Type 1 diabetes is an autoimmune disease characterized by the body's inability to produce insulin. It results from the destruction of insulin-producing beta cells in the pancreas. The disease presents with symptoms of hyperglycemia and if left untreated can lead to serious acute complications such as diabetic ketoacidosis. Management involves insulin therapy, dietary changes, exercise, glucose monitoring and patient education to prevent acute complications and reduce the risk of long-term complications affecting the eyes, kidneys, nerves and cardiovascular system. Strict glycemic control is important for improving health outcomes and quality of life.

1. Type1 Diabetes Mellitus
By : Ziad Eidhah Sharaf (MBBS)
e-mail: Ziad5050@Hotmail.com
&
Areej Eidhah Sharaf

2. Objectives :
1. Definition
2. Pathophysiology
3. Clinical Presentation
4. Diagnosis
5. Acute and Chronic complications eg; focusing on:
DKA: Triggering factors, Diagnosis and management
6. Management including:
Insulin therapy ( types, storage, injection sites, side effects and compliance.
Education (Diet, Exercise, Travelling, Schooling, Sick day management, HBGM).
7. Follow up

3. Type 1 diabetes is a chronic illness characterized by the
body’s inability to produce insulin due to the autoimmune
destruction of the beta cells in the pancreas. Although onset
frequently occurs in childhood, the disease can also develop
in adults.
Type 1 diabetes mellitus is a metabolic disorder characterized
by hyperglycemia due to absolute insulin deficiency.
Definition :
introduction

4. There are four stages in the development of Type 1 DM:
1. Preclinical period with positive β-cell antibodies
2. Hyperglycemia when 80-90% of the β- cells are destroyed.
3. Transient remission (honeymoon phase).
4. Establishment of the diseas
Pathophysiology of Type 1 DM

5. Etiology and pathophysiology
• It is polygenic disease .
• Progressive destruction of pancreatic cells.
• Autoantibodies cause a reduction of 80% to 90% of normal cell function
before manifestations occur.
• Up to 90% of patients will have autoantibodies to at least one of 4 antigens:
1- Glutamic acid decarboxylase (GAD).
2- insulin.
3- tyrosine-phosphatase-like molecule, islet auto-antigen-2
4- β-cell-specific zinc transporter 8 autoantibodies.

6. Pathophysiology:
 Pathogenesis of Type 1A DM is explained on the basis of 3
mutually-interlinked mechanisms:
 Pathogenesis of Type 1B DM remains idiopathic.
A. Genetic susceptibility.
B. Autoimmune factors.
C. Certain environmental factors.

7. Genetic issues :
o Monozygotic twins have 60% lifetime concordance for developing IDDM (insulin
dependent DM) .
o Dizygotic twins have an 8% risk of concordance, which is similar to the risk among
other siblings
o The frequency of diabetes developing in children with a diabetic mother is 2-3% and
5-6% if the father has IDDM
o The risk to children rises to almost 30% if both parents are diabetic.
o HLA class II molecules DR3 & DR4 are associated strongly with IDDM (risk
developing other autoimmune endocrinopathies & celiac disease in positive DR3)

8. Clinical
Presentation
Early symptoms of type 1 diabetes :

9. Advanced symptoms of type 1 diabetes

11.  Full history and physical examination
 Initial evaluation and testing
 Basic metabolic panel
 CBC
Diagnosis
• Eelectrolytes , urinalysis
• Venous or arterial blood gas
• Liver function tests, and calcium, magnesium,
phosphorus

12. Random blood sugar test. This is the primary screening test for type 1
diabetes. A blood sugar level of 200 (mg/dL), or 11.1 (mmol/L), or higher
suggests diabetes.
Glycated hemoglobin (A1C) test.
An A1C level of 6.5 percent or higher on two separate tests indicates
diabetes.
Fasting blood sugar test. A fasting blood sugar level of 126 mg/dL (7.0
mmol/L) or higher suggests type 1 diabetes.
Diagnostic tests of diabetes in children:
(Criteria)

13.  The diagnosis of type 1 diabetes is often obvious from the clinical
presentation, but can be confirmed through additional testing:
In addition to the Diagnostic Criteria :
1- Low C-peptide levels
2- Presence of one or more autoimmune markers are consistent
with a diagnosis of type 1 diabetes

14. Acute complication Chronic complication
Complications of diabetes mellitus 1
Diabetic ketoacidosis (DKA)
Hypoglycemic coma
HHC
Microvascular
• Retinopathy
• Nephropathy
• Neuropathy
Macrovascular
• Cerebrovascular
• Cardiovascular
• Peripheral Vascular disease

15. 15
Acute complications of diabetes mellitus
Diabetic
ketoacidosis
Diabetic nonketotic
hyperosmolar coma
Hypoglycemia

16. Diabetic keto acidosis DKA :
• It is one of the acute complication of the
type 1 DM and sometime it is the first
presentation of the patient.
• Occurs in the absence of insulin and
Results in metabolic acidosis.
• characterized by hyperglycemia,
ketoacidosis, and ketonuria

17. 17
Diabetic ketoacidosis (DKA)
May be the 1
st
presentation of type 1 DM.
Mortality rate around 5%.
Result from absolute insulin deficiency or increase requirement.
Major, life-threatening complication of diabetes characterized by
hyperglycemia, ketoacidosis, and ketonuria.

18. 18
Predisposing factors for DKA
o Inappropriate withdrawal insulin
o Low socioeconomic status
o Delayed diagnosis
o young age
o Infection
o Stress
o Others

19. 19
Pathogenesis
=> glycosuria,
osmotic diuresis &
dehydration
Hepatic glucose
production increase ↑ &
↓glucose utilization of
peripheral tissue
Insulin decrease↓
Lead to the release of free
fatty acid into circulation
from fatty tissue.
Unrestrained hepatic fatty acid
oxidation to ketone bodies (β-
hydroxybutyrate, acetone,
acetoacetate)
=> resulting in ketonemia
and metabolic acidosis.

20. Clinical presentation of DKA

21. Diagnosis
• The diagnosis of DKA is based on identification of the biochemical triad of
hyperglycaemia, acidaemia and ketonaemia/ketonuria.
• Immediate investigations to establish diagnosis of DKA:
o Laboratory glucose: > 11.0 mmol/L
o Venous/arterial blood gas: pH < 7.3 or bicarbonate < 15 mmol/L
o Ketone testing: capillary blood ketone ≥ 3 mmol/L or *urinary ketones +++ or above

23. Investigations
The main investigations in the management of DKA include a laboratory
glucose, venous/arterial blood gas and a ketone measurement (blood/urine).
Nevertheless, a full set of investigations are essential to properly assess for any DKA precipitants
and monitor for complications (e.g. electrolyte derangements, acute kidney injury).
Bedside tests
• ECG
• Urinalysis +/- MSU
• Urinary pregnancy test
Blood tests
• FBC
• U&Es
• CRP
• LFTs
• Blood cultures
• Troponin
Imaging
• Chest X-ray

24. 24
Complication of DKA
Respiratory distress
syndrome
MI
Infection
Vascular thrombosis
Cerebral edema

25. Treatment:
25
• Fluid replacement
• Insulin therapy for hyperglycemia.
• Electrolyte correction.
• Acidosis correction.
• Treatment of precipitating cause.

26. 26
Treatment
• Fluid replacement
• Insulin therapy for hyperglycemia.
• Electrolyte correction.
• Acidosis correction.
• Treatment of precipitating cause.
summary

27. 27
Hypoglycemic coma
Hypoglycemia is the level of blood glucose at
which autonomic and neurological dysfunction
begins
Hypoglycemia is the most frequent acute complication in
diabetes.

28. 28
Predisposing factors
Missed meal
Alcohol ingestion
Alterations or errors in insulin dosage
Change in physical activity

29. 29
Autonomic dysfunctions
Clinical manifestations of hypoglycemia
Hunger Tremor Palpitation
Anxiety Pallor Sweating

30. 30
Neurologic dysfunctions
Clinical manifestations of hypoglycemia:
Impaired thinking Change of mood Irritability
Headache Convulsion Coma

31. 31
Treatment of hypoglycemia
In mild cases oral rapidly
absorbed carbohydrate
In sever cases (comatose patient)
iv hypertonic glucose 25% or 50%
concentration
Glucagons injection

32. 32
Chronic complications of diabetes mellitus
Macrovascular
Microvascular
• Retinopathy
• Nephropathy
• Neuropathy
• Cerebrovascular
• Cardiovascular
• Peripheral Vascular disease

33. 33
Macrovascular Microvascular
Stroke
Heart disease and
hypertension
Ulcers & amputation
Diabetic eye disease
(retinopathy and cataracts)
Renal disease (Kidney)
Neuropathy
Foot problems
Peripheral
vascular disease
Diabetes Complications

34. 34
Macrovascular
Peripheral Artery
Disease
Coronary heart disease
cerebrovascular
disease

35.  Nephropathy by ACR (albumin creatinine ration ) > 30-300 mg/g (give ACE inhibitors ) .
 Retinopathy : by ophthalmologist >> if severe non-proliferative retinopathy or worse
and/or diabetic macular edema >> Laser treatment (photocoagulation ) and intravitreal
injections of anti-VEGF agents reduce the rate of visual loss.
 Neuropathy >> by neurological examination .
Screening of the chronic complication (Nephropathy , Neuropathy , Retinopathy)
should start from age 11 years with 2 to 5 years diabetes duration.

36. Strict glycemic control.
Control the blood pressure.
Control the lipid profile.
Limitation of protein diet.
Prevention of chronic complication by:

37. Management of
type 1 DM

38. 38
Objectives
Site of injection
Adverse affect
Storage
Type of insulin therapy

39. Type of DM

40. TYPE OF INSULINType of insulin therapy

41. Common Site of injection
41

42. 42
Storage of insulin
Store at room temperature ( 15 - 25 c ) after use .
Rapid acting in use should be stored at 4c .

43. 43
Six Essential Tips for Storing Insulin
2 4
31
Do not keep in
hot places.
Do not leave
in sunlight.
Write the date down
Never use insulin
if expired.
Do not keep in
freezing places.
5
6
Inspect your insulin
before each use

44. 44
Adverse affect
Hypoglycemia Hypokalemia Hypersensitivity
reactions

45. 45
Adverse affect
insulin resistant
Local adverse affect

46. Education & Follow up
of Type 1 DM

47. 47
Diabetes education
“Diabetes education is an interactive process that facilitates
and supports the individual and/or their families, those who
provide care or significant social contacts to acquire and
apply the knowledge, confidence, and practical, problem
solving and coping skills, needed to manage their life with
diabetes in order to achieve the best possible outcomes
within their own unique circumstances”

48. 48
Collaborative Care to Achieve Control of DM1
Patient teaching
Nutritional therapy
Drug therapy
,
Exercise
Self-monitoring of
blood glucose
Sick day management

49. - Physician
- Diabetic educator
- Dietician
- Patient  parents
- Psychologist /
psychiatric
- Social worker
To Achieve Tight Control of
DM1 By 2 ways : Components of
Therapy ( education )
49
Diabetic Team
Approach
insulin
exercise
nutrition

50. HEALTH
1- Equipment and supplies needed to effectively manage insulin
therapy at home:
• Insulin
• Syringes or pen needles
• Blood glucose meter and strips
• Lancets and lancing device
• Glucagon emergency kit
• Contact information of diabetes care provider
Patient education : Insulin therapy

51. HEALTH
Patient education : Insulin therapy
2- What Patients Need to Know About Insulin and Delivery
Devices:
• Storage and expiration
• When it should be refrigerated
• When it can be at room temperature
• When medication expires after first use
• How to prepare product for first use
• How to properly use the device
• How to dispose of the device

52. HEALTH
• Glucagon emergency kit• Lancets and lancing device
1- Patient education :

53. HEALTH
• Current dietary management of diabetes emphasizes a healthy, balanced diet
that is high in carbohydrates and fiber and low in fat.
• The following are among the most recent dietary consensus recommendations
(although they should be viewed in the context of the patient’s culture) :
Nutrition therapy
Should provide 50-55% of daily energy intake :Carbohydrate intake should emphasize
nutrient-dense carbohydrate sources that are high in fiber, including vegetables, fruits,
legumes, whole grains, as well as dairy products.
1- Carbohydrates

54. Nutrition therapy
2- Fat
• Should provide 30-35% of daily energy intake
• diet rich in monounsaturated and polyunsaturated fats may be considered to improve
glucose metabolism and lower cardiovascular disease risk and can be an effective
alternative to a diet low in total fat but relatively high in carbohydrates
• Should provide 10-15% of daily energy intake
3- Protein

55. HEALTH3- Eexercise
Regular physical activity ≥3 times per week for ≥60 minutes
each time should be encouraged for all children with diabetes

56. HEALTH4- Home self-monitoring of glucose
 tracks immediate and daily levels of glucose control.
 Helps to determine immediate and ongoing basal and bolus insulin
requirements.
 Detects hypoglycemia and assists in its management.
 Assists in the appropriate management of hyperglycemia.
 Helps guide insulin adjustments to decrease glucose fluctuations.

57. HEALTH4- Home self-monitoring of glucose
• For most patients who require insulin, HMBG is recommended two to four
times daily (usually before meals and at bedtime).
• For patients who take insulin before each meal, SMBG is required at least
three times daily before meals To determine each dose.

58. 58
Sick day management
 sick day :A sick day is when there is illness or infection.
 this needs to make changes to usual diabetes management plan to
keep blood glucose levels fin normal level

59. 59
Sick day management
Some illnesses, especially those associated with fever, raise blood glucose levels because
of higher levels of stress hormones promoting glycogenolysis, gluconeogenesis, and insulin
resistance.
 Illness often increases ketone body production due to inadequate insulin levels and the
counter-regulatory hormone response.
In contrast, illness associated with vomiting and diarrhea (eg, viral gastroenteritis) may
lower glucose levels with the increased possibility of hypoglycemia rather than
hyperglycemia.
Why it’s important to manage sick days

60. 60
Sick day guidelines in management
. 5. Treat any
underlying,
precipitating
illness.
4. Monitor and
maintain hydration
with adequate salt
and water balance
3. DO NOT
STOP INSULIN
2-More frequent
blood glucose
and ketone
(blood or urine)
monitoring.
1- Sick day guidelines
including insulin
adjustments, should be
taught soon after
diagnosis and reviewed
at least annually with
patients and family
members in order to
reduce risk for DKA and
for severe hypoglycemia
(with GI illnesses).

61. Patient with diabetes Follow up
 interval medical history,
 assessment of medication- “taking behavior and intolerance/ side effects”
 physical examination
 laboratory evaluation as appropriate to assess attainment of A1C and metabolic targets,
 assessment of risk for complications
 diabetes self-management behaviors, nutrition, psychosocial health
 and the need for referrals, immunizations, or other routine health maintenance screening.
 If tests are normal for diabetes , repeat testing carried out at a minimum of 3-year intervals
is reasonable.
Most components of the initial comprehensive medical evaluation
including:

62. DONE