1. Polyuria and polydepsia
DR Badi AlEnazi
Consultant pediatric endocrinology and diabetologest

2. Polyuria causes DM Diabetes inspidus Hypokalemia Cerbral salt wasting
Psychotic polydepsia
Chronic Renal disease
Hypercalcaemia

3. What investigations needed?
Glucose
Serum K
Serum ca
Serum cretenin
Serum osmolality
Urin osmolality
Urine sp gravity
Water deprivation test
MRI brain

4. What Diabetes is NOT Diabetes is NOT “a touch of sugar”
DRAFT - Jan4Kitchener.ppt
What Diabetes is NOT
Diabetes is NOT “a touch of sugar”
It is a serious chronic disease that can lead to complications such as heart attack, stroke, blindness, amputation, kidney disease, and nerve damage 4

5. Diabetes MellitusDiagnosis 2011
Fasting Glucose > 125 mg/dl
2 Hour PP Glucose > 200 mg/dl
A1C >6.5%
Pre-Diabetes
Fasting Glucose: mg/dl
2 Hour PP Glucose: mg/dl
A1C: % (underestimates DM)* *

6. The Worldwide Epidemic: Diabetes Trends
DRAFT - Jan4Kitchener.ppt
The Worldwide Epidemic: Diabetes Trends
30million
million Sept 2002 Fact Sheet#236
million
million Zimmet
million Sept 2002 Fact Sheet#236
million 6

7. Myocardial Infarction
Diabetes Mellitus
26-28 Million Americans in 2010
Type 2 DM
Type 1 DM
Leading US Cause
Myocardial Infarction
Kidney Failure
Amputations
Blindness 5%
95 %
~ 4,300 New Cases Every Day
> 1,000,000 New Cases Every Year

8. Prevalence in Saudi Arabia
Obesity
Obesity
45%
15%
Diabetes
Diabetes
23%
7.5%
1990
2005

10. Type 1 diabetes mellitus
most common form of diabetes mellitus in children and adolescents(90% of cases).
It is an autoimmune disorder characterized by T-cell mediated destruction and progressive loss of pancreatic B-cells leading to eventual insulin deficiency and hyperglycemia.

12. Epidemiology
The incidence of Type 1 diabetes mellitus (T1DM) has been increasing, but shows marked geographical variation. In Europe the highest incidence rates are seen in (Finland, Sweden).
During childhood there are two peaks in presentation, one between ages 5 and 7yrs and before or at the onset of puberty.
seen in the winter months.

13. Etiology
The cause of T1DM involves both genetic and environmental factors.

14. Pathophysiology T1DM is a chronic autoimmune condition.
Immune tolerance is broken and antibodies against specifi c B-cell autoantigens are generated (e.g. anti-islet cell; anti-insulin; anti-GluAD; anti-IA2 antibodies).

15. Pathophysiology
T-cell activation leads to B-cell inflammation (‘insulitis’) and to subsequent cell loss through apotosis.
The rate of B-cell loss varies (months–years) and the timing and presentation of symptomatic diabetes may depend on factors that
increase insulin requirements (e.g. puberty).

16. Clinical presentation
The onset of symptoms evolves over a period of weeks. Symptoms are a reflection of insulin deficiency resulting in increased catabolism and hyperglycaemia.
In the majority, first presentation is usually made in the early symptomatic phase with:
weight loss;
polyuria/polydipsia;
nocturia/nocturnal enuresis.
Other less common symptoms include:
candida infection (e.g. oral thrush, vulovaginitis)
skin infections.

17. Clinical presentation
Failure to recognize these symptoms will result in delayed or late diagnosis
And presentation with DKA

18. Assessment of new patient
History: duration of symptoms.
Family history: of diabetes/other autoimmune disease.
Examination: weight/BMI; signs of DKA

19. Diagnosis and investigations
The diagnosis is readily established in a symptomatic child with a random blood glucose level >11.1mmol/L. Other investigations:
U&E.
Blood pH (to exclude DKA).
Diabetes-related autoantibodies: islet cell antibody (ICA)/anti-insulin
antibody (IAA)/anti-GluAD antibody (GluAD)/anti-IA-2.
Other autoimmune disease screen: thyroid function test/thyroid antibodies; coeliac disease antibody screen.

20. Type 1 diabetes mellitus: management
All newly diagnosed patients must start insulin therapy as soon as possible.
An intensive programme of education and support is needed for the child and parents. The aims of management of T1DM are:
• education of child and family about diabetes;
• insulin therapy;
• nutritional management;
• monitoring of glycaemic control;

21. avoidance and management of hypoglycaemia;
• management of acute illness and avoidance of DKA
• screening for development of associated illness
• screening for diabetes-related microvascular complications
• prevention and treatment of microvascular complications

22. Education, counselling, and support
An intensive programme of education and counselling is needed in the first few days/weeks to cover the fundamental principles about T1DM andits management. • Basic pathophyisology of T1DM. • Insulin therapy: • actions of insulin; • SC injection techniques; • dose adjustment principles, including carbohydrate counting Tchniques. • Home/self blood glucose monitoring.

23. Education, counselling, and support
Acute complications:
• avoidance, symptom recognition, and treatment of hypoglycaemia
and diabetic ketoacidosis
• ‘sick day rules’ during illness to prevent DKA
• Diet:
• healthy, low-fat;
• high complex carbohydrate.
• Long-term complications: risk factors and avoidance.
• Psychological issues.

24. Nutritional management
Diet and insulin regimen need to be matched to optimize glycaemic control.
Instruction on and application of carbohydrate counting techniques
are required. A healthy diet is recommended with a high complex carbohydrate
and relatively low fat content.

25. Blood glucose monitoring
• Regular daily blood glucose monitoring and testing when blood levels are suspected to be low or high is recommended. • Home blood glucose monitoring is normally carried out using a portable glucose meter and finger-pricking device. .

26. Blood glucose monitoring
• Regular testing is required to assist with insulin dose-adjustment decisions, and to learn and predict how changes in lifestyle, food, and exercise affect glycaemic control. • A minimal testing frequency of 4 times per day should be encouraged. • SC continuous glucose monitoring (CGM) devices are also now available and in certain select situations may offer some advantages and benefi ts to patients

27. Insulin type

28. Insulin regimens The daily requirement for insulin varies with age:
• at diagnosis, 0.5U/kg/day;
• childhood/prepubertal, 0.5–1.0U/kg/day;
• puberty, 1.2–2.0U/kg/day;
• post-puberty, 0.7–1.2U/kg/day.
Insulin is administered SC, usually as a bolus injection.
A number of patients receive insulin in the form of a continuous SC insulin infusion (CSII) delivered by a pump device.

29. Insulin regimens
Insulin injection sites include the SC tissues of the upper arm, the anterior and lateral thigh, the abdomen, and buttocks.
The choice of regime is a compromise between achieving optimal therapy
and minimizing psychosocial development. The patient and family must have input into the choice.

30. Insulin regimens
Two dose regimen The simplest regimen. Two injections per day. Each injection is a mix of short/rapid-acting insulin plus an intermediate-acting insulin. Traditionally 2/3 of the total daily dose is given at breakfast and 1/3 given before/at the evening meal. Disadvantages • Need to mix insulins. • Peak action of insulin does not correspond with timing of main meals. • Increased frequency of between meal and nocturnal hypoglycaemia. • Between meal snacks required to minimize hypoglycaemia. Note: Less hypoglycaemia with rapid analogue insulin use.

31. Three-dose regimen Improvement and intensification of the two-dose
• Basal insulin: once a day intermediate- or long-acting insulin
(traditionally at bedtime).
• Fast-acting insulin: At meal times (i.e. 3 per day) and with between
meal snacks.
Advantages
• Increased flexibility with meal times/exercise planning.
• Insulin dose adjustment— carbohydrate (CHO) counting.
Disadvantages
• Need for more injections.
• Need more frequent blood glucose monitoring.

40. Hypoglycaemia
All children with T1DM will experience an episode of hypoglycaemia.
Symptoms develop when blood glucose <3.5mmol/L. The frequency of hypoglycaemia is higher with more intensive insulin regimens and in young
children. Symptoms and signs include:
• feeling of hunger;
• sweatiness;
• feeling faint/dizzy;
• irritability/confusion.
• pallor.

41. Hypoglycaemia Hypoglycaemia: management
Acute episodes of mild to moderate symptomatic hypoglycaemia can be managed with oral glucose (glucose tablets or sugary drink). Oral glucose
gels applied to the buccal mucosa can be used in the child who is unwilling or unable to cooperate to eat. Severe hypoglycaemia can be managed in
the home with an intramuscular injection of glucagon 1mg

42. Diabetes Complications
DRAFT - Jan4Kitchener.ppt
Diabetes Complications
Macrovascular
Microvascular
Stroke
Diabetic eye disease
(retinopathy and cataracts)
Heart disease and hypertension
Renal disease (Kidney)
Peripheral
vascular disease
Neuropathy
Foot problems
Ulcers and amputation 42

43. Type 2 diabetes mellitus
T2DM is a multifactorial and heterogeneous condition in which the balance between insulin sensitivity and insulin secretion is impaired.
is characterized by hyperinsulinaemia; however, there is relative insulin insufficiency to overcome underlying concomitant tissue insulin resistance.

44. Epidemiology
T2DM is emerging as a significant health problem with increasing incidence in most developing countries.
The increasing frequency of T2DM parallels
the upward trend in childhood obesity in these populations.
T2DM now accounts for up to 45% of the new cases of diabetes diagnosed in childhood in USA

45. CHEESEBURGER Today 20 Years Ago 333 calories 590 calories
Calorie Difference: 257 calories

46. Aetiology T2DM is not an autoimmune disease.
a strong genetic basis, which is thought to
be polygenic.
risk factors for the development of T2DM are
as follows.
• Obesity.
• Family history of T2DM.
• Ethnic origin:
• Asian;
• Polycystic ovarian syndrome.
• Small for gestational age (SGA).

47. Clinical features
Clinical presentation ranges from mild incidental hyperglycaemia to the typical manifestations of insulin deficiency.
Presentation with DKA may occasionally be seen.
acanthosis nigricans.

50. Diagnosis
Current diagnostic prerequisites for T2DM are: • presence of T2DM risk factors • lack of absolute/persistent insulin defi ciency; • absence of pancreatic autoantibodies.

51. Management
All patients with T2DM require the same type and degree of educational support and clinical follow-up as for patients with T1DM.
Specific treatment goals should in addition include the following:
• aim to improve insulin sensitivity and insulin secretion;
• manage obesity and its comorbidities via lifestyle changes;
• screening and management of T2DM comorbidities such as hyperlipdaemia and hypertension.

52. Management
Mild (incidental) T2DM should initially be managed with lifestyle interventions
aimed at lowering caloric intake (low fat; reduced CHO diet)
and increasing physical activity. Where these interventions fail, pharmacological
therapy is added. In children, the oral insulin sensitizing agent
metformin is added as a fi rst step; however, if glycaemic targets remain
diffi cult to achieve insulin therapy should be included.

56. THANK YOU