Diabetes Insipidus

By Deborah S. Greco, DVM, PhD, DACVIM, Senior Research Scientist, Nestle Purina PetCare

The Pituitary Gland
Overview of the Pituitary Gland
Cushing Disease (Hyperadrenocorticism)
Nonfunctional Pituitary Tumors
Hirsutism Associated with Adenomas of the Pars Intermedia
Adult-onset Panhypopituitarism
Juvenile-onset Panhypopituitarism

Central diabetes insipidus is caused by reduced secretion of antidiuretic hormone (ADH). When target cells in the kidney lack the biochemical machinery necessary to respond to the secretion of normal or increased circulating levels of ADH, nephrogenic diabetes insipidus results. It occurs infrequently in dogs, cats, and laboratory rats, and rarely in other animals.

The hypophyseal form develops as a result of compression and destruction of the pars nervosa, infundibular stalk, or supraoptic nucleus in the hypothalamus. The lesions responsible for the disruption of ADH synthesis or secretion in hypophyseal diabetes insipidus include large pituitary neoplasms (endocrinologically active or inactive), a dorsally expanding cyst or inflammatory granuloma, and traumatic injury to the skull with hemorrhage and glial proliferation in the neurohypophyseal system.

Clinical Findings:

Affected animals excrete large volumes of hypotonic urine and drink equally large amounts of water. Urine osmolality is decreased below normal plasma osmolality (

300 mOsm/kg) in both hypophyseal and nephrogenic forms, even if the animal is deprived of water. The increase of urine osmolality above that of plasma in response to exogenous ADH in the hypophyseal form, but not in the nephrogenic form, is useful in the clinical differentiation of the two forms of the disease.

The posterior lobe, infundibular stalk, and hypothalamus are compressed or disrupted by neoplastic cells. This interrupts the nonmyelinated axons that transport ADH from its site of production (hypothalamus) to its site of release (pars nervosa).

This is based on chronic polyuria that does not respond to dehydration and is not due to primary renal disease. To evaluate the ability to concentrate urine, a water deprivation test should be done if the animal is not dehydrated and does not have renal disease. The bladder is emptied, and water and food are withheld (usually 3–8 hr) to provide a maximum stimulus for ADH secretion. The animal should be monitored carefully to prevent a loss of >5% body wt and severe dehydration. Urine and plasma osmolality should be determined; however, because these tests are not readily available to most practitioners, urine specific gravity is frequently used instead. At the end of the test, urine specific gravity is >1.025 in those animals with only a partial ADH deficiency or with antagonism to ADH action caused by hypercortisolism. There is little change in specific gravity in those animals with a complete lack of ADH activity, whether due to a primary loss of ADH or to unresponsiveness of the kidneys.

An ADH response test should follow to differentiate among conditions that may result in large volumes of urine that is chronically low in specific gravity but otherwise normal. These include nephrogenic diabetes insipidus (an inability of the kidneys to respond to ADH), psychogenic diabetes insipidus (a polydipsia in response to some psychological disturbance but a normal response to ADH), and hypercortisolism (which results in a partial deficiency of ADH activity due to the antagonistic effect of cortisol on ADH activity in the kidneys). This test also can be used to evaluate animals in which a water deprivation test could not be performed. Urine specific gravity is determined at the start of the test, desmopressin acetate is administered (2–4 drops in the conjunctival sac), the bladder is emptied at 2 hr, and urine specific gravity is measured at set intervals (4, 8, 12, 18, and 24 hr) after ADH administration. Specific gravity peaks at >1.026 in animals with a primary ADH deficiency, is significantly increased above the level induced with water deprivation in those with a partial deficiency in ADH activity, and shows little change in those with nephrogenic diabetes insipidus.

If osmolality is measured, the ratio of urine to plasma osmolality after water deprivation is >3 in healthy animals, 1.8–3 in those with moderate ADH deficiency, and 2 in animals with primary ADH deficiency, between 1.1 and 2 in those with inhibitors to ADH action, and 50%) during the first treatment day strongly suggests an ADH deficiency and a diagnosis of central diabetes insipidus or partial nephrogenic diabetes insipidus.

Diabetes insipidus also needs to be distinguished from other diseases with polyuria. The most common are diabetes mellitus with glycosuria and high urine specific gravity, and chronic nephritis with a urine specific gravity that is usually low and shows evidence of renal failure (protein, casts, etc).

Polyuria may be controlled using desmopressin acetate, a synthetic analogue of ADH. The initial dose is 2 drops applied to the nasal mucosae or conjunctivae; this is gradually increased until the minimal effective dose is determined. Maximal effect usually occurs in 2–6 hr and lasts for 10–12 hr. Water should not be restricted. Treatment should be continued once or twice daily for the life of the animal.

The Pituitary Gland
Overview of the Pituitary Gland
Cushing Disease (Hyperadrenocorticism)
Nonfunctional Pituitary Tumors
Hirsutism Associated with Adenomas of the Pars Intermedia
Adult-onset Panhypopituitarism
Juvenile-onset Panhypopituitarism

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Camilla Stefansdotter - Hundtränarblogg

Lyckliga hundar lyder gärna!

fredag 8 februari 2013

Diabetes hos hund

I januari skrev jag om sköldkörtelsjukdomar hos hund. Den här månadens reportage handlar om en annan sjukdom som ökar bland både katter och hundar - och människor - nämligen Diabetes. Den absolut vanligaste orsaken till att hundar får diabetes är övervikt. Det vanligaste symptomet är såna som man i vardagen ser hos hundar med just övervikt; trötthet. Andra symtpom är ökad törst och därmed ökad kissning (ökad urinmängd och frekvens av "toabesök"). Övervikt är ju ofta boven vid diabetes och ironiskt nog ökar även aptiten hos en hund med diabetes och hunden får också svårare att bli av med övervikten (enligt Agria) eller avmagrat rejält (enligt SLU).

Symptomen kan också vara varningstecken på andra sjukdomar än diabetes. Som hos människan kan ofta diabetes och ämnesomsättningsstörningar gå hand i hand. Hunden riskerar också gråstarr, njursvikt och ökad infektionsrisk.

Enligt Agria (som baserar sin information på de hundar som är försäkrade hos de) så är det oftast äldre eller medelålders hundar som får diabetes. Diabetes är vanligast hos tikar och tikar med diabetes måste alltid kastreras.

SLU:s hemsida har en bra beskrivning för nybörjare och ett avsnitt för vanliga frågor och svar där det bl.a. finns svar om ärftliget, ögonbesvär, livslängs och kostnader vid diabetesbehandling. Där finns även ett diabeteslexikon.

På Agrias hemsida kan man läsa om vad som täcks och vad som inte täcks av just deras försäkringar. T.ex. så täcks kastrationen av tikar med diabetes.

1 kommentar:

Som diabetiker själv tycker jag att det är bra skrivet. Men eftersom jag vet vilken svår sjukdom det är, så skulle jag också välja att avliva min hund. Det låter så lätt: Äta rätt på bestämda tider och ta sina sprutor. Men det är det inte. En liten extra sväng upp för trapporna kan ställa till det. En liten förkylning likaså. Och jag har lärt mig känna tecknen på både för högt och för lågt blodsocker. Men en hund kommer aldrig att kunna det. Och gå med den oron i magen varje dag som hundägare skulle inte jag mäkta med.

Hund diabetes

for diagnosing diabetics

Cushing's Disease (or syndrome) occurs when the adrenal glands produce excess amounts of cortisol, also known as cortisone. Cushing's is also known as hyperadrenocorticism. Hyper = above normal; adreno = relating to the adrenal glands; corticism = relating to the cortex & cortisol production. So, Cushings is a disease of elevated cortisol production by the adrenal cortex. Cushing's is much more common in dogs than in cats, so this page focuses on Cushings in dogs.

Reasons why the balance between ACTH and cortisol can be upset:

Pituitary gland tumor- also called Pituitary Dependent Hyperadrenocorticism (PDH) – This is the most common type of Cushings and it is found in about 85% of all cases. A tumor in the pituitary gland causes an increased production of ACTH, which in turn tells the adrenal cortex to produce more cortisol. The pituitary tumor can be very tiny or large and it can be benign or malignant. Poodles, terriers, German shepherds, Dachshunds, beagles, and boxers are more commonly diagnosed with PDH than other breeds.

Not all of these signs may be present, but as the disease progresses, they may become more pronounced or more signs may be seen. How common the sign is is shown for many of the items.

Increased appetite (polyphagia) - 80-95% will show this sign.
Increased drinking (polydypsia) and urination urination (polyuria) - due to interference with production of antidiuretic hormone. 80-90%.
Muscle weakness, lethargy, lack of activity - excess cortisol causes protein breakdown (catabolism) which leads to muscle weakness. 75-80%
Obesity, bloated abdomen, and "potbelly" - due to an increase of fat in the abdomen, increase in liver size (hepatomegaly), cronically full bladder, stretching of the abdominal wall, and the abdominal well becoming weaker. 90-95%
Panting - due to increased fat in the rib area (thorax), muscle weakness, and increased abdominal contents exerting pressure on the diaphragm. A "common" sign.
Poor hair coat, thinning hair (usually on the sides), hair does not regrow . "Common".
Skin infections - due to excess corticosteroids suppressing the immune system.
Thin skin, flaky or greasy skin & bruising - many processes that control skin structure and health are effected.
Fasting hyperglycemia (elevated blood glucose) - seen in 40-60% of dogs.
Insulin resistance - seen in up to 85% of dogs

So as you can, some of the signs of diabetes and Cushing's are identical.

Diagnosis of Cushing’s can be complicated and difficult. It is important to determine the type of Cushings (adrenal, pituitary, or iatrogenic) so that the appropriate treatment can be undertaken.

Routine lab tests are usually performed – complete blood count, biochemistry, urinalysis – and abnormalities in these tests may suggest Cushing’s.
An abdominal x-ray may show an enlarged liver or adrenal gland changes.
An abdominal ultrasound is often performed to evaluate liver and adrenal glands.
A urine test measuring cortisol to creatinine ration is sometimes performed, but it is not a very specific test because many health problems can cause abnormal test results. This is a screening test only – a negative result rules out Cushing’s. A positive result does not confirm Cushing’s and more tests will need to be performed.
More definitive diagnostic testing looks at adrenal gland function. Cortisol levels in the blood are measured before and after a drug that would normally effect cortisol levels is given. Two commonly used tests are the ACTH stimulation test and the Low-dose dexamethasone suppression test . During the ACTH stimulation test, a pre-test blood sample is taken, then a dose of ACTH is given. After 2 hours, cortisol levels are measured again. If the cortisol levels are higher than expected, Cushing’s may be diagnosed. Dexamethasone is a cortisone-type drug that provides negative feedback on the pituitary gland to turn off ACTH production, and that in turn causes a decrease in adrenal cortisol production. In a normal animal (non-Cushing’s) a dip in cortisol would be seen 8 hours after giving dexamethasone. If a pituitary tumor exists, no drop in cortisol level is seen during the low-dose dexamethasone test. During a high-dose dexamethasone suppression test , cortisol levels will be suppressed in about 75% of dogs with PDH and will not be suppressed in the remaining 25% of dogs with PDH or in 100% of dogs with an adrenal tumor.

Diabetic animals can pose a special problem when testing for Cushing's .

As you can see, diabetes and Cushing’s share many of the same signs (increased drinking, urination, eating, lethargy, enlarged liver). Uncontrolled diabetes can lead to complications that in turn cause increased cortisol levels and signs that are identical to Cushing’s. Testing and diagnosis of Cushing’s in a non-diabetic dog can be complicated, and it can be extremely complicated in a dog that has diabetes. The situation is even worse for a stressed or poorly controlled diabetic because stressed diabetics and Cushing’s dogs can have similar blood panel abnormalities and blood chemistry abnormalities. Plasma ACTH levels, the ACTH stimulation test results, and low-dose dexamethasone suppression test results can be abnormal in a stressed DM dog; the high-dose dexamethasone suppression test results can be abnormal in an unregulated DM dog. There are clinical signs that help distinguish the two disease so your general vet and specialist must consider the “whole picture” of your dog’s physical condition and test results.

Cushings caused by a pituitary gland tumor (PDH) . Surgery to remove a tumor in the pituitary gland is very risky and is rarely performed. Controlling the growth of the tumor may be attempted with radiation. Medication is used to control this type of Cushings.

The drug most commonly used is o,p’DDD, also know as Lysodren or mitotane. This drug works by destroying the cortisol-producing cells in the adrenal cortex. Careful monitoring is required during treatment to be sure that too much drug is not given and too many adrenal cortex cells are not killed. Too much drug would result in too little cortisol being produced (resulting in Addison’s disease, the opposite of Cushing’s). Treatment involves an “induction” or “loading” phase where Lysodren is given on a daily basis. This loading phase rapidly brings the some of the Cushing’s symptoms under control. Owners are usually instructed to closely monitor their dog’s eating and drinking. When drinking is normal (about 50-60 mL water per pound body weight per day) induction is complete and the “maintenance” phase begins. In maintenance, Lysodren is given two to three times a week to keep the cortisol levels within acceptable levels. ACTH stimulation tests are repeated every three to four months to ensure adequate control and dosing.

Anipryl or L-deprenyl is another drug that is used to treat pituitary-dependent Cushing’s. It was approved for use in the United States in 1997. Anipryl is used to treat cognitive dysfunction in dogs and has shown to be effective in clinical trials in controlling Cushing’s in about 70% of dogs. The drug works by influencing dopamine concentrations (a chemical used to by brain cells to communicate with each other), which in turn influences production of ACTH by the pituitary gland. The effectiveness of this drug is controversial, but since the side effects are less severe than those of Lysodren, it is used in some dogs, especially those who are older or have multiple health problems. Anipryl does not involve an induction or loading phase.

Ketoconazole is another drug used to treat PDH or dogs who have adrenal gland tumors. It works by blocking production of cortisol in the adrenal gland. It has the potential to damage the liver.

Cushings caused by an adrenal gland tumor may be treated surgically or with Lysodren or Ketoconazole . Surgery is difficult and may have many complications. Removal of the adrenal gland may require life-long supplementation with glucocorticoids and mineralocorticoids (both normally produced by the adrenal gland).

Iatrogenic Cushing’s – treatment requires slowly discontinuing the cortisone that is being given. This must be done in a controlled manner so that other problems do not occur. The disease that is being treated with cortisone will probably recur. If damages has been done to the adrenal glands, that will need to be addressed.

With a possible diabetic and/or Cushoid animal there are three different scenarios that can occur:

Your animal may be both diabetic and have Cushing's. As the Cushing's is brought under control your animal's insulin needs will be greatly reduced. Therefore it's very important to monitor your animal's blood glucose until the correct maintenance dose is determined so an overdose of insulin doesn't happen.

You can read Kiri's story - she lived with diabetes, Cushing's and hypothyroidism for over 6 years.

Your animal may only have Cushing's. The increased blood glucose levels may be a side effect of the Cushing's and once the Cushing's is brought under control there may be no need for insulin anymore.

Your animal may only be diabetic. The Cushing's tests may have been altered by one of the previously mentioned causes, resulting in false positive results.

With a diabetic it is very important to take every means possible to stabilize them on their insulin before a Cushing's test is even tried. Some questions to ask your vet:

If your animal is unregulated--ask your vet at what amount of insulin they would consider your animal to be needing to bring the glucose levels under control.
If your animal has only been on one type of insulin, are they willing to try another type.
Would a change in food, feeding schedule, or amount of food make a difference.

Updated April 2006

This site is for information purposes only. Please consult your veterinarian.

Sukkersyge

Hvad er sukkersyge hos hunde?

Sukkersyge er en tilstand, hvor blodets sukkerindhold forhøjes på grund af problemer med det sukkerregulerende stof insulin. Sygdommen findes i flere forskellige former:

Type 1 diabetes skyldes en nedsat produktion af insulin i bugspytkirtlen.
Type 2 diabetes skyldes, at kroppens insulin ikke har den effekt, som det skal have. Denne type sukkersyge kaldes også insulinresistens.
Sekundær diabetes er sukkersyge, der opstår som følge af en anden sygdom eller af medicinsk behandling.

Hos hunde er type 1 diabetes langt den hyppigste.

Hvad er symptomerne på sukkersyge?

Øget drikkelyst og tissetrang
Vægttab trods øget appetit
Nedsat syn og grålig uklarhed i øjets linse (grå stær/katarakt)

Hvordan kan din dyrlæge stille diagnosen sukkersyge?

Dyrlægen kan undersøge for sukkersyge på urin- og blodprøver. Når en hund har sukkersyge, udskilles der sukker i urinen, og dette kan afsløres ved at dyppe en sukker-urinstix i urinen. Hvis urinprøven er positiv, vil dyrlægen tage en blodprøve for at måle blodets sukkerindhold. Blodsukkeret afhænger af, hvornår hunden har spist, og af andre faktorer som stress og medicin. Dyrlægen kan derfor komme frem til en mere præcis diagnose ved at måle blodets indhold af fructosamin. Testen viser, om blodsukkeret har været forhøjet gennem længere tid.

Hvordan behandles sukkersyge?

Hos hunde er type 1 diabetes den hyppigste form for sukkersyge, og behandlingen består som regel i diæt og indsprøjtninger med insulin.

Overvægtige hunde med sukkersyge bør tabe sig ved hjælp af diæt og øget motionering. De diæter, der oftest anvendes ved sukkersyge, er færdigfremstillede specialdiæter.

Insulinindsprøjtninger kan være en krævende opgave for hundeejere, og det er vigtigt nøje at overholde dyrlægens anvisninger om dosis og behandlingsintervaller. Insulinindsprøjtninger skal altid gives i forbindelse med et måltid.

Det er også vigtigt at få foretaget kontrolblodprøver hos dyrlægen, så man sikrer den rette insulinmængde. Hvis hunden får for meget insulin, kan den få insulinchok. Symptomerne på insulinchok kan være slaphed, vaklende gang og evt. bevidstløshed. Ved mistanke om insulinchok skal man give hunden druesukker eller en anden sukkeropløsning ind i munden og kontakte sin dyrlæge.

Hvordan er fremtiden for din hund, hvis den har sukkersyge?

Hvis sukkersygen er under kontrol, og behandlingen er startet tidligt i sygdomsforløbet, kan hunde med sukkersyge blive lige så gamle som hunde uden sukkersyge. Normaliseres hundens drikkelyst, er det et umiddelbart tegn på, at sukkersygen er under kontrol. Hvis sukkersygen er ude af kontrol, kan den medføre blindhed som følge af grå stær.

Sukkersyge kan også forårsage lidelser i lever, bugspytkirtel og nyrer.

Hvorfor får hunde sukkersyge?

Hunde kan udvikle type 1 diabetes efter forskellige sygdomme i bugspytkirtlen.

Der kan også være tale om, at de celler, der producerer insulinen i bugspytkirtlen simpelthen udmattes.

Type 2 diabetes kan skyldes flere ting, blandt andet overvægt.

Sekundær diabetes kan ligeledes skyldes flere ting. Hyppige årsager hos hunde er behandling med medicin som prednison-tabletter og p-sprøjter , men sekundær diabetes kan også skyldes sygdomme som cushings syndrom og pyometra. De hunlige kønshormoner kan også påvirke sukkerreguleringen, så hvis en tævehund får sukkersyge, vil dyrlægen ofte anbefale, at hunden bliver steriliseret.

Af dyrlæge Henning Ingeman. Hvad er overvægt hos hunde? Overvægt betyder, at kroppen indeholder for meget fedt - enten i vævene eller samlet som depoter. Hvad er symptomerne på overvægt? De synlig…

Overvægt hos hunde

af dyrlæger Henrik Strange og Kirsten Boeck Cushings syndrom er betegnelsen for et sygdomskompleks, der opstår, når organismen igennem længere tid udsættes for en øget mængde binyrebarkhormon. Disse …

Hvad er grå stær hos hunde? Grå stær er en sygdom, hvor der optræder uklarheder i linsen i hundens øje. Sygdommen benævnes også Kataract. Hvad er symptomerne på grå stær? Pupillerne på hunde, der …

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Hund diabetes

Diabetes insipidus (DI) is a disorder of water balance. The animal is unable to concentrate urine, so the urine volume is very high and the urine is dilute. "Insipid" means tasteless -- referring to the dilute urine. This disease is rare in both dogs and cats. The condition is usually permanent, and the prognosis is good. Without treatment, dehydration leads to stupor, coma, and death. This is a completely different disease from Diabetes Mellitus (DM), a disorder of sugar metabolism involving the hormone insulin. We include the information here because people are often looking for resources and we had some owners of pets with DM who also have experience with DI.

Types of diabetes insipidus

Central Diabetes Insipidus - caused when the pituitary gland does not secrete enough antidiuretic hormone (ADH) [also called vasopressin]. This type of DI may be the caused by a congenital defect, trauma, a tumor on the pituitary gland, or unknown causes.

Nephrogenic Diabetes Insipidus - caused when the kidneys do not respond to the ADH that is produced by the pituitary gland. This type of DI may be caused by a congenital defect, drugs, or caused by other metabolic disorders

Diagnosis

Diagnosis includes ruling out other diseases such as hyperadrenocorticism (Cushing's disease), diabetes mellitus, hyperthyroidism (in cats), renal failure, liver disease, pyometra (infection of the uterus), and other disorders.

Images of the pituitary gland may be taken to determine if there is a tumor.

A water deprivation test or an ADH trial with DDAVP may be done. These tests determine if the animal is able to produce more concentrated urine as water is withheld or following the injection of DDAVP (the drug used to treat DI).

Treatment

Central DI is treated with desmopressin , a drug that mimics the actions of ADH. It is available under the trade name DDAVP and as a generic. DDAVP is available in several formulations: as a nasal spray pump; as a liquid for use with rhinal tube; as an injectable liquid; and in tablets. Most pet owners use the nasal spray or rhinal liquid formulations and use them as eye drops, nose drops, or inject it subcutaneously.

Nephrogenic DI is commonly treated with thiazide diuretics. These drugs help to concentrate the urine. An oral drug called chlorothiazide acts on the kidneys to help concentrate the urine. Other treatments may include chloropropamide, which increases the effects of ADH on the kidney. But chloropropamide is not always successful. Nonsteroidal anti-inflammatory drugs may be used in dogs.

No therapy may be chosen, and the pets can survive as long as plenty of water is always available . You CAN NOT limit their water intake . When Sonny's DI first started, he would lay in front of his water bowl and just drink and drink and drink. Of course he also had to go outside very frequently, and his urine was like water - literally.

Ziggy, Puff, and Simone are three kitties with DI. Ziggy also has diabetes mellitus (yes, both diseases can occur together . remember they are totally separate diseases).

I did lose a few drops (expensive and precious, I might add) the first few times I used it. The drops come out of the bottle very easily, so I make sure I have Ferris' eye ready to receive the drop before I even turn the bottle over.

I have tried other eye drop bottles but found the Clear Eyes one to be sleekly designed and thus I can get every drop of Desmopressin out of it.

References

The 5 Minute Veterinary Consult: Canine and Feline Larry Tilly and Francis W.K. Smith, Jr. 1997.
Veterinary Drug Handbook. Second Edition. Donald C. Plumb. 1995.
Pocket Companion to the Fourth Edition of Textbook of Veterinary Internal Medicine Stephen J. Ettinger.
The Cornell Book of Cats : A Comprehensive and Authoritative Medical Reference for Every Cat and Kitten. Mordecai Siegal (Editor), et al.1997.

Updated June 2002

This site is for information purposes only. Please consult your veterinarian.

Hund diabetes

Bei dem zentralen Diabetes insipidus (Syn. Diabetes insipidus neurohormonalis) ist die Ursache ein Fehlen oder eine unzureichende Produktion des "antidiuretischen Hormons" ADH (Syn.: Vasopressin) im Hypothalamus, ein fehlender Transport des ADH vom Hypothalamus über den Hypophysenstiel in die Hypophysenhinterlappen oder ein Fehlen der Speicherung oder ausbleibende Sekretion des ADH im Hypophysenhinterlappen. Das ADH wirkt auf die Nierentubuli antidiuretisch - es wirkt also der Harnausscheidung entgegen - und führt zur Bildung eines konzentrierteren Urins. Für den ADH-Mangel können ein Schädel-Hirn-Trauma mit Abriss des Hypophysenstiels, eine Zyste, eine Operation, eine Entzündung, eine infiltrative Erkrankung, eine Blutung, ein Infarkt oder ein Tumor im Hypothalamus oder der Hypophyse verantwortlich sein. Aber auch ein familiärer Diabetes insipidus mit einem congenitalen, autosomal-dominant vererbten Erbfehler ist möglich als Ursache. Bei einem Drittel aller Diabetes insipidus-Fälle ist die Ursache nicht bekannt und es wird eine Autoimmunerkrankung mit Autoantikörper gegen die vasopressinproduzierenden Zellen vermutet.

Bei beiden Formen scheidet die Niere vermehrt Wasser aus. Wenn Wasser nicht genügend durch Trinken ersetzt wird, kommt es zu einer Konzentrierung von Natrium im Blut (Hypernatriämie), einer sogenannten hypertonen Dehydration.

Das auffälligste Symptom für den Hundebesitzer ist ein, oft plötzlich einsetzender, unstillbarer Durst (Polydipsie) verbunden mit einer stark erhöhten Ausscheidung von Urin (Polyurie).

Die Hunde scheinen ihren Durst kaum stillen zu können und reagieren bei Wasserentzug schnell mit Anzeichen einer Dehydration. Anzeichen einer Dehydration sind, je nach Schweregrad

- der Speichel wird zunehmend zähflüssiger

- angehobene Hautfalte verstreicht nur langsam, bis hin zum völligem „stehen bleiben“ der Falte

- schwacher Puls im fortgeschrittenen Stadium

- Bewusstseinsstörungen bis hin zum Koma

- Der Harn verändert sich in eine unkonzentrierte Flüssigkeit und erscheint „dünner“ als normal, weniger gefärbt und geruchloser.

Wie alles begann und Leben mit der Krankheit:

Eines Tages wurde Nigel krank. Er war apathisch und fühlte sich nur wohl, wenn er stundenlang in der prallen Sonne liegen konnte. Stellte ich ihm einen Sonnenschirm an seinen Liegeplatz, dann schob er sich Zentimeter für Zentimeter wieder in die Sonne. Es dauerte lange, bis er endlich wieder richtig auf den Pfoten war. Kurz darauf begann er Tag für Tag seinen ganzen Napf (1 ½ Liter) leer zu trinken. Hat mich zwar gewundert, aber nicht beunruhigt. Nach wenigen Tagen musste ich innerhalb kürzester Zeit nachfüllen und Nigel trank wieder alles leer. Schließlich begann er zu betteln, weil er noch mehr haben wollte. Gleichzeitig wollte er das viele Wasser umgehend wieder los werden.

Ich brachte ihn zum Tierarzt, denn das Ganze sah irgendwie nach Diabetes mellitus aus. Der Zuckertest fiel negativ aus und ich zog mit langem Gesicht wieder ab. Als Nigel dann pro Tag mehr als fünf, mitunter sogar über zehn Liter trank packte mich die Panik. Vor allem, weil ich keine Nacht mehr durchschlafen konnte. Ständig weckte er mich, weil die Blase drückte. Etwa alle zwanzig Minuten kam er winselnd an mein Bett. Ich war körperlich und nervlich völlig am Ende. Also drängte ich auf eine große Diagnose, die dann das ganze Ausmaß der Katastrophe zu Tage brachte. Der niederschmetternde Befund lautete: Diabetes insipidus.

Nigel bekommt seitdem jeden Abend 2 Tropfen Minirin in die Augen. Damit trinkt er etwas weniger, schläft dann ungefähr zwei Stunden am Stück. Ich habe mich inzwischen daran gewöhnt, 2 x oder öfter pro Nacht aufstehen zu müssen. Denn trotz allem trinkt er noch immer mindestens vier Liter. Und regt er sich über irgendetwas auf, dann kann es durchaus noch ein Napf mehr sein.

Inzwischen leben wir vier volle Jahre mit der Krankheit. Das heißt: er mit der Krankheit, ich mit den Folgen. Eine noch höhere Medikamentendosis ist in sofern nicht sinnvoll, da Nigel dann benommen wirkt und teilnahmslos in der Ecke liegt. Solange er keine Schmerzen, guten Appetit und Freude am Leben hat nehme ich gern allen Stress auf mich. Zugleich geht die Behandlung richtig ins Geld. 2,5 ml Minirin kosten durchschnittlich 50 Euro, reichen aber nicht mal einen Monat, dann kommen noch die Tierarzt- und Rezeptkosten. Ich weiß oft nicht wie es weitergehen soll, nur, dass ich für Nigel mein letztes Hemd weggeben würde.

Schmerzen hat Nigel definitiv nicht. Ich gehe mit ihm regelmäßig alle 6 Wochen zum Arzt, schon weil wir dann ein neues Rezept für die nächsten 1 1/2 Monate brauchen. Er fühlt sich oft schlapp, was bei seinen Diagnosen durchaus normal ist. Wir gehen also nur noch kurze Runden. Sollte sich sein Zustand so verschlimmern, dass er Schmerzen bekäme oder er das Fressen verweigern würde, dann wäre ich die Letzte, die ihn leiden ließe. Ich hoffe inständig, dass mir das erspart bleibt und dass ich ihn irgendwann am Morgen leblos finde, weil er friedlich in der Nacht für immer eingeschlafen ist.

Niemand kann mir wirklich erklären, wie die Nieren und das Herz diesen Marathon durchhalten.

Da fliegt die Menschheit zum Mond, verpulvert Milliarden in sinnlosen Kriegen und ist einfach nicht in der Lage ein wirksames Medikament zu entwickeln, welches Diabetes insipidus dauerhaft in den Griff bekommt.

Nigel ist ein Phänomen. ich wundere mich immer wieder, wie selbstverständlich er schon seit so vielen Jahren mit all seinen Handicaps lebt.

Nun steuern wir gemeinsam seinen 14 Geburtstag im Juli an. Immerhin werden andere Hunde selbst bei bester Gesundheit nicht so alt.

opheimblog

blandt andet om at have hund med diabetes

Den dag jeg opdagede, at hunde kan få diabetes

Ved du, at hunhunde kan få hormonelt betinget diabetes? Jeg vidste det ikke, men jeg fandt ud af det da Ciewie, min ene border collie, fik det.

Sommeren 2012 – En søndag eftermiddag da vi var på vej i skoven med hundene, ville Ciewie pludselig ikke gå mere. Vi var lige kommet ind i skoven, 500 meter fra vores hjem, så det var ikke distancen, der var problemet. Hun lagde sig ned og nægtede simpelthen at gå længere. Min mand måtte bære hende hjem. Vi regnede med at hun måske var lidt overanstrengt i benene, hun var jo trods alt 9 1/2 år. Men humør og energi var bare væk.

Næste dag blev hun undersøgt af dyrlægen, som konstaterede for lavt stofskifte og voldsom diabetes. Med rigtig dårlig samvittighed fandt vi nu ud af, at flere af de skavanker, vi havde forklaret med høj alder og almindeligt slid pga agility var relateret til stofskiftesygdom.

Hun fik stofskiftemedicin, så var der sådan set styr på den del. Så manglede vi bare at få styr på det med diabetes…

Background

My name is Glenn Kardel. I have polyglandular autoimmune syndrome type II, frequently referred to as Schmidt's syndrome. The classic manifestations of this syndrome are adrenal insufficiency plus autoimmune thyroid disease and/or insulin dependent diabetes mellitus. I have all three of the above conditions: Addison's disease, hypothyroidism, and type I diabetes.

The goals of this site are:

Provide information about Addison's disease, type I diabetes, and the interaction between the two conditions.
Share the techniques I've used to control my diabetes in the face of the added pressure of Addisons.
Provide an opportunity for others to share information, experiences, and advice on Addison's disease and diabetes.

Please consult your physician before implementing any of the

Canine and feline diabetes

Diabetes can be managed successfully with insulin therapy and attention to diet and exercise. Effective diabetes treatment of pets, will restore the quality of life of dogs and cats with diabetes mellitus.

This web site is intended for owners of dogs and cats with diabetes. The site provides disease information on diabetes mellitus. Advice about insulin treatment and suitable diets for managing canine and feline diabetes can also be found.

Answers to questions about diabetes in dogs, canine diabetes treatment and the use of insulin.

Answers to questions about diabetes in cats, feline diabetes treatment and the use of insulin.

In some cases in cats, diabetes may no longer need treatment with insulin but can eventually be stabilised with careful monitoring of diet.

Videos and diagrams describing how to give an insulin injection for the treatment of canine or feline diabetes.

Diabetes insipidus

Diabetes insipidus is an endocrine disease characterized by vasopressin dysregulation [1] , excessive polyuria, polydipsia, and the absence of hyperglycemia and glucosuria.

Diabetes insipidus is entirely different to diabetes mellitus and has two presentations:

Central diabetes insipidus - due to hypothalamic-pituitary trauma [2] , post-transsphenoidal surgery for correction of hyperadrenocorticism[3] , dorsally expanding cysts, inflammatory granuloma, lymphocytic hypophysitis [4] , congenital malformation and neoplasms such as craniopharyngioma, pituitary chromophobe adenoma[5] , pituitary chromophobe adenocarcinoma [6] and metastatic tumors such as metastatic mammary carcinoma, lymphoma[7] , malignant melanoma and pancreatic carcinoma

- results in lack of vasopressin (antidiuretic hormone) production

Nephrogenic diabetes insipidus - due to nephron impairment as a result of genetic or acquired disease

- results in lack of vasopressin sensitivity by nephrons

Central diabetes insipidus (CDI) results in absolute or partial loss of vasopressin (antidiuretic hormone; ADH) production by the central nervous system, causing persistent hyposthenuria (urine specific gravities ≤ 1.006) and severe diuresis, even with severe dehydration.

Nephrogenic diabetes insipidus (NDI), which may be primary (familial; X-link in humans [8] ) or secondary (acquired), results from impaired responsiveness of the nephron to the actions of vasopressin. Plasma vasopressin concentrations are normal or increased in animals with this disorder. Primary NDI is a rare congenital disorder of dogs resulting from a congenital defect involving the cellular mechanisms responsible for insertion of aquaporin-2 water channels into the luminal cell membrane.

Acquired secondary NDI includes a variety of renal and metabolic disorders which interfere with the normal interaction between vasopressin and its renal tubular receptors, affect renal tubular cell function, or decrease the hypertonic renal medullary interstitium, resulting in a loss of the normal osmotic gradient. These disorders are listed below as differential causes od secondary nephrogenic diabetes insipidus.

Clinical signs

Common clinical signs in dogs with diabetes insipidus is polyuria and polydipsia.

In dogs with primary (familial) NDI, clinical signs typically become apparent by the time the dog is 8 to 12 weeks of age, with symptoms of excessive thirst, urination and difficulty in house-breaking [9] .

Neurological signs have been reported, due to electrolyte disturbances or pituitary neoplasia, with depression and seizures observed in rare cases [10] .

Water consumption can often be extreme, sometimes exceeding 800 ml/kg/day, with compensatory urine production exceeding 50 mL/kg/day, .

Blood tests are usually within normal limits apart from a polydipsia-induced hyponatremia.

Urinalysis usually shows hyposthenuria or isosthenuria, and hematuria is not regularly observed unless underlying concurrent nephropathy present. Urine culture and sensitivity is required to eliminate underlying cystitis or pyelonephritis.

Diagnosis is initially one of exclusion of other diseases (see list below), followed by low dose dexamethasone suppression test, water-deprivation tests, vasopressin therapy and central nervous imaging studies to diagnose central diabetes insipidus. The main diagnostic dilemma is differentiating between central diabetes insipidus, psychogenic polydipsia and nephrogenic diabetes insipidus.

Standard hematology and biochemistry assessments are usually unrewarding and in most cases, plasma concentrations of thyroid-stimulating hormone, thyroxine, growth hormone, insulin-like growth factor-1, adrenocorticotropic hormone and plasma α-melanocyte-stimulating hormone are within normal reference levels.

A response to synthetic vasopressin therapy (desmopressin; 0.1 - 0.2 mg orally every 8 hours) or urinary aquaporin-2 excretion testing may help clarify nephrogenic from central diabetes insipidus [11] . Other tests include vasopressin measurements during hypertonic saline infusion [12] . However, the occurrence of spontaneous vasopressin pulses may hamper the interpretation of the curve describing the relationship between plasma osmolality and plasma vasopressin concentration during osmotic stimulation [13] .

An increase in urine specific gravity by 50% or more, compared with pre-treatment specific gravities, supports the diagnosis of CDI, especially if urine specific gravity exceeds 1.030. There should be only minimal improvement in dogs with primary NDI. Dogs with psychogenic water consumption may exhibit a mild decline in urine output and water intake because the chronically low plasma osmolality tends to depress vasopressin production.

Pituitary or hypothalamic neoplasia should be considered in older dogs diagnosed with CDI. A renal biopsy may be warranted in the older dog tentatively considered to have primary NDI.

A differential diagnosis would include:

Diabetes mellitus - osmotic diuresis

Chronic renal disease osmotic diuresis

Primary renal glycosuria - osmotic diuresis

Post-urolithiasis diuresis - osmotic diuresis, down-regulation of aquaporin-2

Pyometra - bacterial endotoxin-induced reduced tubular sensitivity to vasopressin

Escherichia coli septicemia - bacterial endotoxin-induced reduced tubular sensitivity to vasopressin

Hypercalcemia - interference with action of vasopressin on renal tubules

Hepatitis - loss of medullary hypertonicity, impaired hormone metabolism

Hyperadrenocorticism - impaired tubular response to vasopressin

Hyperaldosteronism - impaired tubular response to vasopressin

Pyelonephritis - bacterial endotoxin-induced reduced tubular sensitivity to vasopressin, damaged countercurrent mechanism

Fanconi's syndrome - osmotic diuresis

Hypokalemia - down-regulation of aquaporin-2, loss of medullary hypertonicity

Hyponatremia - loss of medullary hypertonicity

Hypoadrenocorticism - loss of medullary hypertonicity

Hyperthyroidism - loss of medullary hypertonicity

Leptospirosis - action unknown

Polycythemia - action of natriuretic peptide

Pheochromocytoma - excessive catecholamines

Portosystemic shunt - loss of medullary hypertonicity, increased GFR

Dwarfism - action unknown [14]

Acromegaly - osmotic diuresis due to diabetes mellitus [15]

Psychogenic polydipsia - loss of medullary hypertonicity

Intestinal leiomyosarcoma - impaired tubular response to vasopressin [16]

Very low protein diet - loss of medullary hypertonicity

Gastrointestinal disease (e.g. ulcerative colitis) [17]

X-link hereditary nephropathy - loss of medullary hypertonicity, increased GFR

Renal dysplasia - loss of medullary hypertonicity, increased GFR

With hypophyseal tumors, a transsphenoidal hypophysectomy is usually recommended. In dogs which develop CDI secondary to hypophysectomy may spontaneously resolve within 2 - 4 weeks [18] [19] .

Prophylactic use of desmopressin at 4 μg twice daily has been shown effective at minimizing onset of CDI [20] .

In dogs with primary NDI, long-term therapy with low sodium diet, unlimited water access, hydrochlorothiazide (used to increase urine osmolality) [21] or desmopressin tablets or nasal spray.

Haushund

понедельник, 18 июня 2018 г.

hund_diabetes

Diabetes Insipidus