DIABETES MELLITUS an up-to-date 2017- 2018

1. TOPIC : DIABETES MELLITUS
Group E & F, 55th MBBS
Chittagong Medical College
Integrated Teaching Program

2. CHAIRPERSON: Professor Dr. Asok Kumar Dutta
CHIEF GUEST : Professor Dr. Selim Mohammad
Jahangir
SPECIAL GUEST: Brigadier General Dr. Jalal Uddin
Professor Dr. Pradip Kumar Dutta

3. UMME KANIJ FATEMA
MD. ZAHIRUL ISLAM MD.EBNUL AKIL
NOWSHIN SAMREEN
MD. ISMAIL HOSSAIN
FARIA HOSSAIN
NAREN CHOWDHURY
ISRAT SHAHRIN AZAD
Presented By

4. INTRODUCTION AND
APPROACH
MD. ISMAIL HOSSAIN HRIDOY

5. INCIDENCE WORLDWIDE

6. DEFINITION
A metabolic disorder of multiple etiology
characterized by chronic hyperglycemia with
disturbances of CHO, fat and protein metabolism
resulting from defects in insulin secretion, insulin
action or both.

7. CLASSIFICATION
• Type 1 diabetes
• Type 2 diabetes
• Gestational diabetes
• Other specific types

8. GLUCOSE HOMEOSTASIS

9. GLUCOSE HOMEOSTASIS (CONT.)
Blood Glucose
Glucagon
GH
Cortisol
Insulin

10. GLUCOSE TRANSPORTERS

12. PATHOGENESIS OF TYPE 1 DIABETES

13. TYPE 2 DIABETES
• The central pathology is insulin resistance and abnormal insulin
secretion.
• The disease is polygenic and multi-factorial (obesity, nutrition,
physical activity)
• In-utero environment also contributes the pathogenesis of
diabetes mellitus.

14. PATHOGENESIS
INSULIN RESISTENCE
COMPENSATORY HYPERINSUNAEMIA
IGT
IFG
TYPE 2 DM

15. INSULIN SENSITIVITY

16. FEATURES

17. PREVENTION
• Prevention of type 1 diabetes is not possible yet
• As IFG and IGT are pre-diabetic conditions, extensive life
style and dietary modification can delay or prevent type 2
diabetes
• Some experts also suggest Metformin as a preventive drug

18. APPROACH TO THE PATIENT
Patient may present with variable presentations:
1. Asymptomatic
2. Hyperglycemia
3. Complications secondary to hyperglycemia
4. Diabetic Ketoacidosis

19. ASYMPTOMATIC
Most of the patients are diagnosed by routine
investigations during check ups or medical
conditions or before surgery.

20. HYPERGLYCEMIA
Symptoms
 Thirst and dry mouth
 Polyuria
 Nocturia
 Tiredness and fatigue
 Mood change
• Weight loss
• Blurring of vision
• Genital candidiasis
• Nausea and headache

21. COMPLICATIONS SECONDARY TO
HYPERGLYCEMIA
• Eye complications
• Renal complications
• Neurological complications
• Oral complications
• Foot complications
• CVS complications
• Pregnancy related &
dermatological
complications

22. EYE SYMPTOMS
• Dimness of vision

23. RENAL SYMPTOMS
• Chronic kidney disease

24. NEUROLOGICAL SYMPTOMS
Peripheral neuropathy
• Tingling
• Numbness
• Paresthesia
Erectile Dysfunction

25. ORAL SYMPTOMS
• Oral candidiasis

26. DERMATOLOGICAL MANIFESTATIONS
• Fungal infection
• Balanitis
• Acanthosis Nigricans

27. FOOT MANIFESTATIONS
• Blisters
• Fissures
• Cracks
• Ulcers
• Gangrene
• Charcot’s Arthropathy

28. CVS MANIFESTATIONS
• Stroke
• Myocardial Infarction
• Transient Ischaemic Attack

29. PREGNANCY RELATED MANIFESTATIONS
• Big baby
• Difficult labor

30. DIABETIC KETOACIDOSIS
• Type 1 diabetes mellitus may manifest as DKA in 30% cases
It is a medical emergency.
Symptoms
• Polyuria, thirst
• Weight loss
• Weakness
• Nausea
• Blurred Vision
• Abdominal Pain
• Vomiting

31. HISTORY ,
EXAMINATION ,
ORAL DRUGS
UMME KANIJ FATEMA

32. HISTORY
A complete history with special emphasis on:
1) Weight
2) Family history of DM and it’s complications
3) Risk factors for cardiovascular diseases
4) Exercise
5) Smoking
6) Ethanol use

33. HISTORY (cont.)
In diagnosed case of DM, emphasize on prior diabetic
care:
Type of therapy
HbA1c level
Self monitoring blood glucose result
Frequency of hypoglycemia
Presence of any complication
Patient education
Exercise
Nutrition

34. EXAMINATION

35. INVESTIGATION
• Blood glucose - fasting and 2 hours after 75gm oral glucose
load
• Glycated hemoglobin
• Urine testing for glucose and protein

36. ORAL GLUCOSE TOLERANCE TEST
• Whom to test
Age >45 years
Body mass index >25, In case of Asian >23
History of big baby
History of GDM
History of Impaired glucose tolerance

37. OGTT

38. OGTT(cont.)

39. GLYCATED HEMOGLOBIN
• HbA1c is a reflection of glycemic history over the previous 2-3
months.
• Advantages of measuring HbA1c
Greater convenience(fasting not required).
More pre-analytical stability.
Less day to day perturbations during stress and illness .

40. LIMITATIONS
• Hemoglobinopathies
• Anemias
• Reticulocytosis
• Uremia interfere with HbA1c result
• Pregnancy

41. DIAGNOSIS
• Symptoms of diabetes plus random blood glucose
concentration ≥11.1mmol/L (200mg/dl) or
• Fasting plasma glucose ≥7mmol/L (126mg/dl) or
• HbA1c ≥6.5% or
• 2 hour plasma glucose ≥11.1mmol/L (200mg/dl) during an
OGTT
Note: In the absence of unequivocal hyperglycemia and acute metabolic
decompensation, this criteria should be confirmed by repeat testing on
a different day.

42. PRE-DIABETIC CONDITION
• Impaired fasting glucose (IFG)
• Impaired glucose tolerance (IGT)
Fasting plasma glucose 5.6-6.9mmol/L (100-125mg/dl)
Plasma glucose level 7.8-11mmol/L (140-199mg/dl)

43. MANAGEMENT
 Diet
 Drugs
 Discipline ( Lifestyle )

44. GOALS OF NUTRITION THERAPY FOR ADULTS
WITH DIABETES
○ Achieve and maintain body weight goals
○ Attain individualized glycemic, blood pressure, and lipid goals
○ Delay or prevent the complications of diabetes

45. DEFINITIVE MANAGEMENT GOALS

46. LIFESTYLE
• Nutrition
• Physical Activity
• Alcohol
• Quit Smoking
• Psychological Issues

47. NUTRITION THERAPY
What to eat?
What not to eat?
How much I will eat?
Can i take sugar?

48. MEDICAL NUTRITION THERAPY
• Diet should be provided by a Dietitian.
• Macronutrient distribution should be individualized.
• Carbohydrate -whole grains, vegetables, fruits, legumes and foods rich
in fiber and lower in glycemic load
• Daily intake of protein should be individualized
• Diet rich in monounsaturated fat

50. PHYSICAL ACTIVITY
• People are advised to engage in 150min/week of moderate
intensity or 75min/week of vigorous intensity aerobic
physical activity.
• Reduce the amount of time spent in sedentary activity
• Individuals taking insulin and insulin secretogogues should
titrate their dose according to physical activity.

51. DRUGS
 Oral
 Parenteral
 Others

52. ORAL DRUGS AVAILABLE
V
VGlibenclamide
Glyburide
Repaglinide

53. ORAL DRUGS AVAILABLE (CONT.)
SGLT2 inhibitors Inhibition of reabsorption Dapagliflozin
of glucose at proximal Canagliflozin
tubules

54. World Health Day 2016
Poster by WHO

55. INSULIN AND
MANAGEMENT
MD. ZAHIRUL ISLAM

56. PARENTEAL DRUGS AVAILABLE

57. TYPES OF INSULIN
• Human Insulin
• Animal Insulin
• Insulin Analogues

58. INSULIN STRUCTURE

59. INSULIN ANALOGS

60. ADVANTAGES OF INSULIN ANALOGUES
• Full biologic activity like insulin
Short Acting
• More rapid absorption, onset of duration, shorter duration of action
less tendency for self aggregation. So preferred for prandial coverage
Long Acting
• Longer duration of action, less pronounced peak, lower incidence of
hypoglycemia

61. INSULIN PREPARATIONS AVAILABLE

62. DURATION OF ACTION OF INSULIN ANALOGS

63. DIFFERENT COMMERCIAL
PREPARATIONS

64. ROUTE AND SITE
Most patients injects insulin subcutaneously
Site can be
• Anterior abdominal wall
• Upper arms
• Outer thighs
• Buttocks

66. ALTERNATIVE INSULIN THERAPIES
• Continuous subcutaneous (CSII)
• Intraperitoneal or intravenous infusion of insulin
• Artificial pancreas
• Intrapulmonary (inhalation)
• Transdermal

67. DEVICES FOR INSULIN INJECTION
Insulin Pen CSII Insulin Syringe

68. SIDE EFFECTS
• Hypoglycemia

69. • Weight Gain

70. • Lipohypertrophy

71. • Lipodystrophy

72. • Peripheral Edema

73. Local Allergy

74. Insulin Dosing RegimenINSULIN REGIMEN

75. REGIMEN DEPENDS ON
• Desired degree of glycemic control
• Severity of insulin deficiency
• Patient’s lifestyle
• Ability to adjust the insulin dose

76. PHARMACOLOGIC THERAPY
FOR
TYPE 1 DM

77. RECOMMENDATIONS
• Most people with type 1 diabetes should be treated with multiple
daily injections of prandial insulin and basal insulin or continuous
subcutaneous insulin infusion
• Consider educating individuals with type 1 diabetes on matching
prandial insulin doses to carbohydrate intake, premeal blood
glucose levels, and anticipated physical activity

78. • Insulin is the mainstay of therapy for individuals with type 1
diabetes dose is based on weight, with doses ranging from 0.4 to
1.0 units/kg/day of total insulin with higher amounts required
during puberty
• 0.5 units/kg/day as a typical starting dose in patients who are
metabolically stable

79. OTHERS
• (FDA)–approved Pramlintide
for use in adults with type 1 diabetes
• Pancreas and Islet Transplantation

80. PHARMACOLOGIC THERAPY
FOR
TYPE 2 DM

81. RECOMMENDATIONS
• Metformin, if not contraindicated and if tolerated, is the
preferred initial pharmacologic agent for the treatment of
type 2 diabetes
• Who are symptomatic and/or have A1C ≥ 10%
(86mmol/mol) and/or blood glucose levels ≥300 mg/dL
(16.7 mmol/L) - Consider initiating Insulin therapy

82. RECOMMENDATIONS(COTD.)
• A patient-centered approach should be used to guide the choice of
pharmacologic agents. Considerations include efficacy,
hypoglycemia risk, impact on weight, potential side effects, cost,
and patient preferences
• For patients with type 2 diabetes who are not achieving glycemic
goals, insulin therapy should not be delayed

83. RECOMMENDATIONS(COTD.)
In patients with long-standing sub optimally controlled type 2
diabetes and established atherosclerotic cardiovascular
disease
empagliflozin or liraglutide should
be considered

84. Antihyperglycemic therapy in type 2 diabetes: General recommendations

86. ACUTE
EMERGENCIES
OF DIABETES
NAREN CHOWDHURY

87. ACUTE EMERGENCIES OF DIABETES
• Diabetic Ketoacidosis
• Hyperglycemic Hyperosmolar State
• Hypoglycemia

88. DIABETIC KETOACIDOSIS
It is a life-threatening condition that develops when
cells in the body are unable to get the sugar (glucose)
they need for energy because there is not
enough insulin.

89. • DKA is characteristic of type 1 diabetes and is often the
presenting problem in newly diagnosed patients.
• An increasing number of patients presenting with DKA
have underlying type 2 diabetes
• Particularly prevalent in African-American and Hispanic
populations

90. FEATURES
• The cardinal biochemical features are-
Hyperketonaemia ≥ 3 mmol/L
Ketonuria >2+ on standard urine
sticks
Hyperglycaemia Blood glucose ≥ 11
mmol/L
Metabolic acidosis
(venous bicarbonate)
< 15 mmol/L

91. FEATURES
>11
mmol/l
<15 mmol/l
+2 on urine
sticks

92. RISK FACTORS
The risk of diabetic ketoacidosis is highest in
• Type 1 diabetes
• Inadequate insulin administration
• Infection (pneumonia/UTI/gastroenteritis/sepsis)
• Infarction (cerebral, coronary, mesenteric, peripheral)
• Drugs (cocaine)
• Pregnancy

93. INVESTIGATIONS
• Venous blood for urea,
electrolytes, glucose and
bicarbonate.
• Urine or blood analysis
for ketones .
• Blood Gas Analysis.

94. MANAGEMENT
• By cardinal biochemical changes
Confirm
Diagnosis
• ICU is needed if pH is <7.00 or
unconsciousHospitalization
• 2–3 L of 0.9% saline over first 1–3 h
• 150–250 mL/h when plasma
glucose reaches 250 mg/dL
Fluid Therapy

95. MANAGEMENT(CONT.)
• IV (0.1 units/kg) short acting insulin
• Then 0.1 units/kg per hour by continuous IV
infusion
Short Acting
Insulin
• Assess and measure biochemical status
• Precipitating eventsAssess Patient
• 10 meq/h when plasma K+ <5.0–5.2 meq/L
• If initial serum potassium is >5.2 mmol/L dont
supplement K+
Replace K+

96. MANAGEMENT(CONT.)
• It is not usually necessary
• In severe acidosis (arterial pH<7.0), the
ADA advises bicarbonate
Replace
Bicarbonate
• As soon as patient is eating.
• Allow for a 2–4 hour overlap in insulin
infusion and SC insulin injection.
Long Acting
Insulin

97. HYPERGLYCEMIC HYPEROSMOLAR STATE
Hyperglycaemic hyperosmolar state (HHS) is characterised by
Severe hyperglycaemia > 30 mmol/L
Hyperosmolality S.osmolality > 320
mOsm/kg
Dehydration in the
absence of significant
hyperketonaemia
< 3 mmol/L
Acidosis pH > 7.3, bicarbonate
> 15 mmol/L

98. DETECTING PLASMA OSMOLARITY
• If osmolality cannot be measured frequently,
osmolarity can be calculated as follows and used as a
surrogate(based on plasma values in mmol/L):
Plasma osmolarity = 2[Na+ ]+[glucose]+[urea]
• The normal value is 280–290 mmol/L and
consciousness is impaired when it is high (> 340
mmol/L), as commonly occurs in HHS.

99. PATHOPHYSIOLOGY
• Relative insulin deficiency and inadequate fluid intake are
the underlying causes of HHS
• Insulin deficiency increases hepatic glucose production
(through glycogenolysis and gluconeogenesis) and impairs
glucose utilization in skeletal muscle

100. PRESENTATION
• Elderly individual
• With type 2 DM, with a several-week history of polyuria,
weight loss, and diminished oral intake that culminates in
mental confusion, lethargy, or coma

101. MANAGEMENT
Calculate S. osmolality and start fluid
replacement
• 0.9% NaCl if osmolality is stable.
• If osmolality is increasing then give 0.45% NaCl.
• Goal is positive fluid balance of 3–6 L by 12 hrs and
replacement of remaining over next 12 hrs.

102. MANAGEMENT(CONT.)
Insulin infusion
• 0.05 U/kg body weight/hr only when blood glucose is not
falling or,
• Significant ketonaemia, 3β-hydroxybutyrate > 1 mmol/L or
• Urine ketones > 2+
Treat comorbid conditions and give prophylactic
anticoagulants

103. HYPOGLYCEMIA
• Hypoglycemia occurs when blood glucose is < 3.5
mmol/L (63 mg/dL).
• In diabetes it results in
mostly from insulin therapy.

104. SYMPTOMS
Autonomic
• Sweating
• Trembling
• Anxiety
• hunger
Neuroglycopenic
• Confusion
• Drowsiness
• Irritability
• Speech
Difficulty
Non-specific
• Nausea
• Tiredness
• Headache

105. Risk Factors
 Strict glycaemic control
 Impaired awareness of hypoglycaemia
 Age (very young and elderly)
 Long duration of diabetes
 Sleep
 Renal impairment
 Genetic, e.g. ACE genotype

106. TREATMENT
Mild (Self treated)
• Oral fast-acting carbohydrate (10–15 g) is taken as glucose drink or
tablets or confectionery
• Followed with a snack containing complex carbohydrate
Severe(External help needed)
• If unconscious, IV 75 mL 20% dextrose or IM glucagon 1 mg
• If conscious, oral refined glucose as drink or sweets or apply
glucose gel or jam or honey to buccal mucosa

107. DELAYED COMPLICATIONS
FARIA HOSSAIN

108. DELAYED COMPLICATIONS
• Despite all the treatments available, the outcome for
patients with diabetes remains disappointing.
• Long term complications still cause significant morbidity
and mortality.

109. COMPLICATIONS(CONT.)
Microvascular
• Retinopathy
• Nephropathy
• Peripheral and Autonomic Neuropathy
• Foot Disease

110. COMPLICATIONS(CONT.)
Macrovascular
• Coronary Artery Disease
• Peripheral Arterial Disease
• Cerebrovascular Disease
Others
• Gastrointestinal
• Genitourinary
• Dermatological

111. MORTALITY OF DIABETES
70%
10%
10%
6% 1%3%
Cardiovascular Disease Renal Failure Cancer
Infections Diabetic Ketoacidosis Others

112. MICROVASCULAR
cOMPLICATIONS

113. RISK FACTORS FOR INCREASED MORTALITY
AND MORBIDITY
• Duration of diabetes
• Early age at onset
• High glycated Hb (HbA1c)
• Raised Blood Pressure
• Dyslipidemia
• Obesity

114. DIABETIC RETINOPATHY
• Diabetic Retinopathy is one of the most common cause of
blindness between 30 to 65 years of age.
• Prevalence is almost inevitable in type 1 diabetes and
majority of type 2 diabetic patient will develop it after 20
years.

115. FEATURES
• Microaneurysm
• Hemorrhages
• Hard exudates & Cotton wool spots
• Venous beading
• Neovascularization & Vitreous hemorrhages

116. STAGES OF RETINOPATHY
A. Microaneurysm B. Hemorrhages

117. STAGES OF RETINOPATHY(CONT.)
C. Hard exudates D. Cotton wool spots

118. STAGES OF RETINOPATHY(CONT.)
E. Venous beading F. Neovascularization

119. STAGES OF RETINOPATHY(CONT.)
F. Neovascularization G. Vitreous hemorrhages

120. SCREENING
• Annual screening is essential for all diabetic patients to
detect in early stages when treatment is most effective.
• Most preferred method is to do Slit Lamp Biomicroscopy
• Direct Ophthalmoscopy maybe done in dilated pupils.

121. MANAGEMENT
• Maintain good glycaemic control and blood
pressureEarly stages
• Novel agents like Ranibizumab,a VEGF-A
• Retinal photocoagulation (laser treatment)
Advanced
stages
• Vitrectomy in Type 1 diabetesSelected cases

122. DIABETIC NEPHROPATHY
Diabetic Nephropathy is the leading cause of chronic kidney
disease(CKD), ESRD, and CKD requiring renal replacement therapy.

123. NATURAL HISTORY

124. NATURAL HISTORY(CONT.)
Nodular Diabetic Glomerulosclerosis

125. TIME COURSE

126. Screening

127. MANAGEMENT
Type 1 Diabetes
• ACE inhibitors*
Type 2 Diabetes
• ARBs*
*Risk of potential hyperkalemia, thus electrolyte and renal function should be checked.
*Alternatives include CCBs.
**Recent studies shows Renal Transplantation dramatically improves the life.

128. DIABETIC NEUROPATHY
• Diabetic neuropathy occurs in ~50% of individuals with long-standing
type 1 and type 2 DM.
• It may manifest as,
 Polyneuropathy
 Mononeuropathy
 Autonomic neuropathy

129. DIABETIC PERIPHERAL NEUROPATHY

130. CLASSIFICATION

131. SCREENING
• 5 years after diagnosis
• Then at least annually*
Type 1 diabetes
• Immediately after diagnosis*Type 2 Diabetes
•Assessment of either temperature or pinprick
sensation (small-fiber function) and vibration
sensation using a 128-Hz tuning fork (for large-fiber
function)
*ADA 2017 Guideline

132. MANAGEMENT
Glycaemic Control
• In type 1 DM, near normal blood glucose prevent development of
neuropathy.
• In type 2 DM, it delays neuropathy. Insulin sensitizers shown better
effect than insulin/sulfonylurea *.
Neuropathic Pain
• Pregabalin and Dulexetine remains mainstay of treatment.
• *ADA 2017 Guideline

133. MANAGEMENT(CONT.)
Orthostatic Hypotension
• Adequate salt itake,avoid precipitating drugs and
compressive garments
• Midodrine and Droxidopa is recommended by FDA
Gastroparesis
• Small meals,decreasing fat and fibre while avoiding certain
drugs like opioid.
• Metoclopramide(FDA approved)

134. MANAGEMENT(CONT.)
Atonic Bladder
• Intermittent self cathetarization
Erectile Dysfunction
• Phosphodiesterase inhibitors
• Intracorporeal or intraurethral Prostaglandins
• Vacuum devices or penile prostheses

135. DIABETIC FOOT
Any condition involving the foot in a person of
diabetes originating in a chronic or acute
injury to the soft tissues of the foot with
evidence of preexisting neuropathy and/or
ischaemia.

136. CLASSIFICATION
Diabetic
Foot
Neuropathic Foot
(Neuropathy
Predominant)
Neuroischaemic
Foot
(Vascular
Involvement)
With
Infection
Without
Infection
Without
Infection
With
Infection

137. NEUROPATHIC FOOT
Clawing of toes Neuropathic UlcerCharcot foot

138. NEUROISCHAEMIC FOOT
Proximal Arterial Occlusion Digital Gangrene

139. FOOT CARE
• Inspection and washing of foot every day
• Moisturizing feet if dry & cutting toenails regularly
• Avoidance of walking barefooted & refraining from bursting
blisters
• Wearing suitable shoes
• Covering of cuts with sterile dressings

140. SCREENING
• Via proper examination of feet specially pulses
• 10 g Monofilament test
10 g Monofilament test

141. MANAGEMENT
Removal of Callus
Eradication of Infection
Reduction of weight bearing forces

142. SPECIAL
SITUATIONS
NOWSHIN SAMREEN

143. SPECIAL SITUATIONS
SPECIAL ACTIONS

144. DIABETES IN CHILDREN AND ADOLESCENTS
Type 1 Diabetes
• Three-quarters of all cases are diagnosed in <18years olds
Type 2 Diabetes
• Incidence is increasing over the past 20 years
• Different from adult in that there is rapid development of
complications

145. TYPE 1 DIABETES IN YOUTH
• Changes in insulin sensitivity related to physical growth
and sexual maturation.
• Ability to provide self-care.
• Supervision in the school environment.
• Neurological vulnerability to hypoglycemia and
hyperglycemia.
• Adverse neurocognitive effects of DKA.
The unique aspects of youths with type 1diabetes

146. MANAGEMENT
• Youth of type 1 DM and their
caregivers should receive DSME &
DSMS according to national
standards at diagnosis ad
routinely thereafter.
DSME &
DSMS*
• Close communication and
cooperation of school personnel
are essential
School
Care
*Diabetes Self-management Education and Support

147. MANAGEMENT(CONT.)
• Assessment of family stresses and
issues
• Encouraging developmentally
appropriate family environment.
Psychological
Issues
• Lowering glucose as safely as
possible by stepwise goals
Glycaemic
Control

148. MANAGEMENT(CONT.)
An A1C goal of 7.5%(58mmol/mol) is recommended across all
pediatric age-groups

149. MANAGEMENT(CONT.)
It should also include consideration of:
• Autoimmune conditions
• Thyroid diseases
• Cardiovascular risk managements
• Smoking control
• Treatment of complications

150. TYPE 2 DIABETES IN YOUTH
• Rapid decline of beta cell function.
• Additional risk factors like adiposity, family history of
diabetes, female sex, and low socioeconomic status
The unique aspects of youths with type 2 diabetes

151. TESTING FOR TYPE 2 DIABETES OR PREDIABETES IN
ASYMPTOMATIC CHILDREN

152. MANAGEMENT
Only approved drugs are insulin and metformin
Strict lifestyle modifications are essential to
prevent comorbidities
Same as type 1 diabetes plus some additional information as follows:

153. 14November
World Diabetes Day
Theme for this year
‘Women and diabetes –
Our right to a healthy future’
World Diabetes Day became an official United Nations Day since 2006

154. DIABETES AND PREGNANCY
Diabetes and Pregnancy
Gestational diabetes
mellitus
Pregnancy in preexisting
diabetes

155. PREGNANCY IN PREEXISTING DIABETES
General Principle
A1C target 6-6.5% ( relaxed up to 7%)
Fasting and postprandial self-monitoring of blood glucose
DM with HTN , BP target 120-160/80-105 mm-hg

156. PLANNING PREGNANCY IN PREEXISTING DIABETES
Preconception counseling
• Starting at puberty, education on risks of unplanned pregnancy
• Family planning
• Addressing importance of glycaemic control
Risk factors assessment
• Counseling on the risk of developing or progression of diabetic retinopathy

157. PLANNING PREGNANCY IN PREEXISTING
DIABETES(CONT.)
Preconception testing
• Rubella, syphilis, hepatitis B
virus and HIV testing
• Pap smear, cervical cultures
• Blood typing
• A1C,TSH
• Creatinine, and urinary
albumin creatinine ratio
• Review of teratogenic drugs,
i.e., ACEI,ARB and statins
• Comprehensive eye exam

158. MANAGEMENT OF PREEXISTING T1 AND T2
DIABETES
Drug of choice –Insulin
Titration needed as
• 1st trimester- ↓ requirements
• 2nd trimester- ↑requirements ( increasing insulin resistance)
• 3rd trimester- slight ↓in requirements

159. PRECAUTIONS

160. IN PREEXISTING TYPE 1 DM
• Ketone Strip to recognize Diabetic Ketoacidosis
• Education of patients and family members about Prevention,
Recognition and Treatment of hypoglycemia
• Address preexisting retinopathy (may worsen)

161. IN PREEXISTING TYPE 2 DM
• Risk of development of HTN
• Pregnancy loss is more in third trimester compared with type 1 in
first trimester
• Glycemic control is often easier to achieve but may need higher
doses of insulin

162. GESTATIONAL DIABETES MELLITUS
• Gestational diabetes is defined as diabetes with first onset or
recognition during pregnancy.
• This definition include a few patients who develop type 1 and
type 2 diabetes, or had unknown preexisting type 2 diabetes,
in whom the diabetes does not remit after pregnancy.

163. EFFECTS OF GDM
In pregnancy
• Abortion
• Preterm labor
• Preeclampsia
• Polyhydramnios
• Retinopathy &
nephhropathy
In labor
• Prolonged labor
• Shoulder dystocia
• Perineal injuries
• PPH
• Operative
interference
In puerperium
• Puerperal sepsis
• Lactational failure
Maternal Effects:

164. EFFECTS OF GDM(CONT.)
• Fetal macrosomia
• Congenital malformations:
Fetal and Neonatal Effects:
CNS & Skeletal
• Neural tube
defects
• Sacral agenesis
Cardiovascular
• VSD, ASD, TOF
• Coarctation of
aorta
Renal & GIT
• Renal agenesis
• Duodenal Atresia

165. DIAGNOSIS

166. MANAGEMENT
• Insulin is the first line agent
• Orally : Metformin
Glyburide
( RCT supports efficacy and Short-term safety of Metformin
and Glyburide in GDM, while lack in Long term safety data)

167. FEW WORDS ABOUT METFORMIN
• Lower risk of neonatal hypoglycemia than insulin
• Less maternal weight gain
• Slightly increase the risk of Prematurity
• Crosses placenta and higher concentration in umbilical
cord blood level than maternal circulation

168. DIABETES AND SURGERY
• Patients with diabetes are reported to have up to 50%
higher peri-operative mortality than patients without
diabetes.

169. PRE-OPERATIVE ASSESSMENT
• Assess glycemic control
• Assess cardiovascular status
• Assess foot risk
• For minor/moderate operations where only one meal will
be omitted, plan for the patient to be first on the list

170. PERI-OPERATIVE MANAGEMENT

171. POST-OPERATIVE MANAGEMENT
• Intravenous fluids during prolonged insulin infusion should
therefore include saline and potassium supplementation
• Once a patient’s usual treatment has been reinstated, care must
be taken to continue to control the blood glucose, ideally between
4 and 10 mmol/L in order to optimize wound healing and recovery

172. RAMADAN MUBARAK
“Whoever witnesses
the month (of Ramadan) then he/she should fast. But, if any of you is ill or travelling –
then he or she is exempted from fasting” –Al Quran
DIABETES AND RAMADAN
A MEDICO-RELIGIOUS PERSPECTIVE

173. PATIENT ASSESSMENT

174. SELF MONITORING OF BLOOD GLUCOSE: TIMING

175. WARNING

176. SULFONYLUREA DOSING

177. METFORMIN DOSING

178. LA INSULIN AND SA INSULIN DOSING

179. PREMIXED INSULIN DOSING

180. MULTI DOSE INSULIN IN TYPE 1 DIABETES

181. POINTS TO BE NOTED
•Discipline is Life
•Hypoglycemia is more dangerous than Hyperglycemia
• Education and awareness regarding Diabetes is a must

182. Eat properly

183. Exercise
Regularly

184. Stay Healthy

185. MODERATED BY
ISRAT SHAHRIN AZAD