1. Whole Blood Vs. Plasma Glucose Levels
The difference is that plasma numbers read about 10 - 12% higher than the whole blood numbers.
So if your fasting plasma glucose is mg/dl, it equals mg/dl whole blood.
Most new meters provide blood glucose readings as plasma glucose readings although it use whole blood

2. To convert Whole Blood or Plasma Glucose from mmol/l to mg/dl
To convert Whole Blood or Plasma Glucose from mmol/l to mg/dl. multiply by 18 and vice versa is correct
Hba1c
The Hba1c has several advantages to
the FPG and OGTT, including
Convenient (fasting not needed)
Greater stability, and less day-to-day variations during stress and illness.

3. Also has several disadvantages
Greater cost,
Limited availability of A1C in certain regions of the developing world,
For patients with an abnormal hemoglobin or abnormal red cell turnover, such as
Pregnancy,
Recent blood loss or transfusion,
Anemias as sickle cell trait or if there

4. Is an elevated level of fetal hemoglobin (HbF)
Is an elevated level of fetal hemoglobin (HbF). patients with hemoglobin variants should first find out which method your laboratory is using.
Only blood glucose criteria should be used to diagnose diabetes in all above mentioned situations.

5. Screening
screening test for type 2 DM is recommended because
large number of individuals wirh type 2 DM are asymptomatic and unaware of the disorder,
Epidemiologic studies suggest that type 2 DM may be present for up to a decade before diagnosis,

6. Some individuals with type 2 DM have one or more diabetes complications at the time of their diagnosis,
Early treatment of type 2 DM may favorably alter the natural history of DM.
The ADA recommends screening of all individuals who

7. >45 years every 3 years and
Screening individuals at an earlier age if they are
Overweight (BMI) >25 kg/m2] and have one additional risk factor for diabetes.
In contrast to type 2 DM, a long asymptomatic period is rare in type 1 DM, so screening is usually not needed.

8. Prevention
The Diabetes Prevention Program (DPP) demonstrated that intensive changes in lifestyle (diet and exercise for 30 min/d five times/week) in individuals with IGT prevented or delayed the development of type 2 DM by 58% regardless of age, sex, or ethnic group.

9. In the same study, metformin prevented or delayed diabetes by 31% compared to placebo.
Pharmacologic therapy for individuals with prediabetes is currently controversial because its cost-effectiveness and safety profile are not known.

10. -ADA suggested that metformin be considered in individuals with both IFG and IGT who are at very high risk for progression to diabetes (mentioned )
Individuals with IFG, IGT, or an A1C of 5.7–6.4% should be monitored annually to determine if progressed to diabetes .

11. MODY
Maturity-onset diabetes of the young is a subtype of DM characterized by
AD inheritance,
Early onset of hyperglycemia (usually <25 years),
Impairment in insulin secretion

12. It is due to genetic defects of beta cell function and are of 6 types (MODY1 to MODY6) depending on site of the mutation.
All respond to sulfonylureas except MODY 2 that require insulin treatment

13. LADA
Latent autoimmune diabetes of adults, or slow onset type 1 diabetes or diabetes type 1.5
Form of type 1 DM that occurs in adults, often with a slower course of onset
May initially be diagnosed as having type 2 diabetes based on their age.

14. Raised antibodies against the islets of Langerhans support the diagnosis of type 1 DM rather than type 2 .
It can only be treated with the usual oral treatments for type 2 diabetes for a short period of time, after which insulin treatment is usually necessary,

15. Gestational Diabetes Mellitus (GDM)
Glucose intolerance developing during later pregnancy due to insulin resistance because of metabolic changes of late pregnancy, and the increased insulin requirements may lead to IGT or diabetes.
GDM occurs in 7% (range 2–10%) of pregnancies in the United States;

16. Most women revert to normal glucose tolerance postpartum but have a substantial risk (35–60%) of developing DM in the next 10–20 years.
Diagnosis of GDM
International Diabetes and Pregnancy
Study Groups recommends that diabetes diagnosed at the initial

17. prenatal visit should be classified as "overt" diabetes rather than gestational diabetes
Women not previously diagnosed with overt diabetes at 24–28 weeks of gestation we perform either One-step” 75-g OGTT, after an overnight fast of at least 8 h with plasma glucose measurement, fasting and at 1 and 2 h,

18. Diagnosis of GDM is made when any of
the following plasma glucose values are exceeded:
Fasting: ≥92 mg/dL (5.1 mmol/L)
1 h: ≥ 180 mg/dL (10.0 mmol/L)
2 h: ≥ 153 mg/dL (8.5 mmol/L)
Or the “Two-step” nonfasting

19. If the plasma glucose level measured 1 h after the load is ≥ 140 mg/dL (7.8 mmol/L)., proceed to 100-g OGTT (Step 2).
The 100-g OGTT should be performed
when the patient is fasting.
The diagnosis of GDM is made when the plasma glucose level measured 3 h after the test is ≥ 140 mg/dL (7.8 mmol/L).

20. Diet and life style changes Insulin
Treatment of GDM
Diet and life style changes
Insulin
Oral antidiabetics are recently approved but usually used in limited cases
style change

21. Acute Complications of DM

22. I- DIABETIC KETOACIDOSIS (DKA)
Pathophysiology
DKA results from the combined effects of insulin deficiency and increased counter regulatory hormones ESPECIALLY Glucagon which is necessary for DKA to develop.
Other hormones as catecholamines, cortisol, and growth hormone).also play role.

23. The decreased ratio of insulin to glucagon leads to
Glycolysis stops so energy is formed by
Glycogenolysis,
Gluconeogenesis,
Lipolysis
Increases in substrate delivery from fat and muscle to the liver by increasing the release of FFA and amino acids)
Ketone body formation in the liver.

24. Normally, these free fatty acids are converted to triglycerides or VLDL with little amount of ketone bodies in the liver.
In DKA, hepatic metabolism is altered to favor ketone body formation, rather than triglycerides or VLDL because:
prolonged insulin deficiency stimulate production of mitochondrial HMG-CoA
synthase and of HMG-CoA lyase

25. HMG-CoA (3-hydroxy-3-methylglutaryl-coenzyme A)
These and the exhaustion of substrates notably oxaloacetate for gluconeogenesis and the and citric acid cycle results in shunting of excess acetyl-CoA into the ketone synthesis pathway and leading to the development of diabetic ketoacidosis.

26. Ketone bodies, are neutralized by bicarbonate
Ketone bodies, are neutralized by bicarbonate. As bicarbonate stores are depleted, metabolic acidosis ensues.
Also there is increased lactic acid production which contributes to the acidosis.