DR.

JAVERIA
Topic DR.JAVERIA
Content; DR.JAVERIA
 Diabetes mellitus
 Insulin
 Incidence and prevalence
 Categories of glucose intolerance
 Type 1 DM ,2DM,Gastitional diabetes
 Pathophysiology of T1DM
 Etiology
 Signs and symptoms
 Complication
 Monitoring
 Medical treatment
 Medical nutrition therapy (MNT)
 Mother types of diabetes
 Diagnosis criteria
 Implement of nutrition care process
Diabetes mellitus:
DR.JAVERIA

 Diabetes mellitus is a group of diseases characterized by

high blood glucose, concentrations resulting from defects in
insulin secretion , insulin action or
both.
 Diabetes mellitus contributes to a
considerable increase in morbidity
and mortality rates, which can be
reduces by early diagnosis and
treatment.
 DR.JAVERIA

Insulin:
 Insulin is a hormone produced
by the beta-cell of the pancreas
that is necessary for the use
or storage of body fuels
( carbohydrate, protein, fat) .
 DR.JAVERIA

Incidence and prevalence:

 In 2014 total prevalence of diabetes in the U.S in all ages
was 20.1 million people (15.5 million adult men and 13.4
adult women). Or 9.3% of the population.
 Of these,21.0 million are diagnosed , and 8.1 million
undiagnosed.
 In 2012 1.7 million new cases of diabetes were diagnosed in
people age 20 years or older (CDC,2014)
 Diabetes prevalence also increases with age, affecting 11.2
million people age 65 years and older, or 25.9% of all people
in this age group.
Categories of glucose intolerance: DR.JAVERIA

 Prediabetes
 Type 1 Diabetes
 Type 2 Diabetes
 Gestational diabetes mellitus
Prediabetes: DR.JAVERIA

 Individuals with a stage of impaired glucose

homeostasis that includes IFG and IGT are
referred to as having prediabetes, indicating their
relatively high risk for the development of diabetes
and CVD.
 People at risk may have IFG (fasting plasma
glucose 100-125 mg /dL),IGT(2-hrs post
challenges glucose of 140 – 199 mg/dL), both or a
hemoglobin AlC of 5.7% - 6.4% and should be
counseled about strategies, such as reduced
energy intake, weight loss, and physical activity, to
lower their risk.
Type 1 diabetes: DR.JAVERIA

 juvenile diabetes.
 Insulin-dependent diabetes.
 Type 1 diabetes (T1D) usually adolescent onset but may
occur at any age.
 Chronic condition.
 Pancreatic beta cell destruction and eventually absolute
insulin deficiency.
Pathophysiology of type 1 diabetes: DR.JAVERIA

 Auto Immune destruction Pathologically,

the pancreatic islets are infiltrated with
lymphocytes (in a process termed insulitis).
 After all beta cells are destroyed, the
inflammatory process abates, the islets
become atrophic.
 The autoimmune destruction of pancreatic
β-cells leads to a deficiency of insulin secretion.
 It is this loss of insulin secretion that leads
to the metabolic derangements associated
with IDDM.
Pathophysiology of Type 1
Diabetes Mellitus (contd.) DR.JAVERIA

 In addition to the loss of insulin secretion, the function of

pancreatic α-cells is also abnormal.
 There is excessive secretion of glucagon in IDDM
patients. Normally, hyperglycemia leads to reduced
glucagon secretion.
 However, in patients with IDDM, glucagon secretion is not
suppressed by hyperglycemia.
 The resultant inappropriately elevated glucagon levels
exacerbate the metabolic defects due to insulin
deficiency.
Etiology: DR.JAVERIA

.
Immune mediated
(autoimmunity)(viral
infection, toxic
chemicals, etc.)
Circulating
idiopathic
Auto-antibiodies

Type 1
diabetes
mellitus
Symptoms : DR.JAVERIA

 Hyperglycemia
 Polyuria
 Polydipsia
 Polyphagia
 Weight loss
 Dehydration
 Electrolyte disturbance
 ketoacidosis
Complications: DR.JAVERIA

 Ketoacidosis
 Macrovascular disease:
- coronary heart disease
- peripheral vascular disease
- cerebrovascular disease
 Micovascular disease:
- retinopathy
- nephropathy
 Neuropathy
Monitoring: DR.JAVERIA

 Self monitoring of blood glucose

 A1C testing
 Lipids
 Blood pressure
 Ketones
 Weight and growth in children
Medical treatment: DR.JAVERIA

 Medical nutrition therapy

 Medications
- insulin by injection or insulin infusion pumps
 Self management education
Medical nutrition therapy (MNT): DR.JAVERIA

 Integrate insulin regimen into preferred eating and

physical activity schedule; consistency in timing
and amount of carbohydrate eaten if on fixed
insulin doses.
 Adjust per meal insulin does based on insulin –to-
carbohydrate ratios.
 Energy intake to prevent weight gain in adults.
 Adequate energy and nutrient intake to promote
growth and development in children
 Cardioprotective nutrition intervention.
Types 2 diabetes mellitus: DR.JAVERIA

 Adult onset diabetes

 Non-insulin-dependent DM(NIDDM)
 Chronic disease
 Age :over 40 yrs.
 T2DM is characterized by a combination of insulin
resistance and beta-cell failure.
Pathophysiology of type 2DM: DR.JAVERIA

 Type 2 DM is characterized by impaired insulin secretion, insulin

resistance, excessive hepatic glucose production, and abnormal
fat metabolism.
 In the early stages of the disorder, glucose tolerance remains
near-normal, despite insulin resistance, because the pancreatic
beta cells compensate by increasing insulin output .
 As insulin resistance and compensatory hyperinsulinemia
progress, the pancreatic islets in certain individuals are unable to
sustain the hyperinsulinemia state.
 IGT, characterized by elevations in postprandial glucose, then
develops.
 A further decline in insulin secretion and an increase in hepatic
glucose production lead to overt diabetes with fasting
hyperglycemia.
 Ultimately, beta cell failure may ensue.
DR.JAVERIA
Etiology: DR.JAVERIA

. Risk factors
(obesity, older age,
race of ethnicity, Environmental
prediabetes, history factors
of gestational
Genetic factors diabetes

Types 2 DM Intake of excessive

calories and physical
inactivity
Symptoms: DR.JAVERIA

 Hyperglycemia
 Fatigue
 Excessive thirst
 Frequent urination
Clinical findings: DR.JAVERIA

 Abnormal patterns of insulin secretion and action.

 Decreased cellular uptake of glucose and increased
postprandial glucose.
 Increased release of glucose by
liver(gluconeogenesis) resulting in fasting
hyperglycemia
 Central obesity
 Hypertension
 Dyslipidemia
Monitoring: DR.JAVERIA

 Self monitoring of blood glucose

 A1C testing
 Lipids
 Blood pressure
 Weight
Medical management: DR.JAVERIA

 Medical nutrition therapy

 Physical activity
 Medications:
- glucose lowering medications
- insulin
 Self management education
Medical nutrition therapy (MNT): DR.JAVERIA

 Lifestyle strategies (food / eating and physical

activity) that improve glycaemia, dyslipidemia, and
blood pressure.
 Nutrition education (carbohydrate, counting and fat
modification)
 Energy restriction
 Blood glucose monitoring to determine
adjustments in food or medication
 Cardioprotective nutrition interventions
Gestational diabetes mellitus: DR.JAVERIA

 GDM is defined as carbohydrate intolerance of

variable severity with onset or first recognition during
the present pregnancy.
 Not the same as Type 1 or Type 2 Diabetes Varies
worldwide & among different racial and ethnic groups
within a country.
Etiology: DR.JAVERIA

 Pregnancy pre-diabetic state

 Pregnancy marked insulin resistance increased
insulin requirement GDM
 Complicates 4% of all pregnancies
 60% to 80 % of women with GDM are obese & experience
insulin resistance & GDM
. Pregnancy Pathophysiology: DR.JAVERIA

 Glucose is a teratogen at high levels

 Crosses placenta readily while insulin cannot
 Insulin resistance occurs because hormonal changes
associated with pregnancy partially block the effects of
insulin
 Insulin resistance causes glucose to be shunted from
mother to the fetus to facilitate fetal growth and
development
Conti. DR.JAVERIA

 Subsequent increase in insulin resistance

causes maternal glucose levels to increase
80% of non-pregnant women Increased insulin
resistance Decreased insulin secretion
Increased maternal glucose GDM
 GDM disappears after pregnancy
 Useful physiologic process out of balance
Effects of diabetes on
pregnancy: DR.JAVERIA

 Abortion
 Preterm labour
 Infection
 Increase incidence of pre- eclampsia
 Polyhydramnios
 Maternal distress
 Diabetic retinopathy
 Diabetic nephropathy
 Diabetic ketoacidosis
 Shoulder dystosia
 Prolong labour
 PPH
 Puerperal sepsis
Fetal and Neonatal Hazards : DR.JAVERIA

Fetal:
 Fetal macrosomia
 Congenital malformation
 Birth injury
 Growth restriction
Fetal death B) Neonatal:
 Hypoglycemia
 Respiratory distress syndrome
 Hyperbilirubinemia
 Polycythemia
 Hypocalcaemia
 Hypomagnesaemia
Diagnosis: DR.JAVERIA

  TWO-STEP STRAREGY 
 50g oral glucose challenge 
 Single serum glucose measurement @ 1 hr
 <7.8 mmol/L(<140mg/dL) normal
 >7.8 mmol/L(>140mg/dL)
 100-g oral glucose challenge
 Serum glucose measurements in fasting state, I, II & III hrs
 Normal values
 Fasting < 5.8 mmol/L (<105mg/dL)
 I hr  < 10.5 mmol/L (<190mg/dL )
 II hr  < 9.1 mmol/L (<165mg/dL)
 III hr  < 8.0 mmol/L (<145mg/dL)
Conti. DR.JAVERIA

 Overnight fast of at least 8 hours

 At least 3 days of unrestricted diet and unlimited
physical activity
 > 2 values must be abnormal
 Urine glucose monitoring is not useful in gestational
diabetes mellitus
 Urine ketone monitoring may be useful in detecting
insufficient caloric or carbohydrate intake in women
treated with calorie restriction
Screening: DR.JAVERIA

 Essentially all Indian women have to be screened for gestational

diabetes mellitus as they belong to a high risk ethnicity
 LOW RISK GROUPS:
 <25 yrs of age
 BMI <25kg/sq.m
 No H/O maternal macrosomia
 No H/O diabetes
 No H/O D.M in first degree relative
 Not members of high risk ethnic groups
 Member of an ethnic group with a low prevalence of GDM
 No H/O abnormal glucose tolerance
 No H/O poor obstetric outcome
Treatment :
DR.JAVERIA

 The total first dose of insulin is calculated according to the

patient’s weight as follow
 In the first trimester weight x 0.7
 In the second trimester weight x 0.8
 In the third trimester weight x 0.9
Medical nutrition therapy: DR.JAVERIA

 Approximately 30 kcal/kg of ideal body weight

 >40-45% should be carbohydrates
 6-7 meals daily( 3meals, 3-4 snacks)
 Bed time snack to prevent ketosis
 Calories guided by fetal well being/maternal weight gain/blood
sugars/ ketones
 Energy requirements during the first 6 months of lactation
require an additional 200 calories above the pregnancy meal
plan
Other types of diabetes: DR.JAVERIA

This category include diabetes associated with specific;

 genetic syndromes (such as maturity-onset diabetes of youth)
 genetic defects in insulin action
 diseases of the exocrine pancreas (such as cystic fibrosis)
 endocrinopathies ( such as acromegaly or Cushing's syndrome)
 drugs or chemical induced ( such as in treatment of HIV /AIDS or
after organ transplantation)
 infections and other illness
Such types of diabetes may account for 1% -5% of all diagnosed
cases of diabetes.
Screening and Diagnostic
criteria: DR.JAVERIA

 Screening of diabetes:
 Screening for diabetes should be considered in all adults who are
over weight (BMI >25 kg/m2) and who have one or more addition
al risk factors for T2DM :
 Additional risk factors for diabetes following:
 Physical activity
 First – degree relative with diabetes
 Members of a high risk population (African Americans, Latino,
Native American, Asian American, and Pacific Islander)
Conti. DR.JAVERIA

 Women who have delivered a baby weighing more than 9lb or

have been diagnosed with GDM
 Hypertension (B.P >140/90mg/Hg or taking medication for HT)
 High density lipoprotein (HDL), cholesterol level <35 mg/dl
(0.9mmol/L) and/or a triglyceride level > 250 mg/dl(2.82mmol/L)
 AIC>5.7 %,IGT, or IFG on previous testing
 Other clinical condition associated with insulin resistance (severe
obesity, acanthosis nigricans [gray-brown skin pigmentation])
 History of CVD
Diagnostic Criteria:
Diagnosis Criteria DR.JAVERIA

Diabetes A1C>6.5%
OR
FPG>126mmg/dl(>70mmol/L)
OR
2-h PG >200mg/dl(>11.1mmol/L) during an OGTT
OR
In patient with classic symptoms of hyperglycemia or
hyperglycemic crisis, a random
PG>200mg/dl(>11.1mmol/L)
Prediabetes FPG100-125mg/dL(5.6-6.9mmol/L) [impaired fasting
glucose]
OR
2-hPG in the 75-g OGTT140-199mg/dl(7.8-11.0mmol/L)
[impaired glucose tolerance]
OR
A1C5.7-6.4%

Normal FPG<100mg/dl(<5.7mmol/L)
2-Hpg <140mg/dl(<7,8mmol/L)
A1C 4-5 %
Implement of nutrition care
process: DR.JAVERIA

1. Nutrition assessment
2. Nutrition diagnosis
Nutrition assessment: DR.JAVERIA
Nutrition diagnosis of DM: DR.JAVERIA

 Inconsistent carbohydrates intake

 Excessive carbohydrates intake
 Inappropriate intake of food fats
 Altered laboratory values
 Overweight / obesity
 Food – and nutrition – related knowledge deficit
 No ready for life style change
DR.JAVERIA
DR.JAVERIA