Feline Diabetes Message Board

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Diabetes mellitus is one disease that can attack dog or cat and can occur at any age. Diagnosis of diabetes mellitus can be confirmed by clinical and laboratory examination of the glucose content in the blood. This study aims to evaluate blood glucose levels in pet cats aged five years or more. The study was conducted by taking blood samples from 25 cats with different races and sexes that were different from the age of five years. Before blood sampling, cats are identified for their health through clinical examination. Blood samples were collected through the cephalic vein using an aseptic 25 G needle, dripped onto the EasyTouch® GCU strip then after 10 seconds blood glucose levels were read on the screen. The data obtained were analyzed statistically by t test. The results showed that the average blood glucose level in cats was 114.72 ± 23.73 (at meal time) and 107 ± 21.37 (at meal time). Based on the results of this study concluded that blood pet blood glucose levels are in the normal range. There was no significant difference (P <0.05) between cat blood glucose levels before and after meals.

Diabetes cases that occur in cats are smaller than dogs. However, when that happens, cat’s diabetes can be more difficult to overcome.

When a diabetic cat consumes berglukosa foods, his body can not process glucose properly, so it can cause a buildup of sugar in the bloodstream. Finally, high blood sugar leads to sugar getting into the cat’s urine. The consequences will sometimes threaten the life of the cat.

General Profile

Diabetes can occur in cats of all ages, although most occur after cat age more than six years.

Some cats may be dependent on insulin and may be assisted with lifelong insulin therapy.
Other cats can be non-insulin dependent and only require insulin when stressed. Usually, these cats regain their balance after the stressful conditions end.

History and Physical Examination

Common signs of diabetes are thirst and increased urination, increased appetite and weight loss. However, these signs can occur in cats that have other diseases.

You may see signs of this kind of illness:

  • Gag
  • Diarrhea
  • Loss of appetite
  • Respiratory difficulties
  • Weakness
  • Difficult urination

The above symptoms may appear suddenly for several days, or for several months.

Diagnosis

In many cases, cats with diabetes can be difficult to diagnose because they also suffer from other diseases simultaneously or diseases that can be similar to diabetes.

Some of these diseases are hyperthyroidism, kidney disease or failure, adrenal gland disease, gastrointestinal disease, cancer, liver disease or failure, and some types of drug therapy.

To diagnose cat diabetes, the veterinarian uses the following tests:

Blood Sugar Level

Test results showing a blood sugar level of more than 200 indicate the possibility of diabetes.

However, diabetes because of its own stress can produce higher blood sugar levels (up to 300-400) in cats without diabetes, this is due to the adrenaline waves.

  • Glucose Urine: Diabetes cats have sugar in their urine. They can also have ketones in the urine, which results from the metabolism of damaged fatty acids. Cats without diabetes are under stress may also have some glucose in the urine, but its only temporary.
  • Chemical Blood: Lipemia, which increases fat in the blood can be evidence of liver dysfunction.
  • Urinalysis: In addition to sugar and ketones, there may be signs of bladder infection.

Treatment

Insulin injections are still the most acceptable way to treat insulin-dependent diabetes cats.

Initially, diabetic cats are hospitalized and arranged for three to four days. During that time, several blood sugar tests were administered to establish the right schedule for the cat.

The goal of treatment is to keep blood sugar levels between 100 and 200 in each 24-hour period and to correct or relieve symptoms.

Often, many hospitals monitor serial blood sugar and make adjustments in the required insulin dose.

The nature of the cat easily stress can make the management of diabetes becomes difficult. Because cats have a strong stress response, it can be difficult to interpret their blood sugar test.

Caring For A Cat With Diabetes

Cats with diabetes have the potential to lose significant weight. Therefore, cats will need solid diet energy until their weight will be normal. For obese diabetic cats, it is advisable to enroll the cat on a weight-loss program under the guidance of a veterinarian. This is because obesity in cats will interfere with the effects of insulin to be given. .

Research has shown that low carbohydrates and high protein diets can help reduce insulin requirements and improve diabetes management.

In addition to the diet program, you can see several types of commercial food for cats that are available in the market. Some commercial pet food manufacturers produce foods with low-carbohydrate dietary recipes that are suitable for use in diabetic cats.

It is advisable for your cat to keep the diet consistently both in terms of what is eaten as well as meals and so on. Changing your diet can disrupt the stabilization of diabetes. However, you do not need to set strict cat eating time. If your cat has been applying the diet consistently, you can provide additional food outside of the planned time.

For advanced therapy, your veterinarian may suggest to provide insulin therapy at the beginning of the program. Insulin in cats affected by diabetes is given by injection under the skin of the nape.

Cats injected with insulin will most likely experience good stability. There are several therapeutic programs, which involve injection once or twice daily. The injection site should be changed daily to reduce scarring or injection site reactions that may limit the absorption of insulin. A special insulin syringe with a very fine needle is used so that the cat will not feel the injection process.

Many veterinarians often recommend a diabetic cat to be given food before they receive insulin so the cat is unaware of the injection while eating.

The prospect of cats to survive with diabetes mellitus varies greatly depending on how old they are. Some non-complicated cats will be easier to stabilize than those with other diseases. In one study, the mean survival time for a diabetic cat was about 2 years after diagnosis. Many diabetic cats have excellent quality and experience increased potential after following treatment.

Case Study 1

Bubu, Domestic Short Hair Cats, 7-year-old males come on January 15, 2009 with complaints of difficulty for urination. urine mixed with red blood.

Xray shows the presence of sediment in the bladder and kidney (the bottom of the bladder, radio-opaque look). Ultrasound (ultrasonoghraphy) shows hyper-echoic, indicating sediment in the bladder (sediment appears to float). Urine test with reagent strip on the first day (15/1) obtained Protein: 300 (++) and Glucose: 250 (+). Treatment: Clavulox and Dexamethasone injection for 6 days, the feed is converted to c / d diet (science plan *), fluid therapy and duphalyte (amino acid) for 6 days, diazepam on the first day. With diazepam is expected to relax the spinchter from the urine. the second day, urine clear yellow.

The third day, catheterization (with sedative Zoletil *) is done because the bladder still feels great. The use of Zoletil as an anesthetic here is due to its properties light, and includes short acting. Certainly lighter than combination ketamine-xylazine.

Urine that came out mixed with brownish red color to make catheterization for 3 days. The third day tested urine test Protein: 100 (++) and Glucose 500 (++).

Allegedly cats suffer from FLUTD (Feline Lower Urinary Tractus Disease), caused by the existence of urinary obstruction.

In addition to the FLUTD problem, a high glucose image appears in urine.

on the first day: (+)
second day: (++)
then on the third day, taken blood and examined
via automatic test kit.
glucose test result (17/1)
at 11 am: 10.3 mmol / L
at 3 pm: 8.2 mmol / L
fourth day (18/1)
at 10 am: 4.9 mmol / L
at 12 noon: 6.9 mmol / L
The fifth day (19/1):
1 pm: 11.3 mmol / L
Day 7 (21/1):
at 10 am: 10.2 mmol / L
Eighth day (22/1):
1 pm: 9.4 mmol / L
Day of the ninth (23/1):
at 3 pm: 7.6 mmol / L

While the normal range:

fasting: 3.9-5.6 mmol / L
non fasting: <8.0 mmol / L

Because Bubu suffers from diabetic, it will be very dangerous if performed sediment removal / calculi / kidney stones.

Therefore Bubu given insulin as much as 2 units (not 2 ml), intra muscular with a special syringe insulin.

I.V Fluid continues until the sixth day (20/1).

Similarly, the catheter, stick to the ureter Bubu up day fifth day (total only two days, because after that cat can pee himself)

After that, after the ninth day, the cat began to eat alone, and more sparkling eyes

THIS DIABETIC CASE CAT IS SIGNED

Feline Diabetes Message Board

Case Study 2

This case occurred in November 2010 at Animal Hospital of Bogor Agricultural University. Angora male cats aged ± 13 years monitored significant weight loss, polydipsia and polyuria. Physical examination found clinical findings of pale mucous membranes, odors of urea, dull hair, oily skin and dandruff and skin turgor is difficult to return as before (dehydration).

Cat eyes also have cataracts, heavy and slow breathing sounds. The sound of the heart is bradyrhythmias and visible cordic icons. The limb part tends to be cooler (hypothermia). The result of supporting test (urine and blood) showed no decrease of red blood cell, hemoglobin and hematocrit, but in erythrocyte index seen MCV value in normal range and MCHC decreased (normokitik hipokromik), an increase of relative value of lymphocytes without absolute increase nor leukocytes, elevated blood sedimentation rate, increased urea (uremia) without any creatinine increase, hyperglycemia, hypertriglyceridemia, and urine examination of proteinuria, ketonuria, glucosuria.

From the analysis of supporting test results, the cat is suspected of having diabetes mellitus. Diabetes mellitus (DM) in cats is smaller than that of dogs. But if it happens, DM cat is more difficult to overcome. The therapy given is a lactated ringer infusion fluid. Cats die before further handling.

Signalemen

Bong-Bong cat is male, Angora gray and ± 13 years old.

Anamnesis

Cats look weak and drink a lot.

Clinical Symptoms

Clinical symptoms seen are very weak cats, anorexia, polidipsi and severe polyuria and severe kaheksia. Clinical findings found on physical examination include pale mucous membranes, odor of urea, dull hair, oily skin and dandruff and skin turgor is difficult to return as before (dehydration).

Routine Hematology

Examination Unit Normal Value *
Result Interpretation
RBC/SDM x10⁶/mm³ 5,24-10,89 6,8 Normal
Haemoglobin (Hb) g/dl 9,0-16,7 10,6 Normal
Hematokrit (PCV) % 29,2-51,7 37 Normal
MCV 41,0-56,2 54,4 Normal
MCH pg 13,0-18,0 15,6 Normal
MCHC % 29,5-34,8 28,64 Down
Platelet/Trombosit x10³/mm³ 170-600 540 Normal
Leukosit/WBC/SDP x10³/mm³ 4,2-17,5 17,2 Normal
Neutrofil Relative (%) 35-75 76 Up
Absolut (/mm³) 1.925-14.825 13.07 Normal
Eosinofil Relative (%) 02-Dec 0 Down
Absolut (/mm³) 110-750 0 Down
Basofil Relative (%) 0-1 0 Normal
Absolut (/mm³) 0-190 0 Normal
Examination Unit Normal Value * Hasil Interpretation
Limfosit Relative (%) 20-55 20 Normal
Absolut (/mm³) 1.100-7.000 3.44 Normal
Monosit Relative (%) 01-Apr 4 Normal
Absolut (/mm³) 55-780 688 Normal
Blood Deposit Rate mm/hour 0-2 15 Up

Blood Chemistry

Heart function
AST / SGOT IU / l Dec-40 39 Normal
ALT / SGPT IU / l 28-76 57 Normal
Kidney function
Ureum mg / dl 15-34 257 Increase
Creatinine mg / dl 1.0-2.2 1.79 Normal
Others
Glucose mg / dl 60-130 878 (duplo) Up
Triglycerides mg / dl 34-98 170 Up

Examination Unit Normal Value
Results Interpretation
Heart Function
AST/SGOT IU/l 12-40 39 Normal
ALT/SGPT IU/l 28-76 57 Normal
Kidney Function
Ureum mg/dl 15-34 257 Up
Kreatinin mg/dl 1,0-2,2 1,79 Normal
Others
Glukosa mg/dl 60-130 878 (duplo) Up
Trigliserida mg/dl 34-98 170 Up

 

Urinalysis (Strip Test)

Examination Unit Normal Value Results Interpretation
Leukosit Leukosit/µL Negative Negative Normal
Nitrit Negative Negative Normal
Urobilinogen mg/dL (µmol/L) 0,2 (3,5) Negative Normal
Protein mg/dL (g/L) Negative ++ 100 (1,0) Naik (++)
pH Asam (± 6,8) 8,0 Naik (++)
Blood Eritrosit/µL Negative Negative Normal
SG (BJ) 1,020-1,040 1,005 Down
Keton mg/dL (µmol/L) Negative + 15 (1,5) Naik (+)
Bilirubin mg/dL (µmol/L) Negative Negative Normal
Glukosa mg/dL (µmol/L) Negative ≥ 2000 (110) Up (++++)

* Tilley and Smith (1997)

Diagnosis

From the summary of changes in laboratory results, the suspected diagnosis is diabetes mellitus (DM).

Prognosis

The proposed prognosis is infausta.

Therapy

The therapy given is the infusion of ringer lactate. However, because of the blood vessels collapse can not be installed intravenously.

Results of Analysis

Results of analysis / analysis of supporting test (blood and urine), obtained the following changes:

  1. There was no decrease in red blood cells, hemoglobin and hematocrit, but on the erythrocyte index the MCV values in the normal range and MCHC decreased (hypochromic normocytic)
  2. Increased relative value of lymphocytes without absolute or leukocyte increase
  3. Increased rate of sedimentation of blood
  4. Elevated urea (uremia) without any creatinine enhancement
  5. Increased levels of blood glucose (hyperglycemia)
  6. Increased triglycerides (hypertriglyceridemia)
  7. Urine examination seen the existence of proteinuria, ketonuria, glukosuria and increased pH and decrease BJ urine

Discussion

Results of routine hematological examination data indicate that cats have no problem with erythrocytes. However, in the erythrocyte index, normocytic normocytic features are seen. Hypochromic normocytic anemia is very rare (Stockham and Scott 2002). If it happens, it is more often caused by the validity of the data or the range of normal values that still allow for the increment of numbers.

The increase in lymphocytes is relatively not followed by an increase in absolute values. Therefore, this value does not provide any real change. Lymphocytosis may be caused by chronic inflammation or infection (eg due to bacterial infections, ricketsia, fungi, virus and blood parasites especially Babesia and Theileria), physiological processes of illness, anxiety, stress and drugs (eg epinephrine), neoplasia and hypoadrenokortisism (Stockham and Scott 2002). For other types of leukocytes (neutrophils, eosinophils, basophils and monocytes) did not show significant change in values. As for the cat does not increase leukocytes so the possibility of infection should still be studied first. Increased rate of sedimentation of blood (15 mm / h) indicates the presence of more concentrated blood.

Liver enzyme examinations only AST / SGOT and ALT / SGPT tend to be normal. Examination of renal function seen as an increase in ureum without the increase of creatinine.

According to Stockham and Scott (2002), azotemia can be caused by:

1) decreased urinary excretion, divided into three ie a. pre-renal (hypovolemia due to decreased blood volume and dehydration, coronary insufficiency, shock), b. renal (inflammatory, amyloidosis, toxic nephrosis, ischemia or hypoxic renalis, hypoplasia, hydronephrosis and neoplasia), c. post-renal obstruction (urinary tract obstruction, trauma, neoplasia); and

2) increased production of urea or cretinine (intestinal hemorrhage, increased urea diet, increased protein catabolism). Clinically, the smell of urea in the cat. In the blood chemistry of cats also seen the presence of hyperglycemia and hypertriglyceridemia.

According to Stockham and Scott (2002), increased glucose (hyperglycemia) can be divided into three groups of causes, namely:

1) physiological hyperglycaemia eg postprandial, diestrus, stress / anxiety / fear;

2) pathological hyperglycaemia caused by immune-mediated DM; and

3) pharmacological hyperglycemia due to glucose, drugs that affect insulin and growth hormone.

Elevated triglycerides (hypertriglyceridemia) are caused by:

1) increased production of triglycerides (by hepatocytes and by enterocytes);

2) decreased lipolysis (hypothyroidism, nephrotic syndrome and lipoprotein lipase deficiency); and

3) others (acute pancreatitis, DM, high-fat diet, hyperadrenocortisism, idiopathic hyperlipidemia).

In many cases, a cat with DM can be difficult to diagnose because it also suffers from other diseases simultaneously or a disease similar to that of DM. Some of these diseases are hyperthyroidism, kidney failure, adrenal gland disease, gastrointestinal disease, cancer, liver failure, and diseases caused by some types of drug therapy. Common signs of DM that are sometimes similar to other diseases are thirst (polidipsi) and increased urine (polyuria), increased appetite (polyphagia) with decreased body weight. However, these signs can occur in cats that have other diseases. Other clinical signs are vomiting, diarrhea, loss of appetite, respiratory difficulty, weakness and constipation. These signs may appear suddenly for several days, or for several months. These cats also experience these symptoms, at first cat eat a lot (polipagia), but towards the end of death the cat will not eat.

To diagnose cat diabetes, the veterinarian uses fasting blood glucose, urinalysis, and lipemia (triglyceride or cholesterol) levels. Test results showing a blood glucose level greater than 200 indicate the likelihood of DM. However, DM due to stress can produce higher blood glucose levels (up to 300-400) in cats without DM, this is due to the adrenaline waves. In cats diabetic patients have glucose and ketones in urine. Lipemia, which occurs is hypertriglyceridemia and cholesterolemia. Hyperglycemia occurs when the concentration of glucose in the blood is greater than 130 mg / dl. In the cat is called hyperglycemia if the concentration of glucose is 200-280 mg / dl. Glucosuria causes osmotic diuresis, which then becomes polyuria and polydipsia. In cats with glucose levels 280 mg / dl no symptoms are seen. If mild hyperglycaemia (blood glucose levels less than 180 mg / dl) and glucosuria is absent because polydipsia and polyuria should be considered other than DM (Agna 2009).

A condition where blood glucose levels are very high above normal is called hyperglycemia. Hyperglycemia usually occurs when the insulin hormone produced by the β islets of Langerhans island pancreas can not be used properly or defisiensi (GoWati 1993). As for hyperglycemia with the cause is strongly associated with DM. Diabetes Mellitus (DM) is a disease associated with insulin levels in the blood that is influenced by various factors as its etiology. As it is known that insulin is closely related to the process of metabolism in the body (Agna 2009).

Insulin is a hormone synthesized in the endoplasmic reticulum (RE) β cells of the pancreas Langerhans island (Suryohudoyo 2000). The function of insulin primarily is in the regulation of glucose in the body that is lowering blood glucose levels, by increasing uptake of glucose into the tissues through GLUT-2 and GLUT-4. Other functions include increasing the protein and fat catabolism, inhibiting glucose formation of amino acids and fat in peripheral areas by stimulating the formation of muscle amino acids and fat storage in adipose cells (Agna 2009). Insulin deficiency will cause disruption of the biochemical processes in the body, ie decreased glucose intake into cells and increased release of glucose from the liver into the circulation. This is what causes the occurrence of hyperglycemia.

The most important sign of DM is the persistent hyperglycemia. This disorder is often thought of as a result of insufficient insulin secretion, in which changes in plasma insulin levels in response to carbohydrate loading are abnormal in obese individuals and in diabetics. Severe hyperglycemia occurs in patients who are thin because of lower insulin levels in the circulation. Body cells lack glucose despite hyperglycemia and glucosuria. Cells in low-carbohydrate and high-fat states that cause compensated ketosis and acidosis (Montgomery et al., 1993). In this cat, in addition to the presence of hyperglycemia also detected the presence of glucosuria and ketonuria.

Insulin also works to increase lipoprotein lipase activity in the endothelial surface in taking triglycerides from kilomikron and VLDL (Very Low Density Lipoprotein). Insulin also prevents the decomposition of fatty acids from fatty tissue. Insulin deficiency will result in decreased lipoprotein lipase activity triglyceride levels will increase in blood (hypertriglyceridemia). (Tsutsumi et al 1998, Bierman 1992).

There is a tendency to increase the incidence of heart disease risk with elevated plasma triglyceride levels. Diabetes also has risk factors for heart disease. Therefore, the occurrence of hypertriglyceridemia in diabetics may increase the risk of heart disease (Tsutsumi et al., 1998). This can be seen from the clinical examination of cats where the heart tends to severe bradiarithmia.

There are two types of DM in cats, namely DM type 1 (Dependent Diabetes Mellitus / DDM) that often occurs due to damage to β cells so that the pancreas of the cat does not produce enough insulin hormone, and type 2 DM (Non Dependent Diabetes Mellitus / NDDM) cat cells are less / unresponsive / sensitive to the presence of insulin. DDM is caused by heredity and destruction of the pancreas due to pancreatitis, whereas NDDM is caused by obesity, glucocorticoid hormone, cortisol, toroxin, glucagon, growth hormone, progesterone and epinephrine. Rand and Marshall (2005) say that 80-95% of diabetic in cats is an analog of type 2 DM. In this cat further testing is needed to determine the type of DM.

According to Agna (2009), insulin resistance or insulin ineffectiveness in tissues in cats and dogs is caused by:

1) inactive insulin due to the administration of diabetogenic drugs;

2) insulin is dissolved due to hyperadrenocortism;

3) giving at an inappropriate time when diestrus in dogs;

4) improper doses due to infection especially in the cavity oris and urinary tract,

5) improper insulin delivery frequency due to hypothyroidism in dogs and hyperthyroidism in cats;

6); failure or lack of insulin absorption due to damage to the kidneys, liver and heart; and

7) the presence of anti-insulin antibodies in cases: glucagonoma in dogs, chronic inflammation due to pancreatitis, pancreatic exocrine gland damage, severe obesity, hyperlipidemia, and neoplasia.

DM cases in cats are smaller than dogs. But if it happens, DM cat is more difficult to overcome. When a diabetic cat consumes berglukosa food, his body can not process glucose properly, which can lead to the buildup of glucose in the bloodstream. DM can occur in cats of all ages, although most occur after cat age more than six years. There is no predisposition of race in cats with DM, but explained that as many as 75% of cats who suffer from DM ranged in age from 8-13 years (Tilley and Smith 2007). Some cats may be dependent on insulin and may be assisted with lifelong insulin therapy. Other cats only need insulin when stressed. Usually, these cats regain their balance after the stressful conditions end.

Without insulin, glucose remains in the bloodstream and eventually passes through the urinary tract that can be detected in the urine (glucosuria). This will cause the cat to drink more water due to thirst, and become hungry because his body can not use glucose in the blood. The accumulation of ketone can cause vomiting so that it will happen dehydration. The disease can not be cured, but it can be sustained. If preserved, cats with this disease can lead to a normal life.

In the less insulin state, there is hyperglycemia, but energy remains inadequate so that the metabolism of fat increases. As is known fat metabolism produces ketone bodies, so that if fat metabolism increases the amount of ketone body produced also increases, causing ketonemia and ketonuria. Ketosis causes the acidic state in the blood that causes metabolic acidosis, called diabetic keto-acidosis (Agna 2009).

Insulin is a lipolysis inhibitor and fatty acid oxidation. Relative or absolute insulin deficiency causes increased lipolysis and causes fatty acid mobility to the liver to increase, increasing fatty acids and ketogenesis. Ketones become accumulated in the blood causing metabolic acidosis. The ketone accumulates in the extracellular space, the amount exceeds the threshold of the renal tubules for complete resorption and causes the presence of ketones in urine (ketonuria). This causes osmotic diuresis caused by glycosuria and causes electrolyte excretion (sodium, potassium, and magnesium). In conclusion all this causes water and electrolyte losses that cause azotemia pre renal. In the less insulin state, protein synthesis increases, causing glucose formation in the liver to increase, and the removal of triglycerides and fatty acids by the tissues also decreases. As a result glucose levels remain high, and fatty acids and triglycerides which are glucose precursors continue to circulate in circulation and return to liver, causing glucose formation it is possible to remain high.

In the end, hyperglycemia worsens. In the state of hyperglycemia, the osmotic pressure in the blood increases so that the fluid is drawn into the blood vessels causing hypertension. Because the cell fluids are attracted into the extracellular (blood vessels), then dehydration occurs (Agna 2009). Dehydration causes an increase in appetite (polydipsia) which results in polyuria. Polyuria causes electrolytics (dissolved electrolytes – K +, Na +, Mg + in urine) as osmotic pressure increases. Osmotic pressure is increased due to glycosuria. In addition, because ketones can bind electrolytes to bind electrolytes, in the case of eletrolite ketonuria is carried away and wasted (Agna 2009).

Hyperglycemia causes an increase in plasma osmolality causing osmotic diuresis which even increases plasma osmolality. Increased plasma osmolality causes loss of water and salt and fluid moves out of the cell causing cell dehydration. Figure 2. The condition of Bong-Bong cat towards the end of death

According to Rand and Marshall (2005), the treatment that can be given for DM cases in cats are:

  1. rapid treatment;
  2. regularly controlling blood glucose;
  3. low carbohydrate diet; and
  4. monitor the efficacy of the medicines administered. Provision of insulin preparations should use parameters to determine the given dosage. Early administration of insulin in cats can begin with a dose of 2 U per cat per injection twice daily.

Table 1. The criteria used to determine the dosage of insulin in DM therapy at Cats according to theory (Rand and Marshall 2005)

Parameter Change Dosage If the glucose level> 360 mg / dL is increased 0.5 U If the glucose level 270 <360 mg / dL according to the dose

If the glucose level is 198-252 mg / dL as dose or decreased

If the glucose level <180 mg / dL is decreased 0.5-1 U, stop insulin

If there are symptoms of hypoglycemia lowered to 50% If water content <20 mL / kg in wet food according to dose

or <70 mL / kg in dried food If water content> 40 mL / kg in wet food is increased from 0.5 to 1 U

or> 100 mL / kg in dried food

If urine glucose> 3+ (0-4+ scale) is increased 0.5-1 U

If negative urine glucose rechecks diabetic remission

Conclusion

Bong-Bong cat was diagnosed with diabetes mellitus (DM) after analyzing the results of clinical examination, the symptoms that emerged and the results of laboratory tests on blood and urine. Treatment given infusion of ringer lactate, as yet other therapy has not been given because the cat can not survive.

Reference

  1. Agna. 2009. Diabetes Mellitus. http://dr-agna.livejournal.com/3397.html. [December 25th 2011].
  2. Bierman EL. 1992. Atherogenesis in Diabetes. Arterioscler and Tromb. 12: 647-656. Gough A. 2007. Differential Diagnosis in Small Animal Medicine. Blackwell Publishing. Page 292-293.
  3. Montgomery R, Conway TW, Spector AA. 1993. Clinical-Oriented Biochemistry. Ed. 5. Translator: Lecturer Department of Biochemistry Faculty of Medicine University of Indonesia. Volume 1. Jakarta: Binarupa Aksara.
  4. Morgan RV. 2008. Handbook of Small Animal Practice. Ed. 5. Vol. 2. Page 1269-1271.
  5. Going E. 1993. Efforts to Handling Diabetes. Panasea 65.
  6. Price SA and Wilson LMc. 2006. Editor: H Hartanto. Pathophysiology: Clinical Concept
  7. Disease Processes. Ed. 6. Jakarta: EGC Medical Book Publishers.
  8. Rand J and Marshall R. 2005. Understanding Feline Diabetes Mellitus: Pathogenesis and Management. Diabetes Mellitus and Endocrinologic Disorders. Waltham Focus: PT. Rofaca Kabalmasih Abadi. Pages 5-11.
  9. Suryohudoyo P. 2000. Kapita Selekta Molecular Medicine Science. Jakarta: CV. Sagung Seto. Page 48-57.
  10. Stockham SL and MA Scott. 2002. Fundamentals of Veterinary Clinical Pathology.
  11. Iowa State Press: Blackwell Publishing Company. Page 49-153, 251-275, 381-459.
  12. Tilley LP and Smith JR. 1997. The 5 Minute Veterinary Consults Canine and Feline.
  13. Philadelphia: William & Wilkins A Waverly Company, A Lea & Febiger. Page 1166-1172.
  14. Tsutsumi K, Iwamoto T, Hagi A and Kohri H. 1998. Streptozocin Induced Diabetic Cynomolgus Monkeys is a Model of Hypertriglyceridemia with Low High-Density Lipoprotein Cholesterol. Biol. Pharm. Bull. 21: 693-697.

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