ASSESSMENT AND MANAGEMENT OF PATIENT

WITH DIABETES MELLITUS

A. Definition
DM is a group of metabolic diseases characteristic by
elevated of levels of glucose in the blood (hyperglycemia),
resulting from defects in insulin secretion, insulin action or
both (Expert Committee on the Diagnosis and
Classification of Diabetes Mellitus, 1998 cited by Smeltzer
& Bare, 1999).
B. Classification Of DM
1. Type I (IDDM)
Type I is characteristic by destruction of the pancreatic
beta-cell.
2. Type II (NIDDM).
The main problem is related to insulin resistence and
impaired insulin secretion.
3. DM Associated With Other Conditions or Syndromes.
Accompanied by: pancreatic diseases, hormonal
abnormalities, drugs (corticosteroid and estrogen
containing preparations).
4. Gestational DM
Due to hormones secreted by the placenta, which inhibit
the action of insulin.
C. Clinical Manifestation of DM
Clinical manifestations:
- 3 P (polyuria, polydipsia, polyphagia).
- Fatigue and weakness.
- Sudden vision changes.
- Tingling or numbness in hand and feet.
- Dry skin.
- Sores that are slow to heal.
- Recurrent infection.
- Type I may also associated with nausea, vomiting, or
abdominal pain.

D. RISK FACTOR FOR DM

- Family history of DM.
- Obesity
- Race/ethnicity
- Age more than or = 45 years
- Previously impaired fasting glucose or impaired glucose
tolerance
- Hypertension
- HDL level less than or = 35 mg/dL and/or triglyceride
level more than or = 250 mg/dL.
- History of GDM or delivery of baby > 9 lbs.
E. FUNCTIONS OF INSULIN
1. The relation of insulin to carbohydrates, fat, and protein:
- Promoting liver uptake, storage, and use of glucose.
- Converting liver glucose into fatty acid.
- Increase glucose transport into cell and glucose usage.
- Protein synthesis and storage.
2. Regulation of insulin secretion.
3. Role of insulin in the change of carbohydrates and fat.
F. Criteria for the Diagnosis of DM
1. Symptoms of DM + casual plasma glucose concentration
greater than or equal to 200 mg/dL.
or
2. Fasting plasma glucose greater than or equal to 126
mg/dL.
or
3. 2 hour postload glucose greater than or equal to 200
mg/dL during oral GTT.

G. Pathophysiological Responses
Insulin Deficiency
Two reasons

Decreasing glucose
utilisation

Increase hepatic
glucose production

Lead to
Hyperglycemia

Osmotic diuretic

Excess water and electrolyte loss

Glycosuria
Dehydration

Nausea and vomiting

Result in
Hemoconcentration
Decrease renal
blood flow

Hypotension

Impaired renal
function

Vascular collapse

Anuria

Insulin Deficiency
Responses
Increased lipolysis of adipose tissue
Leads to
Increased plasma free fatty
acids

Increased fatty acids

oxidation

Causes
Hyperglycemia
Kidneys unable to excrete
fatty acids, resulting in
Ketosis

Compromised renal Metabolic

function due to
acidosis
dehydration

Insulin Deficiency
Result in
Breakdown of muscle protein to
amino acids
Leads to
Aminoacidemia

Loss of potassium from tissue

Responses
Increased influx of amino acids
Leads to
Increased gluconeogenesis

Increased hepatic glucose

output

Hyperglycemia

H. Assessment of The Diabetic Patient

1. History:
- Symptoms of hyperglycemia
- Symptoms of hypoglycemia
- Home blood glucose monitoring results
- Status of chronic complications:
@ Nephropathy
@ Retinopathy
@ Macrovascular diseases
@ Neuropathy
- Dietary compliance
- Exercise regimen
2. Physical examination:
- BP
- Weight
- Funduscopic exam
- Feet: lession, infection.
- Neurogenic examination
3. Laboratory Examination:
- HgbA1c (every 3 months)
- Microalbuminuria or 24 hours urine collection.
- Fasting lipid
4. Refferal:
- Ophthalmology
- Podiatry
I. MANAGEMENT
The main goal of DM management is to normalize insulin
activity and blood glucose levels to reduce the development
of the vascular and neurophathic complication.
1. Nutrition management
Nutritional management of the patient with DM is geared
toward the following goal:
a. Providing the entire essential food constituent (vit,
mineral).

b. Achieving and maintaining a reasonable weight.

c. Preventing wide daily fluctuations in blood glucose
levels with blood glucose levels as close to normal as
is safe and practical.
d. Meeting energy needs.
e. Decreasing serum lipid, if elevated.
2. Exercise
a. Its affects on lowering blood glucose and reducing
cardiovascular risk factors.
b. Improve circulation and muscle tone.
c. Increasing the resting metabolic rate.
Avoid exercise if blood glucose level is more than 250
mg/dL and patient has ketone in their urine.
3. Monitoring
a. Self monitoring of blood glucose.
b. Glycosylated Hb.
c. Urine testing for glucose.
d. Urine testing for ketones
4. Pharmacologic therapy
a. Insulin therapy.
b. Oral antidiabetic agents
5. Education.
Survival education is the critical information necessary to
meet the immediate survival needs of the client.
S = Simple pathophysiology (definition and general
information on diabetes).
U = Understand (relationship between food, stress,
medicine, and blood glucose level).
R = Regular exercise.
V = Variety of meal plans (basic nutrition principles)
I = Insulin and/or OHA administration.
V = Value of normalizing blood glucose.
E = Educate entire family (emergency plans,
identification alert, supplies).

J. LONG-TERM COMPLICATIONS OF DIABETES

1.Macrovascular disease :
a. Coronary artery disease
b. Cerebrovascular disease
c. Peripheral vascular disease : gangrene, neurophaty
It can be caused by:
a. Blood vessel walls thicken
b. Scleroses
c. Occluded by plaque
2. Microvascular complications:
a. Retinophaty
b. Nephropaty
c. Cataracts
d. Lens changes
e. Extraocular muscle palsy
f. Glaucoma
3. Neurophaties :
a. Sensorimotor polyneurophaty
b. Autonomic neurophaty