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 90 - 130 mg/dl, it equals 80 - 120 mg/dl whole blood. Most new meters provide blood glucose readings as plasma glucose readings although it use whole blood

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.

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

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.

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,

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

>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.

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.

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.

-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 .

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

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

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.

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,

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;

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

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,

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

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).

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

Acute Complications of DM

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.

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.

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

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.

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.