:
Test Result    Spinal Dysraphism
N/N    No copies of SD mutation. Dog is normal.
N/SD    1 copy of SD mutation. Dog is normal but is a carrier.
SD/SD    2 copies of SD mutation. Dog is affected.

Explanation of Results:
Dogs with N/N genotype will not have spinal dysraphism and cannot transmit this variant to their offspring.
Dogs with N/SD genotype will not be affected by spinal dysraphism, but are carriers. They may transmit this variant to 50% of their offspring. Matings between two carriers are predicted to produce 25% spinal dysraphism-affected puppies.
Dogs with SD/SD genotype will have spinal dysraphism, a non-progressing condition with neurological abnormalities.

Additional Details
Spinal dysraphism (SD) in Weimaraner dogs is a genetic disorder present at birth that results from faulty embryonic development. Affected Weimaraners have a defective spinal canal which leads to neurological abnormalities. Puppies born with SD may have difficulties starting to walk due to weakness of their rear legs. Adults with SD show a typical abnormal gait that includes simultaneous movement of the hind legs or “bunny hopping” in the rear. Additional characteristics include weakness and lack of coordination in the rear, together with normal front end coordination and strength. Rarely a “bunny hopping” gait is observed in the front. The condition is not painful and it does not progress during the life of an affected dog.

SD is an inherited autosomal recessive disease caused by a mutation in the NKX2-8 gene. Two copies of the mutation are necessary for disease signs to be present, with both sexes being affected equally in frequency and severity. Weimaraners that have only one copy of the SD mutation (N/SD genotype) are normal, but they are carriers of the disease. When two carriers are bred to each other, 25% of the resulting puppies are expected to be affected and 50% to be carriers. Approximately 1.4% of Weimaraners are estimated to be carriers of SD (N/SD); however, the number of carriers can change with each generation. Weimaraners that are carriers of SD (N/SD) are completely normal, and they can be safely bred to dogs that are non-carriers (N/N) in order to maintain diversity within the breed and to select for other positive attributes in carrier dogs.

Testing for SD assists Weimaraner owners and breeders in identifying affected and carrier dogs. Breeders can use results from the test as a tool for selection of mating pairs to avoid producing affected dogs.

https://vgl.ucdavis.edu/test/sd-weimaraner
Elbow dysplasia
​Elbow dysplasia is a general term used to identify an inherited polygenic disease in the elbow. Three specific etiologies make up this disease and they can occur independently or in conjunction with one another. These etiologies include:

Pathology involving the medial coronoid of the ulna (FCP)
Osteochondritis of the medial humeral condyle in the elbow joint (OCD)
Ununited anconeal process (UAP)
Studies have shown the inherited polygenic traits causing these etiologies are independent of one another. Clinical signs involve lameness which may remain subtle for long periods of time. No one can predict at what age lameness will occur in a dog due to a large number of genetic and environmental factors such as degree of severity of changes, rate of weight gain, amount of exercise, etc.. Subtle changes in gait may be characterized by excessive inward deviation of the paw which raises the outside of the paw so that it receives less weight and distributes more mechanical weight on the outside (lateral) aspect of the elbow joint away from the lesions located on the inside of the joint. Range of motion in the elbow is also decreased.

Elbow Dysplasia Grades
Elbow dysplasia in dogs has multiple inherited etiologies which may occur singularly or in combination. These etiologies include fragmented medial coronoid (FCP) of the ulna, osteochondritis of the medial humeral condyle and ununited anconeal process (UAP). The most sensitive view used to diagnose secondary degenerative changes in the elbow joint is an extreme flexed mediolateral view of the elbow which is required by the OFA and recommended by the International Elbow Working Group. Veterinary radiologists are most interested in the appearance of the anconeal process of the ulna.

When there is instability of the elbow joint due to elbow dysplasia in a dog, one of the most sensitive radiographic findings is new bone proliferation (osteophytes) on the anconeal process of the ulna associated with secondary developmental degenerative joint disease.

Bone proliferation can be very subtle to visualize in some dogs.  Other arthritic findings such as sclerosis in the area of the trochlear notch of the ulna and bone spurs at joint edges are also reported. If fragmentation of the medial coronoid only involves the cartilage, it may not be seen radiographically but occasionally if the bone is also fragmented, it can be visualized as a separate calcific opacity superimposed over the radius.

Explanation of Elbow Grades
For elbow dysplasia evaluations for dogs, there are no grades for a radiographically normal elbow. The only grades involved are for abnormal elbows with radiographic changes associated with secondary degenerative joint disease. Like the hip certification, the OFA will not certify a normal elbow until the dog is 2 years of age. The OFA also accepts preliminary elbow radiographs. To date, there are no long-term studies for preliminary elbow examinations like there are for hips; however, preliminary screening for elbows along with hips can also provide valuable information to the breeder.

Grade I Elbow Dysplasia: Minimal bone change along anconeal process of ulna (less than 2mm).
Grade II Elbow Dysplasia: Additional bone proliferation along anconeal process (2-5 mm) and subchondral bone changes (trochlear notch sclerosis).
Grade III Elbow Dysplasia: Well developed degenerative joint disease with bone proliferation along anconeal process being greater than 5 mm.

https://ofa.org/diseases/elbow-dysplasia/
Autoimmune thyroiditis
​With Hypothyroidism, the thyroid gland is not making enough of a hormone called thyroxine that controls metabolism (the process of turning food into fuel). Hypothyroidism causes a wide variety of symptoms, but is often suspected in dogs that have trouble with weight gain or obesity and suffer from hair loss and skin problems. The good news is this disease isn’t life-threatening, it’s easy to diagnose with a blood test, and it’s fairly easy and inexpensive to treat. Treatment is typically a thyroid supplement taken daily.

Autoimmune thyroiditis is the most common cause of primary hypothyroidism in dogs. The disease has variable onset, but tends to clinically manifest itself at 2 to 5 years of age. Dogs may be clinically normal for years, only to become hypothyroid at a later date. The marker for autoimmune thyroiditis, thyroglobulin autoantibody formation, usually occurs prior to the occurrence of clinical signs. Therefore, periodic retesting is recommended.

The majority of dogs that develop autoantibodies have them by 3 to 4 years of age. Development of autoantibodies at any time in the dog’s life is an indication that the dog most likely has the genetic form of the disease. Using today’s technology only a small fraction of false positive tests occur.

As a result of the variable onset of the presence of autoantibodies, periodic testing will be necessary. Dogs that are negative at 1 year of age may become positive at 6 years of age. Dogs should be tested every year or two in order to be certain they have not developed the condition. Since the majority of affected dogs will have autoantibodies by 4 years of age, annual testing for the first 4 years is recommended. After that, testing every other year should suffice. Unfortunately, a negative at any one time will not guarantee that the dog will not develop thyroiditis.

The registry data can be used by breeders in determining which dogs are best for their breeding program. Knowing the status of the dog and the status of the dogs lineage, breeders and genetic counselors can decide which matings are most appropriate for reducing the incidence of autoimmune thyroiditis in the offspring.

Dogs should not receive any type of thyroid supplementation for 3 months prior to thyroid testing.  Dogs should not be tested within 30-60 days of vaccinations.

Thyroid Classifications
The method for classifying the thyroid status will be accomplished using state-of-the-art assay technology.
Indices of Thyroiditis

Free T4 (FT4)—this procedure is considered to be the “gold standard” for assessment of thyroid’s production and cellular availability of thyroxine. FT4 concentration is expected to be decreased in dogs with thyroid dysfunction due to autoimmune thyroiditis.
Canine Thyroid Simulating Hormone (cTSH)—this procedure helps determine the site of the lesion in cases of hypothyroidism. In autoimmune thyroiditis the lesion is at the level of the thyroid gland and the pituitary gland functions normally. The cTSH concentration is expected to be abnormally elevated in dogs with thyroid atrophy from autoimmune thyroiditis.
Thyroglobulin Autoantibodies (TgAA)—this procedure is an indication for the presence of the autoimmune process in the dog’s thyroid.
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All other results are considered equivocal.

OFA Thyroid Procedures
Purpose: To identify those dogs that are phenotypically normal for breeding programs and to gather data on the genetic disease autoimmune thyroiditis.
Examination and Classification
Each dog is to be examined by an attending veterinarian and have a serum sample sent to an OFA approved laboratory for testing according to the application and general information instructions.  All OFA forms and the OFA fee are submitted with the sample to the approved lab. Check with the referral laboratory for special sample handling and tests for registry purposes.
Certification
An OFA number will be issued to all dogs found to be normal at 12 months of age. Ages will be used in the certification process since the classification can change as the dog ages and the autoimmune disease progresses. It is recommended that reexamination occur at ages 2, 3, 4, 6, and 8 years.
Preliminary Evaluation
Evaluation of dogs under 12 months of age can be performed for private use of the owner since few dogs are already positive at that age. However, certification will not be possible at that age.
Dogs with Autoimmune Thyroiditis
All data, whether normal or abnormal is to be submitted for purposes of completeness.  Information on results determined to be positive or equivocal will not be made public without explicit written permission of the owner.
Thyroid Abnormalities
Thyroid abnormalities fall into several categories—two types will be defined by the registry.
Autoimmune Thyroiditis (known to be heritable)
Idiopathically Reduced Thyroid Function
Equivocal Results
Those dogs with laboratory results that are questionable, therefore not definitive, will be considered as equivocal. It is recommended that the test be repeated in three to six months.

https://ofa.org/diseases/thyroid/
Mast Cell Tumor
Mast Cell Tumors in Dogs
By Malcolm Weir, DVM, MSc, MPH; Krista Williams, BSc, DVM, CCRP; Christopher Pinard, DVM; Robin Downing, DVM, DAAPM, DACVSMR, CVPPDVM

What is a mast cell?

A mast cell is a type of white blood cell that is found in many tissues of the body. Mast cells are allergy cells and play a role in the allergic response. When exposed to allergens, mast cells release chemicals and compounds (called degranulation). One of these compounds is histamine. Histamine is commonly known for causing itchiness, sneezing, and runny eyes and nose – the common symptoms of allergies.
When histamine and the other compounds are released in excessive amounts (with mass degranulation), it can cause full-body effects, including anaphylaxis, a serious, life-threatening, allergic reaction. Other complications include delayed wound healing, bleeding disorders, and gastrointestinal (GI) ulceration.

What is a mast cell tumor?
A mast cell tumor (MCT) is a type of malignant (cancerous) tumor consisting of mast cells. Mast cell tumors typically form nodules or masses in the skin, but they can also affect other areas of the body, including the spleen, liver, intestine, and bone marrow. MCTs are the most common skin tumor in dogs (7%–21%). Most dogs with MCT (approximately 85%) only develop one tumor.

What causes this cancer?
Why a particular dog develops MCTs or any cancer is not straightforward. Very few cancers have a single known cause. Most seem to be caused by a complex mix of risk factors, some environmental and some genetic or hereditary. Several genetic mutations are known to be involved in the development of MCTs. One well-known mutation affects a protein, called KIT, that is involved in the replication and division of cells.
While any breed of dog can get MCT, certain breeds are more susceptible. MCTs are particularly common in boxers, English bulldogs, Boston terriers, pugs, golden retrievers, cocker spaniels, schnauzers, Staffordshire terriers, beagles, Rhodesian ridgebacks, Weimaraners, Chinese shar peis, and Labrador retrievers. Affected dogs are usually older (average of 8–9 years); males and females are equally affected.

What are the clinical signs of a mast cell tumor?
Mast cell tumors of the skin can occur anywhere on the body and vary in appearance. They can be a raised lump or bump on or just under the skin, and may be red, ulcerated, or swollen. While some may be present for many months without growing much, others can appear suddenly and grow very quickly. Sometimes they can suddenly grow quickly after months of no change. They may appear to fluctuate in size, getting larger or smaller, even daily. These size changes can occur spontaneously or when the tumor is agitated, which causes degranulation and subsequent swelling of the surrounding tissue due to the histamine release.
"While some may be present for many months without growing much, others can appear suddenly and grow very quickly."
When mast cell degranulation occurs, some chemicals and compounds can go into the bloodstream and cause problems elsewhere. Ulcers may form in the stomach or intestines, causing vomiting, loss of appetite, lethargy, and melena (black, tarry stools that are associated with bleeding). Less commonly, these chemicals and compounds can cause anaphylaxis, a serious, life-threatening allergic reaction.
Although very uncommon, MCTs of the skin can spread to the internal organs, causing enlarged lymph nodes, spleen, and liver, sometimes with peritoneal effusion (fluid build-up) in the abdomen, causing the belly to appear rounded or swollen.

How is this cancer diagnosed?
This cancer is typically diagnosed using fine-needle aspiration (FNA). FNA involves taking a small needle with a syringe and suctioning a sample of cells directly from the tumor and placing them on a microscope slide. A veterinary pathologist then examines the slide under a microscope. A tissue biopsy (surgically removed sample) can indicate how aggressive the tumor is, allowing your veterinarian to determine the best course of action.
MCTs have been classically called “the great pretenders” because they may resemble an insect bite, wart, allergic reaction, or other less serious skin tumors. Therefore, any abnormalities of the skin that you notice should be evaluated by your veterinarian.
Once a diagnosis of MCT has been made, your veterinarian or veterinary oncologist (cancer specialist) may recommend a prognostic panel on a tissue sample. This panel provides information on the genetic makeup and abnormalities of the tumor and provides valuable information that your veterinarian will use to determine the prognosis (the likely course of the disease) for your dog.

How does this cancer typically progress?

This tumor's behavior is complex and depends on many factors. Typically, when a biopsy sample is examined under a microscope, the pathologist can assess how aggressive the cancer is based on several criteria. The whole tumor is graded from I-III, with Grade I as much less aggressive than Grade III. Higher-grade tumors have a higher tendency to metastasize (spread to other parts of the body).
Another classification system is also used to classify MCTs as either high-grade or low-grade. The average survival time with high-grade tumors is less than four months, and with low-grade tumors it is more than two years.
Typically, the prognosis is less favorable if:
  • the patient is one of the susceptible breeds,
  • the MCT is located at a junction where the skin meets mucous membranes (e.g., the gums), or
  • the number of cells actively replicating is high, when viewed under the microscope.

How are mast cell tumors treated?
In lower-grade tumors with no evidence of spread, surgery is likely the best option. Surgery for lower-grade tumors provides the best long-term control, with chemotherapy rarely required. However, in higher-grade tumors, even without evidence of spread, a combination of surgery and chemotherapy is often recommended. Radiation therapy is another option if the mass is not in a suitable location for surgical removal or if the surgical removal is incomplete (with cancerous cells left behind).
"A veterinary oncologist is the best resource for determining what is best for your dog."
It is now known there is an underlying genetic basis for MCT, so drugs such as toceranib phosphate (Palladia®) are being designed to target the proteins associated with the development of cancer. Other drugs, such as tigilanol tiglate (Stelfonta®) are designed to cut off the tumor’s blood supply. In patients with non-surgical MCT, or recurrent MCT that has failed to respond to other chemotherapies, targeted therapy becomes a much more appealing option. A veterinary oncologist is the best resource for determining what is best for your dog.

Is there anything else I should know?
You should avoid palpating (feeling) or manipulating the tumor(s), given how reactive MCT is, with degranulation easily triggered with pressure. Do not allow your dog to chew, lick, or scratch it, as this may also trigger degranulation. Degranulation may lead to further itchiness, swelling, discomfort, or even bleeding. Your veterinarian may recommend using an Elizabethan collar (E-collar or cone). Supportive treatments such as diphenhydramine (Benadryl®) and omeprazole (Gastrogard®, Prilosec®) or famotidine (Pepcid®) are recommended for dogs with visible tumors to reduce the side effects of degranulation.

https://vcahospitals.com/know-your-pet/mast-cell-tumors-in-dogs
Entropion
​Entropion occurs when the eyelid rolls inward, allowing the eyelashes to make physical contact with the cornea and cause irritation. If the irritation continues without treatment, painful corneal ulceration will result. Entropion can occur in the upper or lower eyelid, and it can affect one eye or both. It is usually observed within a dog's first year of life.

A group of genes is responsible for the formation of the eyes and their surrounding structures, including the eyelids, the amount of facial tissue around the eyes and the size and shape of the eyes and their orbits. Hereditary entropion can occur if any one of these aspects does not develop just so and the eyelids are not properly anchored in their correct position.

Some signs of entropion include:
  • Squinting or blinking.
  • Yellow, white or green ocular discharge.
  • Excessive tearing.
  • Pawing at the eye.
  • Ocular inflammation.

Once your veterinarian has diagnosed entropion through a physical examination of your Weimaraner's eye, his initial goals will be to prevent secondary eye infection and to treat the eye if corneal ulceration has occurred. These goals are accomplished with the use of ophthalmological medication and, if your dog is persistently pawing or rubbing his eye, an Elizabethan collar. Surgically tacking the eyelids in place is another treatment alternative in some cases.

https://animals.mom.com/causes-of-weimaraner-eye-problems-12358824.html
Distichiasis
​One of the most common congenital ocular conditions, distichiasis, occurs when extra eyelash hairs grow out of one of the glands of the eye, called the meibomian gland, and cause irritation on the cornea. Distichiasis usually presents in dogs under 3 years of age. As in the case of entropion, untreated distichiasis results in corneal ulceration. Signs that your Weimaraner may have distichiasis include squinting or blinking, and excessive tearing.
Treatment for distichiasis involves destroying the follicles of the extra hairs so that regrowth does not occur. The veterinarian will employ one of three methods to accomplish this: electrolysis, surgical removal or cryosurgery, which freezes the follicles at the margin from which they are growing.

https://animals.mom.com/causes-of-weimaraner-eye-problems-12358824.html

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