Diabetes

Mellitus
By
Dr. Hams Attalla
Lecturer of pediatrics, Helwan university
• A 7-year-old girl presents with increased thirst and urination over the last
2 weeks. Despite previously being dry at night, she has wet the bed a few
times over the past week. She has not been ill and has had a good
appetite. She has had no abdominal pain or vomiting. Physical
examination is remarkable for dry, tacky oral mucous membranes. Her
weight is down 3 kg since her last well-child visit. A blood sugar is checked
on a meter and is “high” or too elevated to be read by the meter. A
urinalysis shows positive glucose and ketones in his urine. A basic
metabolic profile reveals sodium of 131 mEq/L, bicarbonate of 20 mEq/L,
and plasma glucose of 652 mg/dL. Hemoglobin A1c is 10.8 percent.
 • It is a metabolic disorder characterized by
hyperglycemia and glucosuria and is end-
DIABETES point of a few disease processes.
MELLITUS
• Resulting from insulin deficiency due to islet
ẞ-cell damage.
Defination:
• A diagnosis of DM is made based on four glucose abnormalities that may be
confirmed by repeated testing:
• (1) fasting serum glucose concentration > 126mg/dL.
• (2) a random venous plasma glucose > 200 mg/dL with symptoms of
hyperglycemia.
• (3) an abnormal oral glucose tolerance test (OGTT) with a 2-hour
postprandial serum glucose concentration > 200 md/dL
• and (4) a HgbA1c > 6.5%.
Types:

Type I DM: caused by autoimmune destruction of insulin-

producing ẞ cells.

Type II DM: results from insulin resistance and relative

insulin deficiency usually associated with obesity.

Others: Gestational diabetes, maturity-onset diabetes of

youth, Mitochondrial diabetes.
 Comparision between type I and type II:

TYPE I TYPE II
Incidence 90% of Children <10% of children
Onset Acute, rapid Insidious
Autoimmunity Yes No
Insulin secretion Absent Variable
Insulin dependence Total and severe Uncommon
Ketosis Common Rare
 **Genetic determinants play a
role in the susceptibility to type I,
although the mode of inheritance
is complex and multigenic.
Epidemiology:
**Genetic factors do not fully
account for the susceptibility,
environmental factors also play a
role.
Pathogensis:
An autoimmune process against the pancreatic ẞ-cells→ beta cell destruction.

Antibodies aganist ẞ-cell destruction could be detected (islet cell -antibodies).

▪ The autoimmune process is related to:

-Triggers of antibody production by environmental factors as(viral infections,

diet, cow’s milk proteins)
**There is an association with other autoimmune disorders as autoimmune
thyroiditis & celiac.
Pathogensis:
 Hyperglycemia results when insulin secretory
capacity becomes inadequate to enhance
peripheral glucose uptake and to suppress
hepatic and renal glucose production.
Insulin
deficiency Insulin deficiency usually first causes
postprandial hyperglycemia and then fasting
result in: hyperglycemia.

Ketogensis is a sign of more complete insulin

deficiency.
• 1.Carbohytdrate:
*Glucose uptake +increased glycogenolysis and gluoneogensis(lack of
suppression)→Hyperglycemia →glucosuria →polyurea →dehydration &
electrolyte disturbance(osmotic diuresis with obligate loss of
sodium,potassium and other electrolytes).
• 2.Fat:
*↑lipolysis →↑ketogensis →ketonuria –fruity mouth odor-vomiting-
acidosis(deep rapid breathing & coma)
• 3.Protein:
*↑Protein catabolism→↓Weight
 • The age at presentation:
-It is uncommon before the age of 1 year.
-A peak 4-6 years of age & a second peak at about
10-14 years of age.
** No overall gender difference in incidence exists.
Clinical • Few weeks of Polyuria - polydipsia – weight
Presentation: loss:
- Secondary nocturnal enuresis
- Marked loss of weight
-Picture of complications(diabetic
ketoacidosis may be 1st presentation in 20%)
 Acute:
a. Hypoglycemia
b. Diabetic ketoacidosis

Chronic:
Complication:
- Microvasclupathy as in
(Retinopathy- Neuropathy-
Nephropathy)
- Ischemic heart disease
Treatment:

The diabetic control and avoidance of complications

requires, established insulin regimen, balanced daily
nutrition with blood glucose monitoring, with the
goal of maintaining blood glucose concentration as
close to normal as possible.

Preprandial blood glucose target concentration 90-

130 mg/dL and concentration before bedtime and
overnight 90-150 mg/dL. A goal of HgbA1c <7.5% is
set for children of all ages.
Insulin Regimen:

**Many types of insulin differ in duration of action and time to peak effect.
**These insulins can be used in various combinations, depending on the
needs and goals of the individual patient.
**The most commonly used regimen is that of multiple injections of fast-
acting (Lispro, aspart& glulisine) insulin given with meals in combination with
long-acting basal insulin (Glargine & detemir) given at bedtime.
**Subcutaneous injection by variety of syringe and needle sizes or Pen-like
devices or subcutaneous infusion pump.
** Insulin pumps provide a continuous SC infusion of short-acting insulin, are
being used by children and adolescents who are highly motivated to achieve
tight control.
II. Diet:
Balancing the daily meal plan with the dosage of insulin is
curucial for maintain serum glucose concentrations within the
target range and avoiding hypoglycemia or hyperglycemia,
• -Food intake is divided into three meals with snacks between
meals and before going to bed.
• -Snacks are also given before exercise (to avoid hypoglycemia).
• -A healthy diet is recommended with:
-A high complex carbohydrate(50-65%)(avoid simple CHO)
-Low fat content (<10% of total calories)(plant source is
better)
-The diet should be high in fibre,(prolong release of
glucose)
III. Blood glucose
monitoring:

a. Regular blood glucose measurement, should be

routinely monitored before each meal and at
bedtime: a record should be kept in a dairy
Target: Fasting 80-120
Postprandial 100-140
b. Transcutenous sensors ( continuous glucose
monitoring system)
c. Detection of ketones in urine or blood samples.
d. Every 3 month: Hb A1c to be measured 4.5%-6%
Treatment of acute complication:
Follow up to avoid long-term
complication:
Patients with typeI diabetes should receive:
- annual ophthalmoloical examination for retinopathy.
-Urine should be collected annually for assessment of microalbuminuria,
which suggest early renal dysfunction and indicates a high risk of
progression to nephropathy.
-early detection of hypertension and hypercholesterolemia with
appropriate intervention can help limit future risk of coronary disease.