ASSESSMENT AND MANAGEMENT OF PATIENT WITH DIABETES MELLITUS

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 Increase hepatic

utilisation glucose production

Lead to

Hyperglycemia

Osmotic diuretic Excess water and electrolyte loss

Glycosuria

Dehydration Nausea and vomiting

Result in

Hemoconcentration

Decrease renal Hypotension

blood flow

Impaired renal Vascular collapse

function

Anuria

Insulin Deficiency

Responses

Increased lipolysis of adipose tissue

Leads to

Increased plasma free fatty Increased fatty acids

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