Polyuria and polydepsia

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Polyuria and polydepsia

• DR Badi AlEnazi
• Consultant pediatric endocrinology and
  diabetologest

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Polyuria causes

• DM
• Diabetes inspidus
• Hypokalemia
• Cerbral salt wasting
• Psychotic polydepsia
• Chronic Renal disease
• Hypercalcaemia

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What investigations needed?

• Glucose
• Serum K
• Serum ca
• Serum cretenin
• Serum osmolality
• Urin osmolality
• Urine sp gravity
• Water deprivation test
• MRI brain

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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

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Diabetes MellitusDiagnosis 2011
Diabetes Mellitus Fasting Glucose gt 125 mg/dl 2
Hour PP Glucose gt 200 mg/dl A1C gt6.5
Pre-Diabetes Fasting Glucose 100-125 mg/dl 2
Hour PP Glucose 140-200 mg/dl A1C 5.7-6.4
(underestimates DM)

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The Worldwide EpidemicDiabetes Trends

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Diabetes Mellitus 26-28 Million Americans in 2010
Type 2 DM Type 1 DM
Leading US Cause Myocardial Infarction Kidney
Failure Amputations Blindness
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95
4,300 New Cases Every Day gt 1,000,000 New
Cases Every Year
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Prevalence in Saudi Arabia
Obesity
Obesity
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Diabetes
Diabetes
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7.5
2005
1990
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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.

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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.

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Etiology

• The cause of T1DM involves both genetic and
  environmental factors.

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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).

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Pathophysiology

• T-cell activation leads to B-cell
  inflammation (insulitis) and to subsequent cell
  loss through apotosis.
• The rate of B-cell loss varies (monthsyears) and
  the timing and presentation of symptomatic
  diabetes may depend on factors that
• increase insulin requirements (e.g. puberty).

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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.

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Clinical presentation

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

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Assessment of new patient

• History duration of symptoms.
• Family history of diabetes/other autoimmune
  disease.
• Examination weight/BMI signs of DKA

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Diagnosis and investigations

• The diagnosis is readily established in a
  symptomatic child with a random blood glucose
  level gt11.1mmol/L. Other investigations
• UE.
• 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.

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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

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• 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

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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.

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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.

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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.

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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.
• .

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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

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Insulin type
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Insulin regimens

• The daily requirement for insulin varies with
  age
• at diagnosis, 0.5U/kg/day
• childhood/prepubertal, 0.51.0U/kg/day
• puberty, 1.22.0U/kg/day
• post-puberty, 0.71.2U/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.

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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.

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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.

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• Three-dose regimen Improvement and
  intensification of the two-dose
• regimen
• 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.

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Hypoglycaemia

• All children with T1DM will experience an episode
  of hypoglycaemia.
• Symptoms develop when blood glucose lt3.5mmol/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.

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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

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

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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

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

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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.

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Diagnosis

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

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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.

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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.

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• THANK YOU