1 - 1 Diagnosis, Classification and Prevention

Diagnosis, classification and
prevention of diabetes
Section 1 | 1 of 4
Curriculum Module II1 | Diagnosis, classification and

presentation of diabetes
Slides current until 2008

Diagnosis and types
Curriculum Module II-1
Slide 2 of 48
Definition of diabetes
Characterized by hyperglycaemia
Defects in insulin production
Autoimmune or other
destruction of beta cells
Insulin insensitivity
Impaired action of insulin on
target tissues
Diagnosis and types
Slide 3 of 48
Definition of diabetes
Chronic hyperglycaemia associated

with long-term damage to:
Eyes
Kidneys
Nerves
Heart and blood vessels
Diagnosis and types
Slide 4 of 48
The diabetes epidemic
230 million affected in 2006
350 million within 20 years
Most rapid in Indian and Asian

subcontinents
IDF Diabetes Atlas

Diagnosis and types
Slide 5 of 48
Classification
Type 1 diabetes
autoimmune
LADA
idiopathic
Type 2 diabetes
Diagnosis and types
Slide 6 of 48
Classification
Other specific types

MODY
Defects in insulin action
Diseases of the pancreas
Endocrine disorders
Drug- or chemical-induced
Infections
Diagnosis and types
Slide 7 of 48
Classification
Uncommon forms of immune-

mediated diabetes
Other genetic syndromes
Gestational diabetes
Diagnosis and types
Slide 8 of 48
Insulin and glucose disposal
Gluconeogenesis
Glycogenolysis
Glycogen synthesis
Insulin
Blood glucose
Glycogen
synthesis Glucose uptake
Free fatty acid release
Diagnosis and types
Slide 9 of 48
Insulin deficiency in
type 1 diabetes
Glucose uptake
Glycogenolysis
Gluconeogenesis (amino acids)
Ketone production (fatty acids)
Blood glucose
Glucose uptake
Protein degradation amino acids
Triglyceride degradation fatty acids

Diagnosis and types
Slide 10 of 48
Insulin insensitivity in
type 2 diabetes
Glucose uptake
Glycolysis
Blood glucose
Glucose uptake
Diagnosis and types
Slide 11 of 48
Insensitivity to insulin in
type 2 diabetes
Glucose uptake
Glycolysis
Blood glucose
Glucose uptake
Glucose uptake
Diagnosis and types
Slide 12 of 48
Effect of insulin resistance in

type 2 diabetes
Glucose uptake
Glycolysis
Blood glucose
Converted to triglycerides
Glucose uptake
Glucose uptake
Diagnosis and types
Slide 13 of 48
Pathogenesis of type 1 diabetes
Immunological activation
Progressive beta-cell destruction
Insufficient beta-cell function
Dependent on exogenous insulin
Risk of ketoacidosis
Diagnosis and types
Slide 14 of 48
Genetic susceptibility
Immune factors
other autoimmune disease
antigen-specific antibodies
Environmental trigger
viruses
bovine serum albumin
nitrosamines: cured meats
chemicals: vacor (rat poison),
streptozotin
Diagnosis and types
Slide 15 of 48
Trigger
Immunological
Genetic abnormalities
Beta-cell
mass Clinical
diabetes
Pre-diabetes Honeymoon
Chronic
phase
Time (months - years)
Diagnosis and types
Slide 16 of 48
Idiopathic type 1 diabetes
Non-autoimmune type 1 diabetes
No autoimmune markers
Permanent insulinopenia
Ketoacidosis
People of African and Asian origin

Diagnosis and types
Slide 17 of 48
Epidemiology of type 1 diabetes
Increasing in recent years
Geographic variation
Relative affluence
Lack of treatment
IDF Diabetes Atlas

Diagnosis and types
Slide 18 of 48
Age of onset peaks

preschool
puberty
Autumn/winter peaks
Diagnosis and types
Slide 19 of 48
Type 2 diabetes
90%-95% of people with

diabetes
Insulin insensitivity and

relative insulin deficiency
Obesity or overweight
Complications often present

at diagnosis
Diagnosis and types
Slide 20 of 48
Multiple genes involved
Hyperinsulinaemia
Poor fetal nutrition beta-cell

formation
Low birth weight/weight change
Thrifty gene
7% beta-cell loss
Diagnosis and types
Slide 21 of 48
The natural history of

type 2 diabetes
Beta-cell loss
Insulin
Primary requirements
Insulin failure with age
requirements
Endogenous
insulin
Age (years)
Diagnosis and types
Slide 22 of 48

type 2 diabetes
Beta-cell loss
Insulin
Hyper-
requirements
insulinaemia
Insulin with age
requirements
Insulin
insensitivity Endogenous
insulin
Age (years)
Diagnosis and types
Slide 23 of 48

type 2 diabetes
Secondary
Beta-cell loss failure
Hyper- Insulin
Effect of requirements
insulinaemia
Insulin oral drugs with age
requirements
Insulin
insensitivity Endogenous
insulin
Age (years)
Diagnosis and types
Slide 24 of 48
Dramatic increase
Aging population
Disturbing trends parallel obesity
epidemic
Especially in adolescents and
minority groups
Increasing in young people
Diagnosis and types
ACTIVITY Curriculum Module II-1
Slide 25 of 48
What are the most common risk

factors for type 2 diabetes for
people in your country?
Are any of these risk factors

modifiable?

Diagnosis and types
Slide 26 of 48
Risk factors for type 2 diabetes
Age > 40 years

First-degree relative with diabetes
Member of high risk population
History of impaired glucose tolerance,
impaired fasting glucose
Vascular disease
History of gestational diabetes
History of delivery of macrosomic
baby
CDA 2003
Diagnosis and types
Slide 27 of 48
Risk factors for type 2 diabetes
Hypertension
Dyslipidaemia
Abdominal obesity
Overweight
Polycystic ovary disease
Acanthosis nigricans
Schizophrenia
Diagnosis and types
Slide 28 of 48
Signs and symptoms
Polydipsia
Polyuria
Nocturia
Visual disturbance
Fatigue
Weight loss
Infections
Diagnosis and types
Slide 29 of 48
Diagnosing diabetes
Normal Impaired fasting glucose* Diabetes

Impaired glucose
tolerance**
FPG <6.1mmol/L 6.1 to 6.9mmol/L* 7.0mmol/L
<110mg/dL 110 to 126mg/dL 126mg/dL
2hr PG <7.8mmol/L 7.8 to 11mmol/L** 11.1mmol/L

<126mg/dL 126 to 200mg/dL 200mg/dL
CDA 2003, ADA 2004, WHO 2002

Diagnosis and types
Slide 30 of 48
Impaired glucose tolerance

Impaired fasting glucose
Intermediate states
Increased risk of developing diabetes
Prevention strategies to prevent or
delay progression
Increased risk of cardiovascular
disease
Diagnosis and types
Slide 31 of 48
Uncertain diagnosis:
Oral glucose tolerance test
75 g glucose load after 8 hours

fasting
Readings taken in fasting state

and at 1 and 2 hours
Possible problems
Diagnosis and types
Slide 32 of 48
Tests for differential diagnosis
Urinary ketones
Antibodies
C-peptide
Diagnosis and types
Slide 33 of 48
Metabolic syndrome
Cluster of risk factors or syndrome

Type 2 diabetes
Different criteria
Three-fold increase in heart
disease and stroke
Two-fold increase in cardiovascular
disease deaths
Diagnosis and types
Slide 34 of 48
Prevention of type 1 diabetes
Early exposure to cows milk

protein
Nicotinamide
Diagnosis and types
Slide 35 of 48
Insulin
Diabetes Prevention Trial
Diabetes Prediction and

Prevention Project
Diagnosis and types
Slide 36 of 48
Lifestyle modification
Da Qing Study
Finnish Diabetes Prevention Study

Diagnosis and types
Slide 37 of 48
Lifestyle vs medication
Diabetes Prevention Program
STOP-NIDDM
Diagnosis and types
ACTIVITY Curriculum Module II-1
Slide 38 of 48
Type 2 diabetes can be delayed in

people with IGT
Lifestyle modification is most
effective
What do you think could be done at

community level to prevent or delay
diabetes?

Diagnosis and types
Slide 39 of 48
Summary
Type 1 diabetes
Results from progressive beta-
cell destruction
People with type 1 diabetes need
insulin therapy to live
Diagnosis and types
Slide 40 of 48
Summary
Type 2 diabetes
Often characterized by insulin
insensitivity and relative rather
than absolute insulin deficiency
A progressive condition
Most people with type 2 diabetes
will need insulin within 5 to 10
years of diagnosis
Diagnosis and types
Slide 41 of 48
Review question
1. The pathogenesis for type 2 diabetes

includes:
a. Insulin deficiency and insulin

insensitivity
b. Insensitivity to insulin and
autoimmune beta-cell destruction
c. Autoimmune beta-cell destruction
and glucagon deficiency
d. Insulin deficiency and glucagon
deficiency
Diagnosis and types
Slide 42 of 48
Review question
2. A person with type 2 diabetes, recently

started on insulin, asks if there is a way
to measure if he/she is still producing any
insulin. The correct response would be:
a. Islet cell antibody tests

b. C-peptide test
c. HbA1c test
d. Serum insulin test
Diagnosis and types
Slide 43 of 48
Review question
3. The Diabetes Prevention Program (DPP):
a. Included people with type 1

diabetes
b. Included only people with IGT
c. Tested the value of exercise
d. Included people with type 2
diabetes
Diagnosis and types
Slide 44 of 48
Review question
4. Type 1 diabetes is usually caused by:
a. Injury to the pancreas

b. An autoimmune reaction
c. Insulin insensitivity in the cells
d. Hypersensitivity to insulin
Diagnosis and types
Slide 45 of 48
Answers
1. a
2. b
3. b
4. b
Diagnosis and types
Slide 46 of 48
References
1. American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes Care
2004; 27(suppl 1): S5-S10.
2. Canadian Diabetes Association Clinical Practice Guidelines Expert Committee. Canadian
Diabetes Association 2003 clinical practice guidelines for the prevention and management of
diabetes in Canada. Can J Diab 2003; 27(suppl 2).
3. Chiasson JL, Josse RG, Gomis R, et al. Acarbose for prevention of type 2 diabetes mellitus:
The STOP-NIDDM randomized trial. Lancet 2002; 346: 393-403.
4. Delahanty LM and Halford BN. The role of Diet Behaviours in Achieving improved glycaemic
control in intensively treated patients in the Diabetes Control and Complications Trial. Diabetes
Care 1993; 16(11): 1453-58.
5. Diabetes Control and Complications Trial Research Group. Effect of intensive diabetes
treatment on the development and progression of long-term complications in adolescents with
insulin dependent diabetes mellitus: Diabetes Control and Complications Trial. The Journal of
Paediatrics 1994; 125(2): 177-88.
6. Diabetes Control and Complications Trial/epidemiology of diabetes interventions and
complications research group intensive diabetes therapy and carotid intima-media thickness in
type 1 diabetes mellitus. New Engl J Med 2003; 348: 2294-303.
7. Diabetes Control and Complications Trial: The effect of intensive treatment of diabetes on the
development and progression of long-term complications in insulin-dependent diabetes
mellitus. N Engl J Med 1993; 329: 977-86.
Diagnosis and types
Slide 47 of 48
References
8. Ford ES, Giles WH, Dietz WH. Prevalence of the metabolic syndrome among US adults: findings
from the third National Health and Nutrition Examination Survey. JAMA 2002; 297: 356-59.
9. Diabetes Atlas 2006. Brussels: International Diabetes Federation, 2006.
10. Isomaa B, Almgren P, Tuomi T, et al. Cardiovascular morbidity and mortality associated with the
metabolic syndrome. Diabetes Care 2001; 24(4): 683-9.
11. Pan X, Li G, Hu Y, et al. Effects of diet and exercise in preventing NIDDM in people with impaired
glucose tolerance: The Da Qing IGT and Diabetes Study. Diabetes Care 1997; 20(4): 537-44.
12. Report of a WHO Consultation. Laboratory Diagnosis and monitoring of Diabetes Mellitus. World
Health Organisation 2002. http://whqlibdoc.who.int/hq/2002/9241590483.pdf cited April 30,
2005.
13. Tuomilehto J, Lindstrom J, Eriksson JG, et al. Prevention of type 2 diabetes mellitus by changes in
lifestyle among subjects with impaired glucose tolerance. N Eng J Med 2001; 344: 1343-50.
14. The Diabetes Prevention Program Research Group. The diabetes prevention Program (DPP).
Diabetes Care 2002; 23(12): 2165-71.
15. UK Prospective Diabetes Study Group. Intensive blood-glucose control with sulpfonylureas or
insulin compared with conventional treatment and risk of complications in patients with type 2
diabetes. Lancet 1998; 352: 837-53.
Diagnosis and types
Slide 48 of 48
References
16. UK Prospective Diabetes Study Group. Tight blood pressure control and risk of
macrovascular and microvascular complications in type 2 diabetes UKPDS 38. BMJ
1998; 317: 703-13.
17. IDF Clinical Guidelines Task Force. Global Guideline for Type 2 Diabetes. Brussels:
International Diabetes Federation, 2005.
18. Harris SB, Ekoe JM, Zdanowicz Y, Webster-Bogaert S. Glycemic Control and
morbidity in the Canadian primary care setting (results of the diabetes in Canada
evaluation study). Diab Research and Clin Pract 2005; 70: 90-7.
Diabetes in clinical reality Diagnosis and types
Global Slide 49 of 48
2000 2030
Ranking Country People with Country People with
diabetes diabetes
(millions) (millions)
1 India 31.7 India 79.4

2 China 20.8 China 42.3
3 US 17.7 US 30.3
4 Indonesia 8.4 Indonesia 21.3
5 Japan 6.8 Pakistan 13.9
6 Pakistan 5.2 Brazil 11.3
7 Russia 4.6 Bangladesh 11.1
8 Brazil 4.6 Japan 8.9
9 Italy 4.3 Philippines 7.8
10 Bangladesh 3.2 Egypt 6.7
Diagnosis and types
Slide 50 of 48
Aims of treatment
Reduce the symptoms of hyperglycaemia
Limit adverse effects of treatment
Maintain quality of life and psychological well-
being
Prevent or delay vascular complications of
diabetes
Hospitalisations account for the majority
Diagnosis and types
of the costs of managing type 2 diabetes Slide 51 of 48
Ambulatory care Anti-diabetic drugs

18% 7%
Other drugs
21%
Hospitalisations
55%
= 29 billion/year ($US 32 billion)
Adapted from Jnsson B. Diabetologia 2002; 45 (Suppl.): S5S12.

Diagnosis and types
Slide 52 of 48
UKPDS: long-term glucose control
9 Conventional
8
HbA1c (%)
Intensive
7
6
0 9
0 3 6 12 15
Years of treatment
UKPDS Study Group 1998
Diagnosis and types
Slide 53 of 48
Natural history of type 2 diabetes

Diagnosis and types
Current recommendations Slide 54 of 48
The Asian-Pacific Type 2 Diabetes Policy Group

recommends that pharmacological therapy should be
started without delay if the patient:
is very symptomatic or
has a very high blood glucose level and diet and
lifestyle changes are unlikely to achieve target
values1
The Global Partnership for Effective Diabetes

Management recommends initial combination therapy
or insulin injection for all patients with HbA1c 9% at
diagnosis2
1.Asian-Pacific Type 2 Diabetes Policy Group. Type 2 diabetes: Practical targets and treatment 4th Ed.
Hong Kong: Asian-Pacific Type 2 Diabetes Policy Group, 2005; 2.Del Prato S et al. Int J Clin Pract 2005; 59: 134555.
Diagnosis and types
UKPDS: reduced micro- and macrovascular Curriculum Module II-1
complications for a 1% decrease in HbA1c Slide 55 of 48
Any Diabetes- All Peripheral Micro-

diabetes-related related cause Myocardial vascular vascular Cataract
endpoint death mortality infarction Stroke disease* disease extraction
0
corresponding to a 1% fall in HbA1c
5
Reduction in relative risk (%)
21 21 14 14 12 43 37 19
10
15

20

25
30
35
40
45
50
*Lower extremity amputation or fatal peripheral vascular disease
p < 0.0001 versus baseline; p = 0.035
Adapted from Stratton IM et al. UKPDS 35. BMJ 2000; 321: 40512.
Inadequate glycaemic controlDiagnosis
in over and types
50% of patients: Diabcare-Asia study Slide 56 of 48
Diabcare Asia study data from 230 centres in

12 countries
Mean HbA1c: 8.62.0% (18211 patients)
55% of patients with measured HbA 1c had
HbA1c > 8%
Prevalence of retinopathy, microalbuminuria,
and neuropathy was higher in patients with
higher HbA1c
Chuang LM et al Diabcare-Asia 1998 Study Group. Diabet Med 2002; 19: 97885.
Diagnosis and types
Majority of type 2 diabetes patients in US Curriculum Module II-1
and EU have inadequate glycaemic control Slide 57 of 48
US1 EU2
100 100
80 80 69%
Subjects (%)
Subjects (%)
64%
60 60
40 36% 31%
40
20 20
0 0
< 7% 7% 6.5% > 6.5%
HbA1c (%) HbA1c (%)
1. Koro CE et al. Diabetes Care 2004; 27: 1720; 2. Liebl A. Diabetologia 2002; 45: S23S28.
Diagnosis and types
Slide 58 of 48
Diabcare-Asia (Sanglah Hospital):

Individual with type 2 diabetes
achieve good glycaemic control (2003)
57
43
Subjects (%)
< 7% >=7%
HbA1C (%)
Diagnosis and types
Slide 59 of 48
Current Recommendations
Diabetes must bediagnosed earlier. And once diagnosed, all types of
diabetes must then be managed must more aggressively
Canadian Diabetes Association
Therefore the results of UKPDS mandate that treatment of type 2 diabetes

include aggressive effort to lower blood glucose levels as close to normal
as possible
American Diabetes Association
C.D.A. Can J Diabetes 2003; 27 (suppl 2): 1-163

ADA. Diabetes Care 2003; 26 : S28-32
Diagnosis and types
Current recommendations Slide 60 of 48
The Asian-Pacific Type 2 Diabetes Policy Group

recommends that pharmacological therapy should be
started without delay if the patient:
is very symptomatic or
has a very high blood glucose level and diet and
lifestyle changes are unlikely to achieve target
values1
The Global Partnership for Effective Diabetes

Management recommends initial combination therapy
or insulin injection for all patients with HbA1c 9% at
diagnosis2
1.Asian-Pacific Type 2 Diabetes Policy Group. Type 2 diabetes: Practical targets and treatment 4th Ed.
Hong Kong: Asian-Pacific Type 2 Diabetes Policy Group, 2005; 2.Del Prato S et al. Int J Clin Pract 2005; 59: 134555.
Diagnosis and types
Slide 61 of 48
Barriers to effective glucose

management
Conservative management
Ineffective diet/exercise initiatives
Delayed efficay due a slow traditional stepwise
approach
Suboptimal health care systems impede achievement
of glycaemic goals
Lack of perceived efficacy
Insufficient communication with patient
Poor adherence to antidiabetic regimens
Lack of knowledge of underlying pathophysiology
Inappropriate prescription ofetmedication
Del Prato al, Int J Clin Prac 60: 1345-1355,2006
Conservative management of glycaemia:
Diagnosis and types
traditional stepwise approach Slide 62 of 48
Diet OAD OAD OAD OAD OAD

monotherapy monotherapy combination + basal insulin + multiple daily
uptitration insulin injections
10
HbA1c (%)
6
Duration of diabetes
Patients remain on monotherapy Diagnosis and types
> 1 year after first HbA1c > 8.0%* Slide 63 of 48
Mean time between first HbA1c > 8.0% and

switch/addition in therapy (months)*
25 20.5
months
20
14.5
months
15
10
0
Metformin only Sulphonylurea only
n = 513 n = 3394
*May include uptitration Brown JB et al. Diabetes Care 2004; 27: 153540.
Proactive management of glycaemia:
Diagnosis and types
early combination approach Slide 64 of 48
Diet
OAD monotherapy
10 OAD combinations
OADs uptitration
9
HbA1c (%)
OAD + basal insulin

OAD + multiple daily
8 insulin injections
6
Duration of diabetes
Diagnosis and types
Slide 65 of 48
Mechanisms of action
GLP-1 (incretins) improve

response to glucose level
Biguanides and thiazolidinediones

reduce glucose production Insulin secretagogues: sulphonylureas and meglitinides
increase insulin production
Alpha-glucosidase inhibitors slow

absorption of sucrose and starch Thiazolidinediones and biguanides reduce
insulin resistance
Expected effect of blood Diagnosis and types Curriculum Module II-1
Slide 66 of 48
glucose-lowering medicines
Class of medicine Expected decrease in
HbA1C in mono-therapy
Alpha-glucosidase inhibitor 0.5-0.8%

Biguanide 1.0-1.5%
Insulin sensitisers 1.0-1.5%
Most insulin secretagogues
1.0-1.5%
Nateglinide
0.5%
Canadian Diabetes Association,2003

Diagnosis and types
Slide 67 of 48
The principles of combination

therapy
Two (or more) oral blood glucose-
lowering medicines that have
different mechanisms of action
Two medications rather than
increase in initial medicine to
maximum dosage
Fewer side effects than mono-
therapy at higher doses
Diagnosis and types
Slide 68 of 48
Strategies to help people

remember :
Check that people understand how
and when to take their medicines
Clarify the benefits of treatment
Keep regimens simple
Minimize costs
Discuss adverse effects
Rubin 2005
Diagnosis and types
Slide 69 of 48
Targets for blood glucose

HbA1C Pre-meal 2 hours
post-meal
Target for people < 6% 4-6 mmol/L 5-8 mmol/L

who can achieve it
(without too much
hypoglycemia)1
Target for most <7% 4-7mmol/L1 5-10mmol/L1

people with
90-130mg/dl*2 <180mg/dl2
diabetes
IDF Global guideline <6.5% <6.0mmol/L <8.0mmol/L

for Type 2 diabetes3
<110mg/dl <145mg/dl
1. CDA 2003, 2. ADA 2004, 3 IDF 2005

Diagnosis and types
Slide 70 of 48
Suggested starting
medicine
HbA1c BMI Suggested medicine
>25 Biguanide alone or in combination

<9%
<25 1 or 2 agents from different classes
>9% 2 medicines from different classes or insulin
CDA, 2003
Diagnosis and types
Slide 71 of 48
Increasing or adding
If goals have not been reached within 2-

3 months, medication should be
increased or medication from a different
class added
Target levels should be reached within 6
months
Insulin should be added if necessary to
reach target levels
Diagnosis and types
Slide 72 of 48
Biguanides
Action not fully understood

Decreases glucose production in liver
Mild and variable effect on muscle
sensitivity to insulin
Side effects
Gastrointestinal (nausea, abdominal
discomfort or diarrhea and occasional
constipation)
Lactic acidosis
Diagnosis and types
Slide 73 of 48
METFORMIN
LKB1,AMPK
Lactate
Anaerobic Gluconeogenesis
Glucose Glycogenolysis Glucose uptake
metabolism FA Oxidation and oxidation
Glycogenesis
FA oxidation
Glukose
turnover Hyperglycemia
Staels, Curr Med Research and Opinion 22,Suppl 2, 2006

Diagnosis and types
Biguanides
Slide 74 of 48
Contraindications
Renal insufficiency
Liver failure
Heart failure
Severe gastrointestinal disease
Advantages
Do not cause hypoglycaemia
when used as mono-therapy
Do not cause weight gain; may
contribute to weight loss
Diagnosis and types
Biguanides
Slide 75 of 48
First-line treatment in overweight or obese

people
Do not cause weight gain
Have some effect on resistance at

the periphery
Diagnosis and types
Biguanides
Slide 76 of 48
Caution
Should be discontinued 24 hours
before procedures requiring
intravenous contrast dye
Can be restarted 48 hours after the
procedure if renal function is not
compromised
Diagnosis and types
Slide 77 of 48
Sulphonylureas
Increase insulin secretion regardless of

blood glucose levels
Many different medicines in this class
Side effects
Hypoglycaemia
Stimulate appetite and provoke weight gain
Nausea, fullness, heartburn
Occasional rash
Swelling
Diagnosis and types
Slide 78 of 48
GLINIDES
Short-acting secretagogues
Meglitinides increase insulin
secretion in response to increasing
blood glucose levels (i.e. after
eating)
Side effects
Hypoglycaemia (probably less than
sulphonylureas)
Weight gain
Diagnosis and types
Slide 79 of 48
Sulphonylureas
Contraindications
Type 1 diabetes
Pregnancy
Breastfeeding
Sulphonylureas - Use cautiously with
liver or kidney disease
Meglitinides - Severe impairment of
liver function
Diagnosis and types
Slide 80 of 48
Sulphonylureas
Things to remember
Some sulphonylureas have slower onset
and lower peak than glibenclamide, thus
may provoke less hypoglycaemia
Some need to be taken only once a day,
therefore may be easier to remember to
take
First generation sulphonylureas, such as
chlorpropamide may accumulate and
cause hypoglycaemia due to their long
duration of action
Diagnosis and types
Slide 81 of 48
Thiazolidinediones
Improve sensitivity to insulin in muscle,

adipose tissue and liver
Reduce glucose output from liver
Changes fat distribution by decreasing
visceral fat and increasing peripheral fat
Side effects
Weight gain, fluid retention
Upper respiratory infection and
headache
Decrease in haemoglobin
Diagnosis and types
Slide 82 of 48
Thiazolidinedione
PPAR
Glucose Uptake Adipogenesis Gluconeogenesis

FA uptake
Lipogenesis
Glucose uptake
Adiponectin
TNF-,Resistin
Hyperglycemia
Plasma NEFA
Staels, Curr Med Research and Opinion 22,Suppl 2, 2006

Diagnosis and types
Slide 83 of 48
Thiazolidinediones
Contraindications
Liver disease, heart failure or history
of heart disease
Pregnancy and breast feeding
They are not contraindicated in renal insufficiency
Potential benefits
Reduced levels of LDL-cholesterol and
increased level of HDL-cholesterol
Diagnosis and types
Slide 84 of 48
Alpha glucosidase inhibitors
Slow digestion of sucrose and starch and

therefore delay absorption
Slow post-meal rise in blood glucose
Side effects
Flatulence, abdominal discomfort ,
diarrhoea
As mono-therapy will not cause
hypoglycaemia
Hypoglycaemia when used with other
medicine (e.g. a sulphonylurea)
Diagnosis and types
Slide 85 of 48
Alpha glucosidase inhibitors
Contraindications
Intestinal diseases, such as
Crohns
Autonomic neuropathy
affecting the gastro-
intestinal tract
Must be taken just before a meal
Diagnosis and types
Slide 86 of 48
GLP-1 (incretin mimetic

agent)
Improves beta-cell responsiveness to increasing
glucose levels
Decreases glucagon secretion
Slows gastric emptying
Results in a feeling of fullness
Must be injected subcutaneously twice a day, within
30-60 minutes before a meal
Reduces HbA1c by ~1%
Side effects
Nausea
Weight loss
Diarrhoea
Risk of hypoglycaemia when used with a
sulphonylurea
Diagnosis and types
Slide 87 of 48
Older people with diabetes
Beware of the possible reductions in

General good health (with other concomitant
conditions)
Kidney function (and increased risk of
hypoglycaemia)
Family support and monitoring
Vision
Flexibility and activities of daily living
Remember also
Poly-pharmacy increases the risk of medicine-
related adverse events
To review all medication and complementary
therapies
Diagnosis and types
Slide 88 of 48
GLP-1 (incretin mimetic

agent)
Contraindications
End-stage kidney disease
or renal impairment
Pregnancy
Severe gastrointestinal
disease
Diagnosis and types
Slide 89 of 48
Always start with the lowest dose

of any blood glucose-lowering
medicine and increase gradually
Using shorter-acting medicines
reduces the risk of
hypoglycaemia
Hypoglycaemia may increase the
risk of falls and heart attack in
older people
Diagnosis and types
Slide 90 of 48

Remember the possibility of
Forgetfulness
Poor motivation
Depression
Cognitive deficits
Poly-pharmacy
Reduced manual dexterity
These impact on the ability to maintain self-care and
achieve maximum benefits from blood glucose-
lowering medicines.
Diagnosis and types
Slide 91 of 48
Ineffectiveness of blood
glucose-lowering medicines
If oral blood glucose-lowering
medicines are ineffective
Check diet and exercise
Consider adding intermediate or
long-acting insulin at bedtime
Maintain metformin
Consider reducing or stopping the
morning sulphonylurea
Diagnosis and types
Simplified ADA-EASD Consensus Algorithm for T2DM
Slide 92 of 48
Lifestyle + metformin
HbA1c 7%
Add Add Add

SU Basal Insulin TZD
HbA1c 7%
Add Add Intensify Add Add

TZD Basal Insulin insulin Basal Insulin TZD
HbA1c 7%
Further intensify insulin or

add basal insulin + metformin TZD*
SU = sulphonylurea; TZD = thiazoidinedione *TZD with insulin is off label in the UK

Diagnosis and types
Slide 93 of 48
Pendahuluan
Diabetes mellitus adalah Peny Kronik

Dapat menimbulkan problem biologi
kimiawi serta anatomi
Akibat dari defisiensi insulin absolut /
relatif serta gangguan fungsi insulin
Diagnosis and types
Slide 94 of 48
Pilar Penanganan Diabetes melitus
Edukasi
Terapi Gizi Medis
Latihan Jasmani
Intervensi Farmakologis
Penanganan Multidisipliner
Diagnosis and types
Slide 95 of 48
Peranan Lat Fisik Pada DM
Kadar Gula Darah

Kepekaan Insulin
Penggunaan Energi
Meningkatkan HDL
LDL dan Trigliserida
Kwalitas Hidup
Mencegah Komplikasi Neuropati
Mengontrol Hipertensi
Diagnosis and types
Slide 96 of 48
Diagnosis and types
Slide 97 of 48
Jenis Lat Fisik Pada DM
Latihan Umum
- Lat Fisik Primer
- Lat Fisik Sekunder
Latihan Khusus
Diagnosis and types
Slide 98 of 48
Latihan Fisik Primer
Pend DM Dianjurkan Lat Ringan 5-10 mnt

Setiap Hari, 1,5 2 Jam Sdh Makan
Contoh : Jalan Sekitar ruangan, Rumah,
Senam ringan
Dapat Dilakukan Ditempat Tidur
Diagnosis and types
Slide 99 of 48
Latihan Fisik Sekunder
Sebelum Lat
Kontrol Gula Darah ( < 250 mg/dl )

Tidak Ada Ketosis
Periksa Jantung EKG
Exercise Stress Test Utk Pend > 30-35 Th
Atau 15 Th Menderita DM atau Dg Gejala
Kardiovaskuler
Diagnosis and types
Slide 100 of 48
Program Latihan
Aerobik
Teratur ( 3 4 Kali / minggu )
Durasi Lama, Intensitas Rendah
Diagnosis and types
Slide 101 of 48
Program Lat Aerobik
High Impact
Gerakan Dg Ada Fase Melayang /
Unspport
Contoh : Lari, Loncat,Jogging, dll
Low Impact
Tdk Ada Fase Melayang, Dimana Kaki
Selalu Kontak Dg Lantai
Contoh : Jalan, Bench Step Aerobik
Diagnosis and types
Slide 102 of 48
Efek Metabolik Lat Teratur
Kapasitas Aerobik
COP, Menurunkan Nadi
Rasio HDL
Jumlah & Ukuran Mitokondria
Mengefektifkan Penggunaan FFA
Menurunkan Konsetrasi Trigliseride
Menghemat glicogen Otot
Diagnosis and types
Slide 103 of 48
Durasi & Intensitas
Durasi Setiap Lat 20 30 Mnt

Intensitas : 50 55 % Kapasitas Aerobik
Maksimal Atau 70 % MHR
Latihan Harus disertai Pemanasan Dan
Pendinginan
Diagnosis and types
Slide 104 of 48
Pencegahan Hipoglikemia Selama Lat
Makan 1- 3 Jam Sebelum Latihan

Pemberian Insulin > 1Jam Sebelum Lat
Monitor Kadar Gula Darah
Diagnosis and types
Slide 105 of 48
Efeks Diabetes Pd Kaki
Gangguan Persarafan (Neuropati )

Gangguan Pembuluh Darah
Kelemahan Otot /Ligamen
Kollap Persendian
Blister dan Callus
Infeksi Tulang
Amputasi
Diagnosis and types
Slide 106 of 48
Pencegahan Komplikasi Pd Kaki
Jaga Kebersihan & Kelembaban Kaki

Hidari Dari tekanan
Jangan Merendam Kaki Dengan Air Panas/Dingin
Lindungi Kaki Dari Suhu Dingin
Harus Selalu Memakai Alas Kaki
Sepatu Harus Pas,Hindari Yg Memakai Paku
Lakukan Lat Ankle Pumping
Diagnosis and types
Slide 107 of 48
Yang Harus Diperhatikan Penderita
Perubahan warna kulit kaki

Pembengkakan kaki
Perubahan Tempratur kaki
Perubahan sensasi kaki
Daerah Kemerahan pada kaki
Kalus , Krak, Ulkus
Diagnosis and types
Slide 108 of 48
Yang Harus Dihindari Penderita
Hindari Panas atau Dingin

Hindari Menyilangkan tungkai
Hindari penggunaan larutan kimia/pisau
untuk menghilangkan kalus
Hindari jalan tanpa alas kaki
Hindari Jalan dg Langkah lebar
Hindari makan berlebihan
Diagnosis and types
Slide 109 of 48
Cara Penentuan Tekanan pd Kaki

(Harris Mat Foot Print)
Pemakai Prinsip Newton : Kaki akan mendapat

reakasi sebesar aksi yg diberikan
Tekanan akan diidentifikasikan oleh cetakan atau
cap
Kegunaannya : - Bentuk pembebanan berat
- Lokasi tekanan
- Tipe lengkung kaki
- Hubungan tumit dan kaki
- Menggambarkan bentuk
kaki
Diagnosis and types
Slide 110 of 48
Pemakaian Sepatu
Pakai kaos kaki yg tebal dari katun

Lama pemakaian 4 6 jam, bila spt baru 2-3 jam
Periksa sepatu sebelum dipakai
Pemilihan sepatu:
- Sesuai ukuran sudah dengan kaos kaki
- Toe Box longgar, Counter Kuat
- Outsole Rigid dg dasar Rocker
- Heel lebar dan tinggi tidak lebih 2 inc
- Insole Lunak , tidak licin
- Hindari yang memakai paku
Diagnosis and types
Slide 111 of 48
Latihan Ankle Pumping
Dikerja Setiap Hari, 2 Kali /Hr

Posisi Sebaiknya Berbaring, Kedua Betis di
Atas Bantal
Lakukan Gerakan:
- Jari-jari kaki keatas dan kebawah
- Dorso Plantarfleksi & Rotasi Ankle
- Ekstensi Fleksi Lutut Secara Bergantian
Diagnosis and types
Slide 112 of 48
Ringkasan
Latihan atau Olah Raga Yg Dianjurkan Pd Pend DM

Adh Aerobik
Lat Teratur Dg Durasi Panjang Intensitas Rendah
Perhatikan Kemungkinan Cedera / Komplikasi
Hipoglisemia
Dg Lat Dapat Memperbaiki Metabolisme Glukosa,
Asam Lemak
Dg Lat Dapat Mencegah / Mengurangi kegemukan
Diagnosis and types
BERBAGAI PENELITIAN Curriculum Module II-1
Slide 113 of 48
MENUNJUKKAN
75 % PENYANDANG DM
TIDAK MENGIKUTI TERAPI NUTRISI
YANG DIANJURKAN.
MENJADI
HAMBATAN U/ TERCAPAI
NYA PELAYANAN DM.
TERAPI NUTRISI KOMPONEN UTAMA

KEBERHASILAN PENATALAKSANAAN
DIABETES.
Diagnosis and types
Slide 114 of 48
REKOMENDASI THE AMERICAN DIABETES
ASSOCIATION (ADA) 2003
DIPERLUKAN PENDEKATAN TIM:

-DOKTER,
-DIETISIEN,
-PERAWAT, dan
-PETUGAS KESEHATAN LAIN serta
-PENYANDANG DM ITU SENDIRI.
MENINGKATKAN KEMAMPUAN SETIAP PENYANDANG DM

DALAM MENCAPAI KONTROL METABOLIK YANG BAIK
ASSESMENT/
Diagnosis and types
PENGKAJIAN Slide 115 of 48
PARAMETER
METABOLIK INDIKATOR
INDIVIDU & KEBERHASILAN
GAYA HIDUP
TERAPI NUTRISI a/
KETERLIBATAN TIM
DALAM 4 HAL
MENDORONG
PENYANDANG
DM
BERPARTISIP
ASI
PD TUJUAN
YANG AKAN MENGEVALUASI
DICAPAI EFEKTIFNYA
PERENCANAAN
MEMILIH PELAYANAN GIZI
INTERVENSI GIZI
YG MEMADAI
Diagnosis and types
Slide 116 of 48
LANGKAH-LANGKAH TERAPI NUTRISI
1. PENGKAJIAN gizi penyandang DM
-TERMASUK DATA KLINIS

(PEMANTAUAN sendiri kadar glucosa darah, kadar lemak darah,
dan hemoglobin glikat)
-DIGUNAKAN PULA U/ apa yang mampu dilakukan o/

penyandang DM dan kesediaan u/ melakukannya.
-ASPEK budaya, etnik, dan keuangan perlu dipertimbangkan

u/ mendptkan KEPATUHAN PENYANDANG DM yg tinggi
-INFORMASI yg dikumpulkan oleh TIM DIABETES perlu dicatat

pada DOKUMEN MEDIK sehingga PERENCANAAN
PENANGANAN DM scr menyeluruh dapat dikembangkan dan
SEMUA ANGGOTA TIM DAPAT MEMBANTUNYA.
2. MENENTUKAN TUJUAN YANG AKAN DICAPAI Diagnosis and types
Slide 117 of 48
HASIL DARI PENGKAJIAN GIZI
DIPERLUKAN MENENTUKAN
TUJUAN YANG AKAN DICAPAI
MEMBANTU
PERUBAHAN YG POSITIP DALAM
KEBIASAAN MAKAN YG AKAN
MENGHASILKAN
PERBAIKAN KADAR GLUCOSA DRH & LEMAK DRH

serta MEMPERBAIKI ASUPAN GIZI.
Diagnosis and types
3. INTERVENSI GIZI Curriculum Module II-1
Slide 118 of 48
PENGKAJIAN & TUJUAN
menentukan DASAR INTERVENSI GIZI
TUJUAN:
U/ MEMBERIKAN INFORMASI PRAKTIS, YG DPT DITERAPKAN PADA
KEHIDUPAN SEHARI-HARI.
MELIBATKAN 2 TAHAP PEMBERIAN INFORMASI:

-INTERVENSI GIZI DASAR
Memberikan gambaran ttg gizi, kebutuhan zat gizi,
petunjuk pelaksanaan, informasi survival-skill yg dianggap
perlu untuk penyandang DM (membaca label dll)
-INTERVENSI GIZI LANJUTAN

Pendekatan perencanaan makan yg lebih MENDALAM,
spt: MENU, DAFTAR PENUKAR BM dll.
4. EVALUASI Diagnosis and types
Slide 119 of 48
BAG PENTING PD PROSES TERAPI NUTRISI.
DIETISIEN DAN KLIEN BER-SAMA MENETAPKAN

HASIL INTERVENSI.
PEMANTAUAN KEADAAN, kadar glucosa darah, hemoglobin

glikat, lipid, tekanan darah, dan fungsi ginjal PENTING u/
MENGEVALUASI HASIL YG BERHUBUNGAN DG GIZI.
KONSISTEN DALAM POLA MAKAN PENTING, AKAN

menghasilkan Hb A1 C yg lebih RENDAH, drpd POLA MAKAN
YANG SERAMPANGAN.
PILAR UTAMA PENATALAKSANAAN DM adalah
1. PERENCANAAN MKN / DIIT / TERAPI NUTRISI/TERAPI GIZI

MEDIS
2. AKTIFITAS JASMANI
3. OBAT (ORAL/INSULIN)
4. PENYULUHAN
DI ANJURKAN MENGIKUTI 3 J :
J1 (JUMLAH KALORI)
TERGANTUNG PENDERITA, DIANJURKAN HABIS
J2 (JADWAL)
DIHARAPKAN TEPAT
JARAK MAKAN + / - 3 JAM
J3 (JENIS MAKANAN)
MAKANAN MANIS ( GULA, SIRUP, MADU DAN HASIL OLAH
NYA DIKURANGI)
POLA DASAR PERENCANAAN MAKAN
3 X makan utama, 2 X snack

3 X makan utama, 3 X snack
DENGAN POLA ATAU KOMPOSISI SBB
Pukul 06.30 MAKAN UTAMA PAGI (20 %)

Pukul 09.30 SNACK / BUAH
Pukul 12.30 MAKAN UTAMA SIANG (30 %)

Pukul 15.30 SNACK
Pukul 18.30 MAKAN UTAMA MALAM (25 %)

Pukul 21,30 SNACK
Makanan ringan/snack: 5-10 % diantaranya

JADWAL DAPAT DIUBAH ASAL INTERVALNYA TETAP 3 JAM
UNTUK PENYANDANG DM YG MENGIDAP PENYAKIT LAIN POLA PENGATURAN MAKAN
DISESUAIKAN DG PENY PENYERTANYA
TERAPI NUTRISI
IDDM / DMTI ( Tergantung Insulin )
- DIANJURKAN MAKAN PADA WAKTU YANG KONSISTEN
DENGAN WAKTU KERJA INSULIN YANG DIGUNAKAN
NIDDM / DMTTI ( Tidak Tergantung Insulin )

- KENDALI GLUKOSA ( menjaga pembuluh darah)
- 10 petunjuk sehat G= Glukosa
U= Uric acid ( asam urat )
L= Lipid ( cholesterol dll )
O= Obesitas ( kegemukan )
H= Hipertensi
S= Sigaret
I= Inaktifitas
S= Stress
A= Alkohol
R= Reguler Check Up
MENGANTISIPASI GULOH SISAR
@JAS BUKE
JEROHAN, ALKOHOL, SARDEN, BURUNG DARA,
UNGGAS, KALDU, EMPING >> ASAM URAT
@ TEK KUK CS2

TELUR, KEJU, KEPITING, UDANG, KERANG, CUMI,
SUSU, SANTAN > CHOLESTEROL

TUJUAN PERENCANAAN MAKAN
MEMBANTU PENYANDANG DM MEMPERBAIKI KEBIASAAN MKN KONTROL
METABOLIK YG LEBIH BAIK
1. MENCEGAH HIPO/HIPERGLIKEMI
2. MAKAN ADEKUAT
3. MEMPERTAHANKAN GULA DARAH BATAS NORMAL
4. MEMPEROLEH / MEMPERTAHANKAN BB N/BB I
5. MENYESUAIKAN DG MKN KEL
6. MELAKSANAKAN AKTIFITAS ORANG NORMAL
7. IBU HAMIL = BAYI NORMAL
- MENCEGAH / MEMPERLAMBAT TIMBULNYA KOMPLIKASI

- MENGUSAHAKAN PERTUMBUHAN DAN PERKEMBANGAN
NORMAL BAGI ANAK DAN REMAJA
- MEMBIASAKAN WAKTU MAKAN TERATUR
- DPT MENGATUR DAN MERAWAT DIRI SECARA OPTIMAL

PERENCANAAN MAKAN PADA PENYANDANG DIABETES
I MAKAN ANEKA RAGAM MAKANAN
A. SUMBER ZAT TENAGA

Beras, jagung, gandum, umbi-umbian, sagu, roti dan
mie, minyak, margarin, dan santan yang mengandung
lemak menghasilkan tenaga, menunjang aktifitas se-
hari
B. SUMBER ZAT PEMBANGUN

Berasal dari bahan makanan Nabati adalah kacang-
kacangan, tempe, tahu.
Sedangkan dari hewani adalah telur, ikan, ayam,
daging,susu serta hasil olahan, berperan sangat penting
untuk Pertumbuhan, Perkembangan, Kecerdasan.

C. SUMBER ZAT PENGATUR
Berasal dari semua sayuran dan buah-buahan. Mengandung Vitamin dan
Mineral yang berperan
untuk melancarkan bekerjanya fungsi organtubuh .
2. MAKAN UNTUK MEMENUHI

KEBUTUHAN ENERGI
Kebutuhan energi penyandang DM tergantung pada:
Umur, Jenis kelamin, BB, TB, aktifitas fisik,
keadaan penyakit dan pengobatannya.
SUSUNAN MAKANAN, sesuai dengan kebutuhan kalori

masingpenyandang DM

3. MAKANLAH SUMBER KH
Pilihlah KH kompleks dan serat, batasi KH sederhana
3 Kelompok KH yaitu
KH Kompleks, KH Sederhana dan Serat
3.1. KH KOMPLEKS atau Tepung-tepungan
Padi padian (beras, gandum, jagung) Umbi-umbian (singkong, ubi

jalar, kentang) , sagu.
Proses penyerapan KH kompleks didalam tubuh
berlangsung lebih lama daripada KH sederhana sehingga tidak

segera merasa lapar.

3.2. KH SEDERHANA
KH sederhana secara alamiah terdapat pada buah, sayur
dan susu. KH sederhana hasil produksi gula, madu,
sirup, cakes, selai dll, langsung diserap dan cepat lapar
Anjuran konsumsi gula pada penyandang DM
adalah 5 % total kalori ( + 3 4 sdm ).
3.3. SERAT MAKANAN
Serat a/bagian dari KH yang tidak dapat di cerna enzim,
tapi berpengaruh baik bagi kesehatan.

TERDIRI ATAS 2 GOLONGAN: Diagnosis and types
Slide 129 of 48
1. SERAT LARUT AIR

PEKTIN, GUM, MUKILASE, banyak terdapat pada
HAVERMOUT, KACANGAN, SAYUR DAN BUAH
BERMANFAAT MENGIKAT ASAM EMPEDU
SHG DPT MENURUNKAN ABSORBSI

LEMAK & KOLESTEROL DARAH SHG MENURUNKAN
RESIKO PJK & DISLIPIDEMIA disamping memp pengaruh
THD PENY DM HIPOGLIKEMIK.
2. SERAT TIDAK LARUT AIR

SELULOSA, HEMISELULOSA & LIGNIN, >> TERDAPAT
DEDAK BERAS, GANDUM, SAYUR DAN BUAH
BERMANFAAT MELANCARKAN DEFEKASI SHG
MENCEGAH OBSTIPASI, HEMORHOID, DIVERTIKULOSIS
KEUNTUNGAN SERAT
- Rasa kenyang, membantu mengendalikan
nafsu makan & menunda rasa lapar.
-Makanan tinggi serat biasanya rendah kalori
- Membantu buang air besar secara teratur
- Meningkatkan waktu transit usus dan massa feses.
- Mencegah ca colon dg mengikat dan mengeluarkan
bahan-bahan karsinogen dalam usus.

4. BATASI KONSUMSI LEMAK, MINYAK, SANTAN
Penyandang DM Peny.Jantung
Makanan jangan terlalu banyak digoreng
atau gunakan minyak tak jenuh seperti :
minyak jagung, minyak kedelai, minyak
biji bunga matahari atau minyak kacang.

5. GUNAKAN GARAM SECUKUPNYA
Penyandang DM asupan natrium tidak lebih dari 3000

mg/hari (6-7 gram / 1 sdt/ hari) yang digunakan dalam
masakan.
6. MAKANLAH MAKANAN SUMBER ZAT

BESI ( Fe)
Kekurangan zat besi yang berkelanjutan dapat

menimbulkan anemia gizi.
BM : sayur hijau, kacangan, hewani

7. BIASAKAN MAKAN PAGI
Makan pagi bermanfaat

memelihara ketahanan fisik
mempertahankan daya tahan tubuh
meningkatkan produktivitas kerja.
Pada penyandang DM
-menggunakan obat glukosa darah
-suntikan insulin
tidak makan pagi, mempunyai resiko
menurunnya kadar gula darah yang membahayakan.

8. MINUMLAH AIR BERSIH AMAN DAN
CUKUP JUMLAHNYA
9. HINDARI MINUMAN BERALKOHOL

Kebiasaan minum alkohol
-Terhambatnya proses penyerapan zat gizi

-Hilangnya zat gizi penting,
-Kurang gizi,
-Penyakit gangguan hati
-Kerusakan saraf otak dan jaringan.


10. MAKAN TERATUR
Penyandang DM selain MAKAN SEIMBANG

perlu juga makan TERATUR dalam hal JUMLAH
JENIS dan WAKTU makan.
11. BACA LABEL MKN YANG DIKEMAS
PERLU MENGETAHUI
KEBUTUHAN KALORI,
KEBUTUHAN BAHAN MAKANAN SEHARI
BERDASARKAN STANDART DIIT DM, dan
DAFTAR PENUKAR BAHAN MAKANAN

Diagnosis and types
Slide 136 of 48
KEBUTUHAN KALORI
KEBUTUAHN KALORI SESUAI UNTUK MENCAPAI DAN

MEMPERTAHANKAN
BB IDAMAN
BB IDAMAN DENGAN RUMUS BROCCA

MODIFIKASI SBB
BB = 90% x (TB dalam cm 100) x 1 kg
Bagi PRIA DG TB 160 dan WANITA TB 150
Modifikasi menjadi
BB IDAMAN = (TB dlm cm 100) x I kg
KEBUTUHAN KALORI UNTUK DM
KALORI BASAL :
LAKI-LAKI= BB Idaman X 30 kal/hari
WANITA = BB Idaman X 25 kal/hari
KOREKSI PENYESUAIAN
Umur > 40-59 thn : - 5% X kal basal
60-69 thn : - 10% X kal basal
> 70 tahun : - 20% X kal basal
Aktifitas : Ringan + 10% X kal basal
Sedang + 20% X kal basal
Berat + 30% X kal basal

BB Gemuk 20% X kal basal
Lebih -10%
Kurang +20%
STRES METABOLIK : +(10-30%X kal basal)
TOTAL KEBUTUHAN KALORI: Total Kal.

KLASIFIKASI IMT
IMT (Indeks Massa Tubuh) BB (kg)
TB (m)
BB Kurang : <18,5
BB Normal : 18,5-22
BB Lebih : >22
Dengan Resiko : 23,0-24,9
Obes I : 25,0-29,9
Obes II: : >30

STATUS GIZI
BB NYATA X 100 %
TB - 100
BB KURANG : 90% BBI

BB NORMAL : 90-110% BBI
BB LEBIH : 110-120% BBI
GEMUK : >120% BBI

MENGGUNAKAN TABEL
KEBUTUHAN ENERGI DM
Kal /Kg BB
DEWASA
Kerja Kerja Kerja
Ringan Sedang Berat
GEMUK 25 30 35
NORMAL 30 35 40
KURUS 35 40 40-50
JENIS AKTIFITAS DIKELOMPOKKAN SBB: Diagnosis and types
Slide 142 of 48
1. KEADAAN ISTIRAHAT
KEBUTUHAN KALORI BASAL + 10 %
2. RINGAN
PEG KANTOR, PEG TOKO, GURU, AHLI HUKUM, IBU RT
3. SEDANG
PEG INDUSTRI RINGAN, MHS, MILITER YG TDK PERANG
4. BERAT
PETANI, BURUH, MILITER DLM KEADAAN LAT, PENARI,
ATLIT.
5. SANGAT BERAT
TUKANG BECAK, TUKANG GALI, PANDE BESI.
SECARA KASAR
GEMUK : 1100 1500 Kal

NORMAL : 1700 2100 Kal
KURUS : 2300 2500 Kal

DENGAN PENENTUAN JUMLAH
KALORI
Kurus : BB X 40-60 Kal/hari

Normal : BB X 30 Kal/hari
Gemuk : BB X 20 Kal/hari
Obes : BB X 1015 kal/hari

Diagnosis and types
Slide 145 of 48
CONTOH KASUS
PASIEN = pria, U= 45 thn

TB = 165 cm, BB = 50 kg,
Mrs dx : DM Keb. Energi,
Protein, Lemak, Karbohidrat?
I. PERKENI
Kal basal = BBI x 30 kal/hr
= 58,5 x 30 kal = 1755 kal
Kor.penys. = 5% x 1755 kal = 87,75 kal -
= 1667,25 kal
Diagnosis and types
Aktifitas = 10% x 1755 kal = 17,55 kal + Slide 146 of 48
= 1684,80 kal
Status gizi = IMT BB (Kg) = kurang (18,37)
TB (m)
= 10 % x 1755 kal = 17,55 kal +
= 1702,35 kal
F. Stres = 20 % x 1755 kal = 351 kal +
TOTAL ENERGI = 2053,35 kal
Diagnosis and types
Bila kita bandingkan dengan Slide 147 of 48
perhitungan secara kasar :
St.gizi Kurus : = BB x 40 60 kkal/hari

= 50 kg x 40 kkal
= 2000 kkal/hr
Kebutuhan KH = 60% - 70% tot.kal

= 60% X 2000 kal = 1200kal
4
= 300 gr
Diagnosis and types
Keb. Protein = 10 % - 15 % total kalori Slide 148 of 48
= 15% x 2000 kal = 300 kal

4
= 75 gr
Keb. Lemak = 20% - 25% total kalori

= 25% x 2000 kal = 500 kal
9
= 56 gr
SELANJUTNYA SUSUN MENU

Khusus Penentuan Kalori
DM pd Kehamilan
(TB-100) X 30 + Y
Y : Trimester 1 = 100 Kal

Trimester 2 = 200 Kal
Trimester 3 = 300 Kal
Laktasi = 400 Kal

Diagnosis and types
KEBUTUHAN KALORI PADA Curriculum Module II-1
Slide 150 of 48
1. BAYI
KEBUTUHAN KALORI LEBIH TINGGI DIBANDING DEWASA:
- TAHUN PERTAMA DPT MENCAPAI 112 kal/kg BB
2. ANAK-ANAK
UMUR 1 TAHUN MEMBUTUHKAN LEBIH KURANG 1000 kal
dan selanjutnya untuk lebih dari 1 tahun mendapat TAMBAHAN 100
kalori UNTUK TIAP TAHUNNYA.
Diagnosis and types
Slide 151 of 48
MACAM DIET DAN INDIKASI

PEMBERIAN
Diet DM A.
- Dari RSCM Jakarta
- Berpedoman pada 8 macam diet DM
Diet DM I III (1100 1500 kal)

- Diberikan pasien gemuk
Diet DM IV V (1700 1900 kal)

- Diberikan pasien BB normal
Diagnosis and types
Diet DM VI VIII (2100 2500 kal) Slide 152 of 48
- Diberikan kurus, remaja dan komplikasi.
DIET DM B
Diet dari RSUD Sutomo Surabaya
Diberikan kepada semua penyandang DM yang
1. Tidak tahan lapar

2. Memp.Hiperkolesterolemia
3. Memp.penyulit penyempitan pembuluh darah
Diagnosis and types
4 Memp.komplikasi ginjal std. I Slide 153 of 48
5. Menderita DM lebih dari 15 tahun.
A. DIET DM B1
Komposisi : Karbohidrat 60 %
Protein 20%
Lemak 20%
Pasien yang memerlukan protein Tinggi:
- Kurus/ RBW < 90%
- Masih muda/pertumbuhan
- Patah tulang
- Hamil/menyusui
- TBC paru
- Gangren diabetik
- Pasca bedah dll
Diagnosis and types
B. DIET DM B2 Slide 154 of 48
- Penderita Nefropati diabetik (Stadium II)

- Sifat-sifat diet DM B2 :
- Tinggi kalori tetapi mengandung

protein 1 gr/kgBB/hr.
- Komposisi sama dengan Diet DM B

(68% KH, 12% Protein, 20% Lemak)
Diagnosis and types
C. DIET DM B 3 Curriculum Module II-1
Slide 155 of 48
- Penderita Nefropati Diabetik (stdm.III)

- Sifat-sifat diet DM B3 :
- Tinggi kalori
- Rendah Protein (40 gr./hr)
D.DIET DM Be (Diet Bebas)
- Penderita DM dengan Nefropati diabetik tipe Be (stdm. Akhir)

- Penderita dibolehkan minum gula/manis
Diagnosis and types
Slide 156 of 48
DM pada saat BULAN RAMADHAN

Boleh apabila :
DM tanpa suntik/suntik insulin < 20 IU

dengan obat OAD atau
diet saja
Kadar glukosa darah 2 jam pp < 200- 250 mg%
Diagnosis and types
PEMBAGIAN MAKAN SEHARI Slide 157 of 48
-Pukul 18.00 (30% Kal Total)

Buka Puasa (Mkn Utama I)
Tablet OAD + Vitamin
-Pk. 21.00 ( 25% Kal Total)

Sehabis Teraweh (Mkn Utama II)
-Sebelum tidur (10% Kal Total)
Mkn kecil, tablet OAD II
-Pk. 03.00 (25% Kal Total)

Sahur (Mkn Utama III)
-Sblm Imsak ( 10 % Kal Total)
Makanan kecil + Vit
Diagnosis and types
Slide 158 of 48
MAKANAN
DIANJURKAN DENGAN
KOMPOSISI SBB
KARBOHIDRAT : 60 70 %
PROTEIN : 10 15 %
LEMAK : 20 25 %
Diagnosis and types
Slide 159 of 48
PRINSIP
Anjuran makan seimbang spt anjuran makan sehat

Tidak ada makanan yang dilarang, hanya dibatasi
sesuai kebutuhan
Menu sama dengan keluarga, gula dalam bumbu
tidak dilarang
Teratur dalam Jadwal, Jumlah dan Jenis makanan
(3J)
DAFTAR BAHAN MAKANAN PENUKAR Diagnosis and types
Slide 160 of 48
Daftar nama bm dg ukuran tertentu

dan dikelompokkan berdasarkan kandungan kalori, protein,
lemak dan karbohidrat
Setiap kelompok bm dianggap mempunyai

nilai gizi yang kurang lebih sama
Bisa dijadikan sebagai pedoman

dlm penyusunan menu sehari
Diagnosis and types
7 KELOMPOK
Slide 161 of 48
BAHAN MAKANAN
Golongan 1 : bm sumber KH
Golongan 2 : bm sumber prot Hewani
Golongan 3 : bm sumber prot Nabati
Golongan 4 : Sayuran
Golongan 5 : Buah-buahan
Golongan 6 : Susu
Golongan 7 : Minyak
Golongan 8 : Makanan tanpa kalori.
Gol. 1 : SUMBER KARBOHIDRAT
1 satuan penukar
= 175 kal
= 4 gr Protein
= 40 gr Karbohidrat
Gol. 2 : SUMBER PROTEIN HEWANI

1 satuan penukar
= 50 kal.
= 7 gr Protein
= 2 gr Lemak

Gol. 3 : SUMBER PROTEIN NABATI
1 satuan penukar
= 75 kal.
= 5 gr Protein
= 3 gr Lemak
= 7 gr Karbohidrat
Gol. 4 : SUMBER SAYURAN

SAYURAN A bebas dimakan.
Kandungan kal. Bisa diabaikan (jumlah sedikit)
SAYURAN B
1 satuan penukar
= 25 kal
= 1 gr Protein
= 50 gr Karbohidrat

Gol. 5 : BUAH DAN GULA
1 satuan penukar
= 50 kal.
= 12 gr Protein
Gol. 6 : SUSU
SUSU TANPA LEMAK
1 satuan penukar
= 75 kal
= 7 gr Protein
= 10 gr Karbohidrat
SUSU RENDAH LEMAK
1 satuan penukar
= 125 kal
= 7 gr Protein
= 6 gr Lemak
= 10 gr Karbohidrat Slides current until 2008
SUSU TINGGI LEMAK
1 satuan penukar
= 150 kal
= 7 gr Protein
= 10 gr Lemak
= 10 gr Karbohidrat
Gol. 7 = MINYAK
1 satuan penukar
= 50 kal
= 5 gr Lemak
Gol. 8 = MAKANAN TANPA KALORI

Agar-agar, Kopi, Teh, Cuka, Air mineral
Kecap, Air kaldu, Gelatin

Diagnosis and types
CONTOH Curriculum Module II-1
Slide 166 of 48
MENU 2000
KALORI
Pagi Siang Sore Snack
Nasi /Penukar 1,5 2 2 -
Ikan /Penukar - 1 1 -
Daging /Penukar 1 - - -
Tempe /Penukar 1 1 1 -
Sayuran A S S S -
Sayuran B - 1 1 -
Buah /Penukar - 1 1 2
Minyak /Penukar 1 2 2 -
Diagnosis and types
KESIMPULAN
Slide 167 of 48
MANAGEMEN NUTRISI penyandang DM
cukup komplek karena harus ada keterlibatan tim kesehatan disamping kesadaran
penyandang DM.
Katalisator keberhasilan untuk mempertahankan kadar gula darah harus senantiasa

dikumandangkan tim kesehatan bagi penyandang DM
Kepatuhan penyandang DM thd pengaturan makanan tdk perlu menjadi BEBAN mengingat
tersedianya penukar bahan makanan yg menjadi pilihan
Diagnosis and types
Slide 168 of 48
Diagnosis and types
Slide 169 of 48
Diagnosis and types
Slide 170 of 48

1 - 1 Diagnosis, Classification and Prevention

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1 - 1 Diagnosis, Classification and Prevention

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Diagnosis, classification and

Curriculum Module II1 | Diagnosis, classification and

Slides current until 2008

Chronic hyperglycaemia associated

The diabetes epidemic

230 million affected in 2006

350 million within 20 years

Most rapid in Indian and Asian

IDF Diabetes Atlas

Other specific types

Uncommon forms of immune-

Insulin and glucose disposal

Triglyceride degradation fatty acids

Effect of insulin resistance in

Pathogenesis of type 1 diabetes

Progressive beta-cell destruction

Insufficient beta-cell function

Dependent on exogenous insulin

Pathogenesis of type 1 diabetes

Pathogenesis of type 1 diabetes

Idiopathic type 1 diabetes

Non-autoimmune type 1 diabetes

People of African and Asian origin

Epidemiology of type 1 diabetes

Increasing in recent years

IDF Diabetes Atlas

Epidemiology of type 1 diabetes

Age of onset peaks

90%-95% of people with

Insulin insensitivity and

Complications often present

Pathogenesis of type 2 diabetes

Multiple genes involved

Poor fetal nutrition beta-cell

Low birth weight/weight change

The natural history of

The natural history of

The natural history of

Epidemiology of type 2 diabetes

What are the most common risk

Are any of these risk factors

Slides current until 2008

Risk factors for type 2 diabetes

Age > 40 years

Risk factors for type 2 diabetes

Signs and symptoms

Normal Impaired fasting glucose* Diabetes

2hr PG <7.8mmol/L 7.8 to 11mmol/L** 11.1mmol/L

CDA 2003, ADA 2004, WHO 2002

Impaired glucose tolerance

75 g glucose load after 8 hours

Readings taken in fasting state

Tests for differential diagnosis

Cluster of risk factors or syndrome

Prevention of type 1 diabetes

Early exposure to cows milk

Prevention of type 1 diabetes

Diabetes Prevention Trial

Diabetes Prediction and

Prevention of type 2 diabetes

Finnish Diabetes Prevention Study

Prevention of type 2 diabetes

Diabetes Prevention Program