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  Pitfalls in diagonsis & management of diabetes 04/24/2024 10:36pm (UTC)
   
 

Pitfalls in diagonsis & management of diabetes mellitus                                                                            Content        Next  
 

   Before doing Laboratory Investigations in Diabetes Mellitus ask yourself for what purpose

are you doing?
 

   (1) Is it for Diagnosis?
        Urine Glucose is not enough. Blood glucose should be done atleast twice and it should

        be in the diagnostic range.
   (2) To Assess control.
       Glycosylated HB Vs Stat Blood Sugar. For Long term assessment Glycosylated

       Haemoglobodin is useful.
   (3) Diagnosis of Hypoglycemia
       Random Blood Glucose at the time of symptoms is diagnostic.
   (4) Diagnosis of Reactive Hypoglycemia. 6 hours extended OGTT is useful.
   (5) Research purpose to study the 1st degree Relatives of Diabetics. OGTT study is done.
   (6) To know whether patient is in Remission.
        C Peptide estimation is useful in addition to routine tests.
   (7) To detect Early Renal Involvement. Microalbuminuria is useful.
   (8) To find out if patient is in ketosis. Urine ketone testing
 

Blood glucose estimation
   
Blood collection in Sodium Fluoride bulb retains the sugar value for several hours at

Room Temp. Several Days if kept in Refrigerator with 10% loss occur. Autoanalyser uses plasma for sugar estimation and the value is 15% higher than whole blood sugar. Follin and Wu's - method gives 20 mgm higher value for blood glucose because of non glucose reducing substances. Somogy Nelson's Method -Estimates True Glucose 20 mgm less than Follin Wu Method. Capillary blood glucose is 20-50 mgm higher both in post meal and fasting.


Advantage of capillary blood sugar estimation is that it is easy to perform in children when repeated blood glucose is to be estimated and when vein is not available.
 

    Dextrometer needs small amount of capillary blood. It is not used for firs*- time diagnosis

of Diabetes.

 
Plasma Glucose Whole Blood Glucose
a. Plasma Glucose not affected by Haematocrit a. Affected bv Haematocrit 10 units decrease will increase Blood sugar by 3.6 mgm.
b. Reflects Concentration of glucose in Extra-celluar fluids. b. Reflects Infra-vascular compartment Blood Glucose.
c. Adaptable for Auto-Analvser c. Not Adaptable.


    Arterial Blood Sugar is 20-50 mgm higher than venous blood sugar in normal adults. In

diabetic Arterial and Venous difference is lost meaning glucose is not utilised by tissues.


Oral Glucose Tolerance Test (OGTT)
   
Low Carbohydrate diet can make OGTT diabetic type. Decreased physical activity gives

diabetic type of curve with OGTT. Infection, Obesity, Carcinoma, Endocrinopathies, can impaire OGTT. Drugs like thiazides, Steroids, Aspirin, O.C.A. Nicotinic Acid and dilantin increase 2 hrs. post meal blood glucose estimation.


   Brittle diabetic mellitus requires 24 hours urinary glucose quantitative estimation.
 

Pitfalls in management of diabetes
    Often Diabetes Mellitus patients on OHA therapy comes for follow up and fasting Blood

Glucose is found raised. Before thinking that he is not well controlled and changing the dose of OHA. Ask him two questions.


   1. Is it really fasting or has he taken break fast before giving blood.
   2. Did he omit his last night OHA. This mistake is often done by patients. They omit the  

       drugs and go for tests. They think that they have taken treatment continuously for 1

       month and want to see the sugar report without drugs. I always explain them most of the

       OHA preparations except Chlorpropamide acts only for that day i.e. 24 hours.
 

       Often patients manupulate the dose of OHA. If they have been prescribed BD dose they

       may make it OD dose. While looking into post meal blood sugar, verify it was really 2 

       hours later or at shorter interval like one hour or one and half hours. This will also raise

       the blood sugar. While reviewing Glycosylated Hb. if there is Anemia or Chronic renal 

       disease, it is bound to cause normal or low values.
    3. Glycosylated Hb is not the correct choice of test during Hypoglycemia or diabetic

       ketoacidosis. Acute blood glucose changes are not reflected in Glycosylated Hb values.
    4. Some general practioners in a known diabetic get post glucose blood sugar value.

       There is no need to give glucose once the diabetes mellitus diagnosis is made. Check

       out this mistake while evaluating postmeal blood glucose values.
    5. In a patient on insulin, if you are getting uncontrolled values, before changing insulin

       dose check out what syringe the patient used. Insulin syringe or ordinary syringe, upto

       which mark he took insulin. This will vary in U80 and U100 Syringes or in the same

       syringe where U40 and U80 is marked and if the patients is taking dosage from mark

       U80 actually he is taking half the dosage only.
    6. Insulin injection technique has to be told to the patient. Some diabetics are in a habit of

       taking insulin at the same site. This is going to make poor absorption of insulin from the

       site of injection and hence uncontrolled diabetic state. Physician has to tell the patient to

       change the site of injection every time so that the site is repeated every 5-7 days.
    7. Once Nephropathy develops there is insulin sensitivity, hence patients are prone to

       hypoglycemic episodes. If the patient is on OHA best is to start regular insulin small

      doses (10 units or 5 units) and then increase.
    8. With Retinopathy patients there is difficulty in seeing and filling syringe upto correct

       mark. Hence they may need help from family members to inject insulin. Some women

      diabetics are in the habit of fasting 3-4 days in a week. Eating less and omitting night

      dose of OHA or insulin or if they take same dose of insulin or OHA they may get frequent

      Hypoglycemia. Best thing is to avoid fasting or in those days she can take food items

      allowed during religious fast and take reduced dose of OHA or insulin.
    9. Sick day rules are to be clearly told to the IDDM patients on insulin. During sickness

       patients stop insulin completely and end up in Diabetic ketoacidosis. We have to explain

       that blood glucose is maintained in normal range in non-diabetic during fasting because

       of Neoglucogenesis and Glycogenolysis in liver. This phenomenon is more so in

       diabetics due to insulin lack and during stressful states like Sickness, blood sugar is

       increased. Best thing is to take regular insulin in a small dose, say, 10 units and check

       urine every 4 hourly and take small repeated doses or consult the Physician

       immediately.
   10. Quite often foot infection i.e. Cellulitis or infected Ulcer occurs and patient is found on

      OHA uncontrolled. He should consult Physician and immediately from OHA he has to 

     switch over to insulin with appropriate antibiotics. Then only the lesion will heal.
   11. Similarly during pregnancy in NIDDM oral agents have to be stopped and insulin

     should be started.
 

CONCLUSION
   
Physician has to be alert in interpreting blood sugar results and he must give enough time

to his patients to avoid the diabetic patients getting into various management problems.
 

REFERENCES
       
1. M. Viswanathan V. Mohar & A Rama Chandran-Diagnosis of Diabetes in Practice of

            Diabetes Mallitus Edited by MMS Ahuja, Vikas Publishing House 1983, Page 79-99.

 
  What is Diabetes?
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
  CONTENTS



1. Diabetes mellitus : a historical review


2. Insulin-some physiological considerations,


3. Epidemiology of diabetes mellitus


4. Pathogenesis of diabetes mellitus in young


5. Impaired glucose tolerance


6. Secondary diabetes mellitus.


7. Laboratory diagnosis and work up for assessment of complications & of diabetes mellitus


8. Oral glucose tolerance test.


9. Neurological involvement in diabetes mellitus


10. Glycation products in diabetes mellitus


11. Diabetes mellitus in adolescence


12. Diabetic keto acidosis


13. Case of brittle diabetes


14. Lipoprotein disorders in diabetes mellitus


15. Diabetes and cardiovascular system


16. Myocardial infarction in diabetes


17. The Syndrome of insulin resistance.


18. Gastro intestinal manifestation of diabetes mellitus


19. Pregnancy and diabetes


20. Skin manifestations of diabetes mellitus


21. Diabetic nephropathy


22. The diabetic foot


23. Sexual dysfunction m diabetes mellitus


24. Joint and Bone manifestation of diabetes mellitus


25. Alcohol and diabetes mellitus


26. Live: and. diabetes mellitus


27. Management of infections m diabetes


28. Diabetes mellitus and surgery


29. Canter arid diabetes


30. Diabetes in elderly


31. Non drug therapy of diabetes mellitus


32. Nutrional approaches in the management of diabetes mellitus


33. Insulin therapy in diabetes mellitus


34. Insulin sensitivity


35. Insulin resistance


36. Oral drugs in non insulin dependent diabetes


37. Lactic acidosis


38. Use of indigenous plant products in diabetes


39. Prevention of diabetes mellitus


40. Pancreatic transplantation in Type I DM (IDDM)


41. Hypoglycemia


42. Diabetes and eye


43. Diabetes mellitus and pulmonary tuberculosis


44. Pitfalls in diagnosis and management of diabetes mellitus


45. Mortality patterns in diabetes mellitus


46. Diabetic education


47. Diabetes mellitus and associated syndromes


48. Diabetes mellitus: socio economic considerations


49. Obesity and diabetes mellitus


50. Proinsulin


51. C-Peptide


52. Glucagon


53. Drug induced diabetes mellitus


54. Insulin anologues


55. Insulin delivery system


56. Micro nutrients in diabetes mellitus


57. Defects in glucose metabolism in neonates


58. Sulphonylurea failure


59. Diabetes control and complications


60. Diabetes mellitus & oral health


61. Common procedures for recording data in diabetes


62. Profile of a lean Type-2 diabetes mellitus


63. Management of post prandial

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