Prediabetes

Individuals with a stage of impaired glucose homeostasis that includes IFG and IGT are
referred to as having prediabetes, indicating their relatively high risk for the development of
diabetes and CVD. People at risk may have IFG (fasting plasma glucose 100-125 mg/dL), IGT
(2-hour postchallenge glucose of 140 to 199 mg/dl), both, or a hemoglobin A1c (A1C) of
5.7% to 6.4% and should be counseled about strategies, such as reduced energy intake,
weight loss, and physical activity, to lower their risks.

Type 1 Diabetes

T1DM accounts for 5% to 10% of all diagnosed cases of diabetes.

At diagnosis, people with type 1 diabetes (T1DM) often experience excessive thirst, frequent
urination, and significant weight loss. The primary defect is pancreatic beta-cell destruction,
usually leading to absolute insulin deficiency and resulting in hyperglycemia, polyuria
(excessive urination), polydipsia (excessive thirst), polyphagia (excessive hunger), weight
loss, dehydration, electrolyte disturbance, and ketoacidosis.

The capacity of a healthy pancreas to secrete insulin is far in Excess of what is needed
normally. Therefore the clinical onset Of diabetes may be preceded by an extensive
asymptomatic Period of months to years.

Hyperglycemia and symptoms develop only after greater than 90%.

Frequently, after diagnosis and the correction of hyperglycemia, metabolic acidosis, and
ketoacidosis, endogenous insulin Secretion recovers. During this honeymoon phase
exogenous Insulin requirements decrease dramatically for up to 1 year or Longer, and good
metabolic control may be easily achieved.

Amylin, a glucoregulatory hormone cosecreted with insulin.

Amylin complements the effects of insulin by regulating postprandial glucose Levels and
suppressing glucagon secretion. T1DM is also an amylin-deficient state

Latent autoimmune diabetes of aging (LADA) may account for as many as 10% of cases of
insulin-requiring diabetes in older individuals and represents a slowly progressive form of
autoimmune diabetes that frequently is confused with T2DM
 Type 2 Diabetes

Type 2 diabetes (T2DM) accounts for 90% to 95% of all diagnosed cases of diabetes and is a
progressive disease that, in many cases, is present long before it is diagnosed.

Most persons with T2DM are obese, and obesity itself causes Some degree of insulin
resistance. Persons who are not obese by traditional weight criteria may have an increased
percentage of body fat distributed predominately in the abdominal region.
Other risk factors include genetic and Environmental factors, including a family history of
diabetes, Older age, physical inactivity, a prior history of gestational Diabetes, prediabetes,
hypertension or dyslipidemia, and race or Ethnicity.

T2DM is characterized by a combination of insulin resistance And beta-cell failure.

Endogenous insulin levels may be normal, Depressed, or elevated, but they are inadequate
to overcome Concomitant insulin resistance.

The inflammatory response to excess weight, insulin resistance, and beta-cell failure occurs
approximately 5 to 10 years before the elevation of glucose above normal. When T2DM is
diagnosed, it is estimated that people already have lost approximately 50% of their beta-cell
function.

Insulin resistance is demonstrated first in target tissues, mainly muscle, liver, and adipose
cells.

Initially there is a compensatory increase in insulin secretion.

Glucotoxicit: over sugar content in the blood results from 2 mean sources:

 Postprandial (after a meal) blood glucose: "Insulin resistance" – increase high

sugar
 Pre-prandial (fasting) blood glucose: "Insulin response" - inadequate in
suppressing alpha-cell glucagon secretion

Lipotoxicity: Insulin resistance also is demonstrated at the adipocyte level, leading to

lipolysis and an elevation in circulating free fatty Acids.

Persons with T2DM may or may not experience the classic Symptoms of uncontrolled
diabetes (polydipsia, polyuria, polyphagia, weight loss) and they are not prone to develop
ketoacidosis except during times of severe stress.

The progressive loss of beta-cell secretory function means that persons with T2DM Require
more medication(s) over time to maintain the same Level of glycemic control; eventually
exogenous insulin will be Required. Insulin is also required sooner for control during periods
of stress-induced hyperglycemia.

Gestational diabetes mellitus (GDM)

Occurs in about 7% of All pregnancies (ranging from 1% to 14% depending on the Population
studied) About 90% of all women With GDM become normoglycemic but are at increased
risk of Developing GDM earlier in subsequent pregnancies.

Women with risk factors for diabetes should be screened For undiagnosed T2DM at the first
prenatal visit,

Macrosomia: "Fetus may Become too large for a normal birth": Extra glucose from the
mother crosses the fetal placenta and the fetus’ pancreas responds by releasing extra insulin
to cope with the excess glucose. The excess glucose is converted to fat. Another Common
problem Neonatal hypoglycemia at birth, because of the supplement of high sugar in the
blood stopped from the mother. And they will usually have extra production of insulin
Women with GDM should be screened for diabetes 6 to 12 weeks postpartum and should
have lifelong Screening for the development of diabetes or prediabetes at Least every 3
years

Women require a minimum of 175 g of carbohydrates Daily the initial Eating Plan may have
approximately 30 g of carbohydrate at breakfast.

Energy intake below Approximately 1700 to 1800 kcal/day is not advised, Also we should
encourage Breastfeeding for GDM after birth

Management goal of DM:

The main goal for both types is glycemic control.

 Type 1 only: glycemic control and percentage of carbs.

 Type 2 only: body weight reduction.

Counterregulatory (stress) hormones:

Have the Opposite effect of insulin, increase blood sugar (glucagon, growth Hormone,
cortisol, epinephrine, and norepinephrine)

*T1DM a flexible, individualized management program using the principles of intensive

insulin therapy Is essential. T2DM is a progressive disease. The “diet” doesn’t Fail; the
pancreas fails to secrete enough insulin to maintain Adequate glucose control. As the
disease progresses, MNT alone Is not enough to keep A1C level at 7% or less.

Bariatric surgery can be an effective weight loss treatment for Severely obese patients
with T2DM
 Macronutrient Percentages:

There is not an ideal percentage of calories from carbohydrate, Protein, and fat for all
persons with diabetes.

There are two main Eating Plans using carbohydrate counting; using insulin-to-carbohydrate
ratios to adjust premeal insulin doses for variable carbohydrate intake, or following a
consistent carbohydrate Eating Plan when using fixed insulin regimens.

 1 unit insulin = 15 g of carbohydrate

High insulin resistance (also called low insulin sensitivity) will result in lower grams of
carbohydrates covered by 1unite of insulin.

Low insulin resistance (also called high insulin sensitivity) will result in higher grams of
carbohydrate covered by one units of insulin.

Insulin to carb ratio (ICR)500 rule.

500/ Total daily does of insulin "Basal and bolus dose"

Adjusting blood sugar:

Correction factor (insulin sensitivity factor). Amount of blood glucose lowering expected
from 1 unit of insulin. Typically added at meal times to get glucose down to target.

Rule of 100 if mmol/l (or1800 if mg/dl)

1 mmol/l = 18mg/dl

Divide by TDD.

I.E: total daily does 50 units.

(if mmol/l):

100/50= 2mmol/l

1 unite will lower 2mmol/l glucose.

 (if mg/dl):

1800/50=36 mg/dl

Glycemic Index and Glycemic Load it's not indicative of glycemic control because has high
various responses

Physical Activity:

Adults with diabetes should be advised to perform at least 150 Min/week of moderate-
intensity aerobic physical activity or at least 90 min/week of Vigorous aerobic exercise
spread over at least 3 days/week with no more than 2 Consecutive days without physical
activity.

Medications:

 Glucose-Lowering Medications for Type 2 Diabetes

  Insulin

Hyperglycemic hyperosmolar state (HHS).

Show mostly in adults, Patients with HHS have a very high blood Glucose level (ranging from
400-2800 mg/dl, [22.2 to 155.6 Mmol/L] without ketones. Patients are markedly
dehydrated.
Treatment consists of hydration and small Doses of insulin to control hyperglycemia.

Diabetic ketoacidosis (DKA)

DKA life-threatening but reversible complication characterized by severe Disturbances in
carbohydrate, protein, and fat metabolism. DKA is always the result of inadequate insulin for
glucose use.

Blood glucose levels (.250 Mg/dl but generally ,600 mg/dl) and the presence of ketones in
the blood and urine. Treatment includes supplemental insulin, fluid and electrolyte
Replacement, and medical monitoring. Acute illnesses such as flu, colds, vomiting, and
diarrhea, if not managed Appropriately, can lead to the development of DKA.
acute complications most common :
 Hypoglycemia
 diabetic ketoacidosis

Long-term complications of diabetes:

 macrovascular diseases
o Dyslipidemia
o Hypertension
 microvascular diseases
o Diabetic Kidney Disease
o Retinopathy
o Neuropathy
 Gastroparesis is characterized by delayed gastric emptying In the
absence of mechanical obstruction of the stomach