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
