DIABETES MELLITUS

Agleham III, Benjamin D.

OBJECTIVES

GENERAL OBJECTIVES:

To be able to discuss Diabetes Mellitus

SPECIFIC OBJECTIVES:

1.
2.
3.
4.

The students would be able to :

Understand the etiology and pathophysiology of
Diabetes Mellitus.
Know how to diagnosis the disease
Identify the management and treatment of the
disease
Enumerate its possible complications

EPIDEMIOLOGY
Worldwide
30 million cases in 1985
177 million in 2000
Trends: >360 million individuals will have
diabetes by the year 2030

The Philippines is one of the worlds emerging

diabetes hotspots. Ranked in the top 15 in the
world for diabetes prevalence, Philippines is
home to more than 4 million people diagnosed
with the disease and a worryingly large
unknown number who are unaware they have
diabetes.
IDF,2012

MORTALITY: TEN (10) LEADING CAUSES

5-Year Average
(2004-2008)

CAUSES

Number

Rate

2009*
Number

Rate

1. Diseases of the
Heart

82,290

94.5

100,908

109.4

2. Diseases of the
Vascular System

55,999

64.3

65,489

71.0

3. Malignant
Neoplasms

43,185

49.6

47,732

51.8

4. Pneumonia
5. Accidents**

35,756
34,704

41.1
39.9

42,642
35,990

46.2
39.0

6. Tuberculosis, all
forms

25,376

29.2

25,470

27.6

7. Chronic lower
20,830
respiratory diseases

24.0

22,755

24.7

8. Diabetes Mellitus 19,805

22.7

22,345

24.2

9.Nephritis,
nephrotic syndrome 11,612
and nephrosis

13.4

13,799

15.0

10. Certain
conditions
12,590
14.5
11,514
originating in the
perinatalperiod
Note: Excludes ill-defined and unknown causes of mortality
* reference year

12.5

WHAT IS DIABETES?

Diabetes Mellitus (DM) refers

to a group of common
metabolic disorders that
share the phenotype of
hyperglycemia.

DIABETES MELLITUS
caused by a complex interaction of genetics and
environmental factors
reduced insulin secretion
decreased glucose utilization
increased glucose production
causes secondary pathophysiologic changes in
multiple organ systems

Blindness

and amputation
Renal failure, nerve damage and heart attacks

TYPES
Type 1 diabetes ( beta-cell destruction,
usually leading to absolute insulin
deficiency)

I.

A.

Immune-mediated
B. Idiopathic

Type 2 diabetes (predominantly

insulin resistance with relative insulin
deficiency to a predominantly insulin
secretory defect with insulin resistance)

II.

TYPE 1 DIABETES MELLITUS

Interactions of genetic, environmental, and
immunologic factors that ultimately lead to the
destruction of the pancreatic beta cells and insulin
deficiency
Autoimmune beta cell destruction
Triggered by an infectious/environmental stimulus and
to be sustained by a beta cellspecific molecule
Diabetes- not evident until a majority of beta cells are
destroyed (80%)
major susceptibility gene located in the HLA region on
chromosome 6

TYPE 1 DIABETES MELLITUS

Autoimmune process in type 1 DM:

(1)

islet cell autoantibodies;

(2) activated lymphocytes in the islets, peripancreatic
lymph nodes, and systemic circulation;
(3) T lymphocytes that proliferate when stimulated
with islet proteins; and
(4) release of cytokines within the insulitis

TYPE 2 DIABETES MELLITUS

WHO SHOULD UNDERGO LABORATORY TESTING?

Considered in all adults >40 y/o

Consider earlier testing if with at least one other
risk factor as follows:

History of impaired glucose test

History of GDM or delivery of a baby weighing >8 lbs
Polycystic ovary syndrome (PCOS)
BMI classified either overweight or obese
Waist circumference >80 cm (females) and >90 cm (males)

First degree relative with Type 2 diabetes

Sedentary lifestyle
Hypertension (BP >140/90 mm Hg)
Diagnosis or history of any vascular diseases
including stroke, peripheral arterial occlusive
disease, coronary artery disease
Acanthosis nigricans
Serum HDL <35 mg/dL (0.9 mmol/L)
Serum Triglycerides >250 mg/dL (2.82 mmol/L)

COMPLICATIONS

CHRONIC COMPLICATIONS

Microvascular
Eye

diseases

Retinopathy (nonproliferative/proliferative)
Macular edema

Neuropathy

Sensory and motor (mono- and polyneuropathy)

Autonomic

Nephropathy

DIABETIC RETINOPATHY
vascular-neuroinflammatory

disease
breakdown of the blood-retinal barrier
(BRB) function and loss of retinal
neurons.
activated macroglia and neuronal
death.
activated microglia exacerbate the
damage.

DIABETIC NEPHROPATHY
rise

in glomerular filtration rate

glomerular

lesions
increased glomerular permeability

microalbuminuria

(30 to 300 mg/day)

diffuse glomerulosclerosis
massive proteinuria - nephrotic
syndrome
Systemic hypertension
progression to ESRD

AUTONOMIC NEUROPATHY

Cardiovascular abnormalities

dysfunction of parasympathetic fibers

impaired sympathetic vasoconstrictor response and
impaired cardiac reflexes
preferential

Altered gastrointestinal function

hypermotility

/ hypomotility
Gastroparesis

Genitourinary alterations
bladder

hypotonia
Erectile dysfunction

ATHEROSCLEROSIS
Lipid abnormalities
Procoagulant state = accentuated platelet
aggregation and adhesion, endothelial cell
dysfunction.
Hyperinsulinemia

The diabetic foot

Chronic

sensorimotor neuropathy
Vascular disease
Abnormal immune function

WAGNER CLASSIFICATION
Grade 0

Pre post ulcerative lesion, completely

epithelized

Grade 1

Partial/full thickness ulcer;

superficial wound

Grade 2

Penetrates tendon or capsule

Grade 3

Deep with osteitis

Grade 4

Partial foot gangrene

Grade 5

Whole foot gangrene

MANAGEMENT

PHARMACOLOGIC THERAPY

Asymptomatic with relatively lower levels of

blood sugar (HbAc <8.0%, FBS <140, RBS <200
mg/dL) MNT, physical activity and exercise
and weight reduction, with an option of starting
pharmacologic therapy (metformin).
If glycemic targets are not reached within 3 months,
then pharmacologic treatment will be started

Combination therapy should be considered when

glycemic targets are not achieved with one drug
given at the maximum effective dose (optimal dose
or half maximum), another drug from another
pharmacologic class should be added rather than
increasing the first drug to its maximum dose

Preferred initial treatment: Metformin

When optimization of therapy is needed, then a
second drug should be chosen according to the
following considerations:

amount of HbA1c lowering

hypoglycemia risk
weight gain
Patient profile (dosing complexity, renal and hepatic
problems, other contraindications and age)

TREATMENT OF DIABETES
MELLITUS 1
Short-acting
Regular

Insulin

human Insulin
Insulin analogue
Aspart
Lispro
Glulisine

Long-acting
NPH

Insulin

analogue

Glargine
Detemir

Insulin

TREATMENT OF DIABETES
MELLITUS 1
Insulin

Combination

75/2575%

protamine lispro, 25% lispro

70/3070% protamine aspart, 30% aspart
50/5050% protamine lispro, 50% lispro
70/3070% NPH, 30% regular insulin
50/5050% NPH, 50% regular insulin

ADVERSE EFFECTS OF INSULIN

1.
2.
3.
4.
5.
6.

Hypoglycemia
Hypokalemia
Anaphylaxis
Lipodystrophy at injection site
Weight gain
Injection complications

TREATMENT OF TYPE 2 DIABETES

Diagnosis
Therapeutic Lifestyle Change
Monotherapy
Combination Therapy - Oral Drugs Only
Combination Therapy - Oral Drug with Insulin

THERAPEUTIC LIFESTYLE CHANGE

Medical Nutrition Therapy
All individuals at risk for diabetes, those with
prediabetes
or
diabetes
and
overweight
individuals with Metabolic Syndrome should be
advised regarding MNT to help attain treatment
targets
MNT should preferably be provided by a
registered dietitian/nutritionist or other health
care professional trained in the principles of
nutrition

MEDICAL NUTRITION THERAPY

The Asian-Pacific Type 2 Diabetes Policy Group has outlined the
following simple reminders:
EAT MOST- Use one or more of these foods as the basis of every meal

Vegetables, legumes, lentils, noodles, rice, bread, grains, barley, wholegrain

cereals, fresh fruit (non-sweet)

EAT MODERATELY

Have small servings of protein-rich foods e.g., fish, seafood, eggs, lean meat,
skinless chicken, low-fat cheese, low-fat yoghurt, low-fat milk, nuts

EAT LEAST

Minimise fats, sugars, salt and alcohol e.g., butter, oil, cream, coconut milk
and cream, processed meat, fried foods, preserved or processed foods,
pastries, sweets, biscuits, soft drink

HOSPITAL-BASED NUTRITION ADVICE

The Asian-Pacific Type 2 Diabetes Policy Group11 recommends

the following macronutrient proportions (of total energy
intake):

Fat: no more than 30% (saturated fat <10%)

Carbohydrate: 50-55% (sucrose <10%)

Protein: 15-20%

salt intake <6 g/day (NaCl) especially for those with

hypertension

higher intakes of dietary fiber (25-50 g/day) for individuals

with diabetes