All what you have to know about Diabetes Mellitus is here.Introduction of Diabetes,Regulation of blood glucose,Predisposing factors of DM,Clinical presentation,DM and pregnancy ,Diabetes ketoacidosis ,Complications of DM ,Diagnosis ,Dietary management of DM & Prevention of DM. Student seminar on Diabetes Mellitus presented by 2007/2008 Batch students of Faculty of Medicine,University of Peradeniya,Sri Lanka.

2. Why DIABETES?
 One of the commonest health problem
 Affects almost all systems of the body
 5%– 10% of total health care expenditure is spent
on DM

3. Trend of The disease
 Each year 7 million people develop
diabetes (each 10 seconds 2 people
develop DM)
 2.3.8 million people die out of DM
each year (one person per each 10
seconds)

4. Future
 By 2007,246 million people were
affected worldwide
 By 2025 380 million people are
expected to have the disease

5. Content
● Introduction - Group 1& 2
● Regulation of blood glucose - Group 3 & 4
● Predisposing factors of DM - Group 5 & 6
● Clinical presentation - Group 7 & 8
● DM and pregnancy - Group 9 & 10
● Diabetes ketoacidosis - Group 11 & 12
● Complications of DM - Group 13 & 14
● Diagnosis - Group 15 & 16
● Dietary management of DM - Group 17 & 18
● Prevention of DM - Group 19 & 20

6. Groups 1 & 2

7. What is Diabetes mellitus ?
 DM is the most common metabolic disorder
encountered in clinical practice.
 Diabetes - Greek word means ‘a passer through a
siphon’.
 Mellitus – Greek word for ‘sweet’

8. Classification of DM
 Type 1 - Insulin dependent DM
Insulin deficiency due to autoimmune
mediate pancreatic islet cell destruction.
 Type 2 - Non insulin dependent DM
Due to tissue insulin resistance.
Associated with ;
- increasing age
- obesity
- ethnicity
- family history.

9. Clinical differences between Type 1
and Type 11 Diabetes
Type 1 Type 11
Ketosis prone Yes Uncommon
Insulin requirement Yes- absolute insulin Often later in disease-
deficiency insulin deficiency+_
deficiency
Onset of symptoms Acute Often insidious
Obese Uncommon Common
Age at onset - years Usually < 30 >30
Family history of 10% 30%
diabetes
Concordance in 30- 50% 90-100%
monozygotic twins

10. Epidemiology
 More than 120 million people worldwide are
suffering from DM.
 It is estimated that it will affect 220 million by
year 2020.

11. Prevalence of diabetes in Sri Lanka

13. Symptoms
 Weight loss.
 Polyuria – increased urine excretion.
 Polydipsia – excessive thirst and
water ingestion.

14. Causes
 Increased prevalence of DM is related to;
 excessive caloric intake
 reduced physical activity.

15. Nature of the Disease
 Usually irreversible.
 Strongly linked to obesity.
 Patients can have a reasonably normal
life style.

16. Insulin
 Coded by chromosome 11 and synthesized in
the beta cells of the pancreatic islets.
 About 50% of secreted insulin is extracted and
degraded in the liver and kidney

17. Action of Insulin
 Prime target organ is the liver.
 Is the key hormone involved in the storage and
controlled release of the chemical energy
available from food within body.

18. Metabolic Changes
 Abnormal carbohydrate metabolism.
(Normal blood glucose level 3.6- 6.1 mmol /l)
 Abnormal lipid homoeostasis.
Hyperglycemia

19. Complications of Diabetes
 Macrovascular diseases
 Coronary heart disease
 Peripheral vascular disease
 Amputations
 Microvascular diseases
 Retinopathy
 Nephropathy
 Neuropathy

20. Prevention & Treatment
 Combination
approach.
 Increased exercise
 Decreases need for
insulin
 Reduce calorie intake
 Improves insulin
sensitivity
 Weight reduction
 Improves insulin action

21. Group 3/4

22. •Normal plasma glucose: 3.9-8.3 mM
•Plasma glucose is tightly regulated by
hormones:
Insulin: ↓Plasma glucose
Glucagon
Epinephrine
Cortisol ↑Plasma glucose
Growth hormone

24. Correlation Between Plasma
Glucose & Insulin Levels

25. Metabolism of Insulin
•Insulin has no plasma carrier proteins
•Short plasma half-life (3-5 min)
• ~50% of insulin is removed during the
first pass through the liver

27. Biological Effects of Insulin
• Major target tissues for insulin:
 liver, skeletal muscle, & adipose
tissue.
• Insulin ↑glucose uptake in muscle
and adipose tissue by regulating
glucose transporter (GLUT4).
• Glucose transporter in the liver
(GLUT 2) is not regulated by insulin.

28. GLUCAGON
The most important hormone
in increasing plasma
glucose.
Glucagon is a single chain
polypeptide (29 amino
acids).

30. REGULATION OF GLUCAGON SECRETION

31. ROLE OF GLUCAGON IN GLUCOSE REGULATION
Glucagon opposes the metabolic actions of insulin.
The major site of action: liver.
The important metabolic effects of glucagon
in the liver include:
Carbohydrates:
↑gluconeogenesis(glucose production)
↑glycogenolysis(glycogen breakdown)
↓glycogen synthesis

32. Fat:
↑Ketogenesis(ketoneproduction)
Protein:
↓Hepatic protein synthesis
↑protein catabolism in the liver
Glucagon DOES NOT affect
muscle proteins.

33. REGULATION OF BLOOD GLUCOSE BY INSULIN & GLUCAGON

36. Overall:
•Insulin
↓plasma glucose by promoting glucose
uptake
& its storage.
•Glucagon
↑plasma glucose by increasing
liver glucose output.

37. GLUCOSE REGULATION DURING
EXERCISE-
ROLE OF EPINEPHRINE

38. Group 5 & 6

39. Diet
Starch
 White bread, sugared breakfast cereals
& potatoes, which all have especially
high glycemic index values & low fiber
contents predispose diabetes.
 Potatoes ,in particular, can become
dietery handgrenades for diabetics when
served as French fries.

40. Diet continue...
 Refined sugars
 Nothing increases blood sugar more readily
than ingesting sugar.
So high fructose corn syrup, candy & sweets such
as cakes are not good for diabetics at all .
 Saturated fats
 Fats do compound many risk factors
for & complications from diabetes
such as obesity, hardening of arteries
& heart attack or stroke.
 Eg: butter, margarine, whole milk

42. Emotional Stress
 Highly stressed life deeply influences the
metabolism of the body. Even grief, anxiety,
worry, death of any close person, etc. may
alter the blood sugar level and lead to the
disease.
 Energy mobilization is a primary result of
the fight & flight response. So stress
stimulates the release of various hormones
like glucocorticoids which elevate blood
glucose level.

43. Obesity
 When a person is overweight,
the cells in the body become less
sensitive to the insulin due to the
high circulating levels of leptin.
 There is some evidence that fat cells
are more resistant to insulin than
myocytes.
 If a person has more fat cells than
muscle cells, then the insulin become
less effective overall,& glucose remain
circulating in the blood instead of being
taken in to the cells to be used as energy.

44. Sedentary Life
 A sedentary life style is
damaging to health & bears
responsibility for the growing
obesity problems.
 Inactivity & being overweight
go hand in hand towards a
diagnosis of type 2 diabetes.
 Muscle cells have more insulin
receptors than fat cells, so a
person can decrease insulin
resistance by exercising.

45. Smoking
 smoking 16 to 25 cigarettes a day
increases your risk for Type 2 diabetes to
three times that of a non-smoker..
 Increases complications esp.
Retinopathy, Cardiovascular conditions
•There is also evidences that
links cigarette smoking with
microvascular diseases in
diabetes.
•Smoking can cause chronic
pancreatitis which leads to
diabetes.

46. Ethnicity
 Incidence high in
 African, Americans, Asians, American
Indians, Hispanic, Caucasians, Latinos,
Mexican-American, Europeans
Age
•It has been observed that as one grows
older, particularly above 45 years of age, in
them the chances to develop diabetes are
increased.
•It is chiefly because due to old age, the person
becomes less active, tends to gain
weight, leading to pancreatic dysfunction.

48. Genetic Predisposition
 People who belong to family background
having history of diabetes are 25% more
prone to develop diabetes.
• The concordance of type 1 DM in identical twins
ranges between 30% and 70%
The major susceptibility gene for type 1
DM is located in the HLA region on
chromosome 6
• The concordance of type 2 DM in identical twins is
between 70% and 90%
•if both parents have type 2 DM, the risk approaches
40%

49. Gestational Diabetes
Human placental Peripheral tissues
Lactogen
Insulin resistance
Estrogen
Pancreas
Progesterone
•Increased Fat stores
•Prolactin
•Changes in insulin receptor
most women revert to normal
glucose tolerance post-partum,
but have a substantial risk (30–
60%) of developing diabetes
mellitus later in life.

50. Infections
 Mumps, Coxsackie B, Cytomegalovirus,
Kilham rat virus and rubella infections
can damage the pancreas.
 Coxsackie virus is the commonest viral
cause
 Some viruses can trigger or maintain
autoimmune beta cell damage.

51. Barker and Hales hypothesis
 Evidence, mainly from animals, suggests
that maternal and therefore fetal
malnutrition during a critical early
phase of fetal development can reduce
Beta-cell mass and permanently impair
insulin secretory reserve.

52. Other factors
 Endocrine
 Acromegaly 25%
 Cushing’s Disease 30%
 Glucagonoma 90%
 Drugs that decrease insulin sensitivity
 Glucocorticoids
 Beta-2 receptor antagonists
 OCP

53. Groups 7 & 8

54. “ The history of diabetic symptoms
is of the greatest importance and an accurate
appreciation of their severity far exceeds an
estimation of the blood sugar as a means of
assessing the need for treatment.”
(John Malins, Clinical Diabetes Mellitus, Eyre & Spottiswoode, 1968)

55. Clinical
presentation
Acute Sub acute
Symptoms Symptoms
•Acute & Sub acute presentations often overlap.
But,
 Asymptomatic diabetes can occur.

56. Acute presentation
Young people often present with a 2-3 weeks
history and report the classical triad of
symptoms. Thirst Polyuria
1.Thirst
2.Polyuria
3.Weight loss
If not
 Ketonuria treated Ketoacidosis

57. Sub acute presentation
 Clinical onset over several months, years
 In older patients
 Classical triad of symptoms are typically present.
But complain of,
 visual – blurring
 pruritus vulvae (female)
 balanitis (male)
lack of energy
 dry mouth
 dysphagia

58. balanitis
Visual blurring
Pruritus vulvae

59. Other symptoms
 Somnolence (the tendency to fall asleep)
 Myopia
 Nausea, headache
 Tiredness, fatigue
 Malaise
 Hyperphagia - predilection for sweet foods

60. Complications
 Macrovascular
 Microvascul
ar diseases
diseases
Cardiovascular diseases
Nehpropathy Eg: Coronary artery
diseases
Neuropathy
Stroke
Retinopathy
• Foot infections
• Erectile dysfunctions gangrene

61. Asymptomatic diabetes
 No symptoms or ill health.
 Accidently detected ;
as glycosuria or hyperglycemia on routine
investigations (for other purposes).
 Both are not diagnostic of diabetes but
indicates a high risk of developing diabetes.

63. Diabetes and pregnancy
Group 9 and 10

64. 1. Already diagnosed diabetes mellitus
woman getting pregnant – Preexisting
diabetes.
2. A woman who hasn’t been diagnosed
diabetes, exhibit high blood glucose
levels during pregnancy – Gestational
diabetes

65. Gestational diabetes
 Gestational diabetes is defined as “Any degree of glucose intolerance
with onset or first recognition during pregnancy"
 Gestational diabetes generally has few symptoms and it is most
commonly diagnosed by screening during pregnancy..

66. Gestational diabetes
During Human placental lactogen
pregnancy level &
Cortisol level increase
• Both are insulin antagonists.
• Cortisol gluconeogenesis
glucose utilization
Blood glucose
• HPL insulin sensitivity
glucose utilization

67. Risk factors
• Obesity BMI > 30
• Family history of diabetes
• Previous babies having high birth weight ( >4.5kg )
• Previous still birth
• Previous babies with congenital abnormalities

68. Maternal complications
 Pre-eclampsia (pregnancy induce hypertension )
 Antepartum hemorrhage due to placental abbruption
 Microvascular
 Nephropathy
 Retinopathy
 Neuropathy
 Macrovascular
 Coronary artery disease
 Hyperglycaemia / hypoglycaemia / ketoacidosis
 Infection
 Thrombo – embolic disease

69. Fetal & neonatal complications
 Increase risk of miscarriage & congenital fetal
abnormalities
 Neural tube defects, congenital heart diseases & spinal anomalies
 Sacral agenesis (caudal regression syndrome)
 Fetal macrosomia
 Late still birth
 Respiratory distress syndrome
 Hypoglycaemia
 Polycythaemia
 Hyperbilirubinaemia
 Hypomagnesemia
Macrosomia

70. Diagnosis of maternal diabetes
 Glucose challenge test (>140mg/dl)
 Oral glucose tolerance test.
 Random blood sugar.
Normal fasting glucose -<7mmol/l
Impaired glucose intolerance -7.8-
11.1mmol/l
Random blood glucose -<11.1mmol/l
If
Diabetes
RBG>11.1mmol/l
mellitus
If FBG>7mmol/l

71. Management
Diabetic women are advised to maintain the blood sugar level close to
normal range for 2 to 3 months in advance, before planning for
pregnancy.
Antenatal care
 Frequent review
 Increase insulin dose
 Vigorous treatment for infection
 Regular urine analysis to detect nephropathy
At term,
 Should not be allowed to continue beyond 38 weeks.
 Caesarean section if needed.
 Delivery before 36 weeks – Dexamethasone.
 Monitor the blood glucose & urine ketone body regularly

72. Newborn,
 Anticipate & treat asphyxia
 Cross monitoring blood glucose level for the first 72h
 Early breast feeding
 Look for congenital malformation.
 Random blood sugar and give dextrose if necessary.
On descharge
 Check the fasting blood sugar
 Complete family early & follow family planning method.

73. References
 Obstetrics by Ten Teachers

74. DIABETIC
KETOACIDOSIS
GROUP 11 & 12
07/08 BATCH

75. Introduction
 Major medical emergency
 Principally with type 1 diabetes
 High blood sugar with ketones in urine and blood
 Body can’t use glucose due to insulin shortage

76. Main cause – Type 1 diabetes
Usually occurs in following circumstances
• Undiagnosed diabetes
• Interruption to insulin therapy
• Stress due to any illness
(Also occurs in type 2 diabetes)

77. Mechanism of Diabetes Ketoacidosis
In adipose cells insulin inhibit the action of intracellular enzyme “Hormone-sensitive lipase”

79. Development of Signs and
Symptoms
 Diabetic ketoacidosis appears to require
Insulin deficiency coupled with a relative
or absolute increase in glucagon
concentration
 Increased glucagon induces maximal
gluconeogenesis and also impairs
peripheral utilization of glucose resulting
in severe hyperglycemia

80.  This induces osmotic diuresis that leads
to volume depletion and dehydration that
characterize the ketoacidotic state.
 Glucagon activates the ketogenic
process and thus metabolic acidosis.

81. Symptoms & signs
 Nausea
 Vomiting
 Excessive thirst
 Frequent urination
 Weakness
 Ketone / Fruity smelly breaths
 Hyperventilation
 Confusion
 Dry skin
 Abdominal pain

83. Diagnosis
 Ketonuria or ketonemia is demonstrated
 Dipstick method for hyperglycemia
 Centrifugation blood for ketonemia ?
 Arterial blood gas analysis

84. Investigations
 Urea & Electrolytes, Blood glucose,
Plasma bicarbonate
 Arterial blood gases to assess the
severity of acidosis
 Urinalysis for ketones
 ECG

85. Treatment
Replace lost fluid & electrolytes
suppressing high blood sugar & ketone
production with insulin
 Fluid replacement
 Insulin therapy
 Potassium
 NaHCO3 ….?

86. Prevention
 Manage diabetes yourself
 Monitoring blood sugar levels
 Adjust insulin dose as needed
 Check urine for ketone levels
 Be prepared to act quickly

87. References
 Kumar & Clark;Clinical Medicine
 Davidson;Clinical medicine
 Harper’s illustrated biochemistry

88. Groups 13-14

89. • Have a considerably reduced life expectancy
• 70%- due to cardio vascular diseases
• Followed by 10% -renal failure
• Pathophysiology
• Non enzymatic glycosylation of protains
• Polyoyl pathway
• Abnormal microvasculr pathway
• Other factors
• Haemodynamic changes

90. • Complications
1.Macrovascular
Hypertension
Smoking
Lipid abnormalities
2.Microvascular
Daibetic eye disese
Diabetic kidney
Diabetic neuropathy
The diabetic foot
Infections
Skin & Joints

91. Diabetic Retinopathy
• Impairment of loss of vision
• Due to damage to blood vessels of retina
• Cause of long standing diabetes
Cataract Glucoma

92. Diabetic nephropathy
• Important cause of morbidity mortality
• Among the most common causes of the end
stage renal failure
• Management is frequently different &
benefits of prevention are substantial

93. Diabetic neuropathy
• Usually causing weakness & numbness
• Symptoms are depended on nerves
which damage
• Most commonly affects legs

94. Complications on foot
 Main cause of the AMPUTATION is diabetes mellitus
 Why it will end up with amputation ????
 Diabetes……….
1) Narrow & hardening the blood vessels
Poor circulation
Less ability to fight with infections
& healing also slow
Foot ulcer
Gangrene

95.  2) Damage the nerves
 Loss of sensation (peripheral neuropathy)
 Injuries cannot be noticed
 Susceptible for infections
 3) Damage to the nerves controlling oil & moisture
 Skin dryness
 Easy to getting cracks
 Susceptible for infections

96.  4) Affects joints
Making them stiffer
 Charcot’s joints

97. Effects of diabetes to blood vessels
Diabetes
mellitus
Part of plaque
Glucose
Travel through circulation
Cholesterol Breakage of
plaque Lodge in a vessel
Deposit in damaged of brain (STROKE)
vessels
Loss of blood supply to
Atheroma ( in damaged inner layer) part of brain
atherosclerosis
Diameter of blood vessels Blood flow

98. Effect of diabetes to heart
 Diabetes mellitus
 Atherosclerosis
Blood glucose In peripheral Blockage of
vessels coronary vessels
blood flow
blood supply
Cardiac muscle to part of
failure heart
Heart has to pump
(cardiomyopathy) more forcefully Ischemic heart
disease
hypertension
Heart
attack

99. GROUP 15-16
DIAGNOSIS of

100. DIAGNOSIS OF DIABETES
If patient complains of symptoms suggesting diabetes
 Test urine for GLUCOSE & KETONES
 Random Blood Glucose (normal <200mg/dL, 11.1mmol/L)
 Fasting Blood glucose (FBG)
if FBG>7.0mmol/l, 126mg/dL-DIABETES
if (6.1 <= FBG < 7.0)mmol/l or (110 <= FBG < 126) mg/dL
IMPAIRED FASTING GLUCOSE (IFG)
 Oral Glucose Tolerance Test (OGTT)
 HbA1C
This can be utilized as an assessment of glycaemic control
in a patient with known diabetic
 other tests - Fructosamine test , Ketone body analysis,
microalbuminuria test

101. URINE TESTS

102. BENEDICT’S TEST
 To assess urine sugar level
 To 5ml Benedict’s solution add 8-10 urine drops,
 Boil and allow to cool then observe color change.
Color change % of sugar
blue Nil
Clear green 0.1
Turbid green 0.3
Green & Yellow 0.5-1.0
Yellow 1.0
Orange 2.0
Brick red >2.0
Maltose, galactose, , sucrose & drugs which contain aldehyde
groups such as Aspirin, Penicillin, Vitamin C, antibiotics (+)ve
results
• detects only blood sugar levels >180mg/dL

103. DIPSTICK METHOD
• A plastic strip coated with reagents
• Reagent strip measure glucose level using glucose oxidase
method.
GLUCOSE OXIDASE
GLUCOSE H2O2 (Change the color of the
indicator)

104. BLOOD TESTS

105. Random blood glucose level
• Measure the blood glucose level other than post prandial
stage or fasting.
• If it is above 11.1mmol (200mg/dl) considered as
diabetes.
• GLUCOMETER
• For rapid diagnosis
of blood glucose levels
(capillary blood )

106. Fasting Plasma Glucose
After 12hr fasting measure the blood glucose level
in venous blood.
4 mmol/L 6.1 7.0
80 mg/dL mmol/L mmol/L
110 126
mg/dL mg/dL
Hypoglycemi Normal Impaired (Hyperglycemic)
c Fasting Diabetes
Glucose

107. OGTT (Oral Glucose Tolerance
Test)
 Unrestricted carbohydrate diet for 3 days before test
 8 Hour overnight fasting is required.
 75g of glucose in 300ml of water is given orally within 5
minutes.
 Measure plasma glucose BEFORE and 2 hours AFTER
the glucose load.
Time Non Diabetic Diabetic Impaired Glucose
_ Tolerance
Fasting(0 <6.1mmol/l >7.0mmol/l 6.1-7.0mmol/l
min) (110mg/dl) (126mg/dl) (110-126mg/dl)
120min <7.8mmol/l >11.1mmol/l >7.8-11.1mmol/l
(140mg/dl) (200mg/l) (140-200mg/dl)

108. HbA1C
 Measure the glycated hemoglobin proportion which
indicates the glycaemic condition
 Glycosylation of hemoglobin α [glucose]
 This can reflect the glycaemic control of the patient over
2 to 3 months
 For every 1% increase of theHbA1c indicate 35mg/dl
incease of blood glucose levels.
4.5% – 6.5 % Reference
range
HbA1c > 8% Poor control

109. HbA1 Mean plasma glucose
c % mg/dl
6 135
7 170
8 205
9 240
10 275
11 310
12 345

110. Fructosamine Test
 Fructosamine = glycosylated plasma proteins,
mainly albumin
 Indicate previous 2-3 week glyceamic control
 Impaired in patients with anemia
, hemoglobinopathies & pregnancy.

111. DIAGNOSIS OF COMPLICATIONS OF
DIABETES
 Diagnosis of Diabetic Neuropathy
Lower limbs
 Peripheral pulses
 Tendon reflexes
 Perception of vibration sensation, light touch and
proprioception
Feet
 Callus skin indicating pressure areas
 Nails
 Need for podiatry
 Ulceration
 DeformityDiabetic Nephropathy

112. Diagnosis of Diabetic Nephropathy
Microalbuminuria test
 In normal people
Albumin excretion =30mg/day
 In kidney damage > 300mg/day
 In diabetic nephropathy ;
Albumin excretion =30-300mg/day
microalbuminuria

113. Diagnosis of Diabetic Retinopathy
Eye examination
 Visual acuities (near and distance)
 Ophthalmoscopy (with pupils dilated)
 Digital photography

114. Group 17 & 18

115.  Diet is an essential part of
the management of
diabetes
 Diet is based on healthy
eating principles

116. Reasons for diet
•Weight control
•Blood glucose control
•Prevention and management of short-term
and long-term complications of diabetes

117. Basic Principles of Diabetic
Diet
•Ensure regular meals
• Base meals on starchy carbohydrates
• Aim for more fruit and vegetables
• Cut down on sugar and sugary foods
• If in doubt read food label
• Encourage relatives to bring low sugar foods
•Reduce salt

118. Eat starchy foods regularly
 Bread
 Potatoes
 Rice
 Cereals
 Plantain
 CHO –to form 45-60% of total energy [cereals,vegetables,legumes]
better use foods which has low glycaemic index

119. Eat fruit and vegetables
 Fresh
 Frozen
 Tinned
 Dried
 Juice
 Encourage food rich in antioxidants - vitamins

120. Reduce protein intake
 Restriction of protein intake to 0.6 -0.8 g/ kg/ day
 Replace red meat with chicken ,fish or vegetable
protein
 To contribute 10-20% of total energy

121. • Aim for low sugar diet
–Not a sugar free diet
–Instead of sweet cakes/ biscuits offer
fruit loaf, plain biscuits, teacakes
 Cut down on sugar and
sugary foods: • Use low sugar foods
– Use drinks labeled diet, low calorie or
sugar- free
– Choose diet or ‘light’ yoghurts instead of
low-fat or whole yoghurts
• Use sugar free/ low sugar - jelly,
custard, rice pudding as dessert ideas

122. Nutrition Claims – Sugar
‘No added Sugar’ – No sugar from any
source added
‘Low Sugar’ – No more than 5gs
sugar/100gs
‘Reduced Sugar’ – 25% less sugar than
regular product
FREE SUGER – do not exceed 50g per day

123. Choose more high fibre foods
To help maintain blood glucose levels and cholesterol levels
Helps to maintain a
 Fruit healthy gut
 Vegetables
 Pulses
• Wholegrain cereals
 Oats
• Wholemeal bread
• Brown rice
 FIBERS – 40g per day or more
half of fiber should be soluble

124. Reduce animal or saturated fat intake
 Use low fat milk
 Use low fat
spread instead of
butter
 Use oil high in
unsaturated
fat, eg olive
oil, rapeseed oil

125. Use less fat in cooking
 Dry-roast
 Microwave
 Steam
 FAT - should not exceed 30 % of total energy
restrict cholesterol to 300mg or less per day

126. Choose the right sort of fat
SATURATED MONO- POLY-
UNSATURATED UNSATURATED
• Full fat dairy
produce (eg • Olive oil • Sunflower oil
cheese, butter, (products)
• Rapeseed oil
full cream milk)
• Oily fish
• Groundnut oil
• Biscuits
• Savoury snacks
• Lard
• Hard vegetable
fat

127. Nutrition Claims – Fat
‘Low Fat’ - . 3g Fat/ 100g or 100mls
‘Less than 5% Fat’ - . 5g fat/ 100g
Reduced Fat’ – 25% less fat than similar
products

128. Reduce salt intake
• Cut down on added salt
• Use alternatives
• Look out for reduced/low sodium foods, eg bread
• Avoid salt substitutes
• SODIUM – restrict to 6g per day

129. Alcohol
• Alcohol in moderation can be
included,
no more than:
– 1-2 units/ day for women
– 2-3 units/ day for men
• Never give alcohol on an empty
stomach
• Remember to use ‘diet’ mixers
•Caution with sweet liqueurs

130. Special diabetic foods
 Not recommended
 May contain more fat or energy than other foods
 May be low in fibers
 Has sorbitol – may cause diarrhoea
 Excessive fructose may be used - Fruit sugar (fructose)
when used excessively as a
sweetener will still affect
blood sugars
in the same way as normal
sugar!!

131. If Residents Overweight
• Weight loss is desirable –via exercising
• Encourage to cut down on fatty foods
e.g. chips, pastry, crisps, biscuits, cheese and fried
foods
• Encourage low-fat food options
e.g. semi-skimmed milk, low-fat spread
• Offer fruit/ low fat yoghurt as a dessert
• Snacks not essential

132. If residents malnourished
• Encourage small frequent meals
and low sugar puddings and snacks:
– Glass of milk/ milky drinks
– Crackers and cheese
– Toast, butter and reduced sugar jam
– Breakfast cereals, nuts
– low fat yoghurt or low sugar milk
pudding
– Plain biscuits, fruit cake, kurakkan
bread,

133. Recommended food meals for a diabetic
patient
Breakfast –chickpea 1 cup or green gram 1 cup or
bread two slices with polsambol 1 tsp.
Lunch – Rice two cups , Vegetables 6 tablespoons ,
green leaves ½ cup, fish or chicken 1 piece, fruit
1 serving
Dinner – Rice 1 cup, vegetable 3 tablespoons, Dhal
3 tablespoons, Fruit 1 serving

134. Key Points
• Ensure regular meals
• Base meals on starchy carbohydrates
• Aim for more fruit and vegetables
• Cut down on sugar and sugary foods
• If in doubt read food label
• Encourage relatives to bring low sugar
foods

135. Group 19-20

136.  CANNOT CURE. But can prevent.
 Kathmandu declaration- life cycle
approach for prevention & care of DM.
o Primary prevention
o Secondary prevention

145. THANK YOU!