PAPERS NURSING MANAGEMENT

OF DIEBETES MEILLITUS

NAME : SISKA

NIM : PO713201151138
 Preface

Thank God we prayed to Allah SWT who has given grace and His gift to us so we
managed to finish the paper on time alhamdulillah titled Nursing care of diabetes
mellitus

This paper contains information about milletus diabetes, complications, pahtofisiologi,

how to cope and ways of treatment. Expected that this paper can give us all the
information about this hereditary disease.

We realize that this paper is far from perfect, therefore criticism and suggestions from all
stakeholders that are built for the perfection we always hoped this paper.

Finally, we say thank you to all those who have participated in the preparation of this
paper from beginning to end. May Allah always be pleased with all our efforts. amen
 CONCEPT OF DM

Diabetes mellitus is a disorder in which the level of blood glucose is persistently raised
above the normal range. Diabetes mellitus is a syndrome with disordered metabolism
and inappropriate hyperglycemia due to either a deficiency of insulin secretion or to a
combination of insulin resistance and inadequate insulin secretion to compensate.
Diabetes mellitus occurs in two primary forms:

 Type 1

characterized by absolute insufficiency, and the more prevalent.

 Type 2

characterized by insulin resistance with varying degrees of insulin secretory

defects.

Diabetes mellitus is a group of metabolic diseases characterized by elevated 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..

Etiology for Diabetes Mellitus

The cause of both type 1 and type 2 diabetes remains unknown, although genetic
factors may play a role. Diabetes mellitus results from insulin deficiency or resistance.
Insulin transports glucose into the cell for use as energy and storage as glycogen. It
also stimulates protein synthesis and free fatty acid storage. Insulin deficiency or
resistance compromises the body tissues’ access to essential nutrients for fuel and
storage. The resulting hyperglycemia can damage many of the body’s organs and
tissues.

 Type 1 diabetes is due to pancreatic islet B cell destruction predominantly by an

autoimmune process, and these patients are prone to ketoacidosis.
  Type 2 diabetes is the more prevalent form and results from insulin resistance
with a defect in compensatory insulin secretion.

 Insulin, a hormone produced by the pancreas, controls the level of glucose in the
blood by regulating the production and storage of glucose.

Risk Factors For Diabetes Mellitus Include

 Obesity

 Physiologic or emotional stress, which can cause prolonged elevation of stress

hormone levels.

 pregnancy, which causes weight gain and increases levels of estrogen and
placental hormones, which antagonize insulin.

 metabolic syndrome, which is considered a precursor to the development of type

2 diabetes mellitus.

 some medications that can antagonize the effects of insulin, including thiazide
diuretics, adrenal corticosteroids, and hormonal contraceptives

Classification of Diabetes Mellitus

There are several different types of diabetes mellitus; they may differ in cause, clinical
course, and treatment. The major classifications of diabetes are:

 Type 1 diabetes (insulin dependent diabetes mellitus) is caused by B-cell

destruction, usually leading to absolute insulin deficiency

a. Immune mediated

b. Idiopathic

 Type 2 diabetes (previously referred to as non insulin dependent diabetes

mellitus) ranges from those with predominant insulin resistance associated with
 relative insulin deficiency, to those with a predominantly insulin secretory defect
with insulin resistance.

Pathophysiology of diabetes

Insulin is secreted by beta cells, which are one of four types of cells in the islets of
Langerhans in the pancreas. Insulin is an anabolic, or storage, hormone. When a
person eats a meal, insulin secretion increases and moves glucose from the blood into
muscle, liver, and fat cells. In those cells, insulin:

 Transports and metabolizes glucose for energy

 Stimulates storage of glucose in the liver and muscle (in the form of glycogen)

 Signals the liver to stop the release of glucose

 Enhances storage of dietary fat in adipose tissue

 Accelerates transport of amino acids (derived from dietary protein) into cells

Insulin also inhibits the breakdown of stored glucose, protein, and fat. During fasting
periods (between meals and overnight), the pancreas continuously releases a small
amount of insulin (basal insulin); another pancreatic hormone called glucagon (secreted
by the alpha cells of the islets of Langerhans) is released when blood glucose levels
decrease and stimulate the liver to release stored glucose. The insulin and the glucagon
together maintain a constant level of glucose in the blood by stimulating the release of
glucose from the liver. Initially, the liver produces glucose through the breakdown of
glycogen (glycogenolysis). After 8 to 12 hours without food, the liver forms glucose from
the breakdown of noncarbohydrate substances, including amino acids
(gluconeogenesis).

Type 1 Diabetes Mellitus

 Type 1 diabetes mellitus is characterized by destruction of the pancreatic beta

cells.
 A common underlying factor in the development of type 1 diabetes is a genetic
susceptibility.

 Destruction of beta cells leads to a decrease in insulin production, unchecked

glucose production by the liver and fasting hyperglycemia.

 Glucose taken from food cannot be stored in the liver anymore but remains in the
blood stream.

 The kidneys will not reabsorb the glucose once it has exceeded the renal
threshold, so it will appear in the urine and be called glycosuria.

 Excessive loss of fluids is accompanied by excessive excretion of glucose in the

urine leading to osmotic diuresis.

 There is fat breakdown which results in ketone production, the by-product of fat
breakdown.

Type 2 Diabetes Mellitus

 Type 2 diabetes mellitus has major problems of insulin resistance and impaired
insulin secretion.

 Insulin could not bind with the special receptors so insulin becomes less effective
at stimulating glucose uptake and at regulating the glucose release.

 There must be increased amounts of insulin to maintain glucose level at a normal

or slightly elevated level.

 However, there is enough insulin to prevent the breakdown of fats and production
of ketones.

 Uncontrolled type 2 diabetes could lead to hyperglycemic, hyperosmolar

nonketotic syndrome.
  The usual symptoms that the patient may feel are polyuria, polydipsia,
polyphagia, fatigue, irritability, poorly healing skin wounds, vaginal infections, or
blurred vision

CLINICAL MANIFESTATIONS/ASSESMENT

Clinical manifestations of all types of diabetes include the “three Ps”: polyuria,
polydipsia, and polyphagia. Polyuria (increased urination) and polydipsia (increased
thirst) occur as a result of the excess loss of fluid associated with osmotic diuresis. The
patient also experiences polyphagia (increased appetite) resulting from the catabolic
state induced by insulin deficiency and the breakdown of proteins and fats. Other
symptoms include fatigue and weakness, sudden vision changes, tingling or numbness
in hands or feet, dry skin, skin lesions or wounds that are slow to heal, and recurrent
infections. The onset of type 1 Diabetes may also be associated with sudden weight
loss or nausea, vomiting, or abdominal pains, if DKA has developed.

Diabetes management

The main goal of diabetes treatment is to normalize insulin activity and blood glucose
levels to reduce the development of vascular and neuropathic complications.

Drugs for Treating Hyperglycemia

The drugs for treating type 2 diabetes fall into several categories:

1. Drugs that primarily stimulate insulin secretion by binding to the sulfonylurea

receptor. Sulfonylureas remain the most widely prescribed drugs for treating
hyperglycemia. The meglitinide analog repaglinide and the D-phenylalanine
derivative nateglinide also bind the sulfonylurea receptor and stimulate insulin
secretion.
 2. Drugs that alter insulin action: Metformin works in the liver. The
thiazolidinediones appear to have their main effect on skeletal muscle and
adipose tissue.

3. Drugs that principally affect absorption of glucose: The glucosidase inhibitors

acarbose and miglitol are such currently available drugs.

4. Drugs that mimic incretin effect or prolong incretin action: Exenatide and DPP 1V
inhibitors fall into this category.

5. Other: Pramlintide lowers glucose by suppressing glucagon and slowing gastric

emptying.

Insulin

Insulin is indicated for type 1 diabetes as well as for type 2 diabetic patients with
insulinopenia whose hyperglycemia does not respond to diet therapy either alone or
combined with other hypoglycemic drugs.

Therefore, the therapeutic goal for diabetes management is to achieve normal blood
glucose levels (euglycemia) without hypoglycemia and without seriously disrupting the
patient’s usual lifestyle and activity.

There are five components of diabetes management

 Nutritional management

 Exercise

 Monitoring

 Pharmacologic therapy

 Education

Nursing diagnosis
1. Lack of fluid volume associated with osmotic, excessive gastric loss, limited
input.

2. Changes in nutrition: less than body requirements related to insufficient insulin

decrease oral input, hipermetabolisme status.

3. Infection associated with high glucose levels, decreased leukocyte function,

circulation changes.

4. Sensory perceptual changes associated with chemical changes in endogenous

(imbalance of glucose / insulin and electrolytes.

5. Powerlessness associated with dependence on others, long-term illness.

6. Lack of knowledge about the disease, prognosis and treatment needs.

Nursing Intervention

1. Lack of fluid volume associated with osmotic diuresis, excessive gastric loss,
limited input.
Data that may arise:
Increased urine output, dilute urine, thirst, weakness,weight decline, dry skin, bad
turgor.

Expected results :
Stable vital signs, good skin turgor, normal urine output, electrolyte levels within
normal limits.

Rational intervention

1. Monitor vital signs of hypovolemia can be characterized by hypotension and

tachycardia.

2. Assessing temperature, color and moisture. Fever, skin redness, dry as a

reflection of dehydration.
 3. Monitor the input and expenditures, note bj urine Provide estimates will need
cairanpengganti, kidney function and effectiveness of therapy.

4. Measure weight every day Gives the best assessment and the fluid status of
ongoing and further in providing replacement fluid.

5. Maintain liquids  2500 cc / day when the income can already be given orally.
Maintaining hydration / volume circulation.

6. Increase comfortable environment with a thin blanket blanket Avoid excessive

heating in patients will lead to the loss of fluid.

7. Write down the things that are reported such as nausea, abdominal pain,
vomiting, gastric distention. Lack of fluids and electrolytes alter gastric motility,
which often lead to vomiting, so there is a lack of fluid or electrolyte.
Collaboration.

8. Give the fluid therapy as indicated

The type and amount of liquid depends on the degree of lack of fluids and
response of the individual patient.

9. Install suction hose NGT and do according to indications. Decompress the

stomach and can eliminate vomiting.

2. Changes in nutrition: less than body requirements related to insufficient insulin,

decreased oral input, hipermetabolisme
Data:

Put the food is inadequate, anorexia, weight decline, weakness, fatigue, poor
muscle tone, diarrhea.

Criteria Results:

Digesting the proper amount of nutrients, showing the energy level usually, stable
weight inclease.

Rational intervention
1. Weigh weight every day Assessing food that adequate revenues (including
absorption).

2. Determine the diet and eating patterns of patients and compare with food
patients spent. Identify deficiencies and deviations from the requirements.

3. Auscultation bowel sounds, record their pain, abdomen, nausea, vomiting.

Hyperglycemia can decrease motility / function of the stomach (distension or
paralytic ileus) that will influence the choice of intervention.

4. Identify the preferred food. If the preferred food can be included in the
digestion of food, this cooperation can be pursued after the return.

5. Involve the family in meal planning as indicated. Provide information on their

families to understand the patient's nutritional needs.

6. Collaboration with dietitians Very helpful in the calculation and adjustment of

the diet to meet patient needs.

7. High risk of infection associated with high glucose levels, decreased

leukocyte function / circulation changes.
Data: -
Expected outcomes : Infections do not occur

Rational intervention

1. Observe signs of infection and inflammation. Patients may sign with an

infection that usually has sparked a state of ketuasidosis or hospital-
acquired infection.

2. Increase prevention by hand washing for everyone associated with the

patients, even though patients themselves. Preventing the emergence of
hospital-acquired infection.

3. Maintain aseptic technique for invasive procedures. High glucose levels

would be the best medium for the growth of germs.
 4. Provide regular skin care and really sugguh, massage depressed area.
Keep the skin stays dry, linen remain dry and tight. Peripheral circulation
can be interrupted which puts patients at increased risk of skin irritation
and infection.

5. Help the patient to perform oral hygiene. Reduce the risk of oral diseases.

6. Suggest to eat and drink adequately. Lowering the possibility of infection.

7. Collaboration on the provision of an appropriate antibiotic treatment early

can help prevent the onset sepsis.

Implementation of Nursing

Implementation is nursing actions implemented to achieve the goal of the action plan
that has been prepared. Every nursing actions performed is recorded in the recording
keperawatn that nursing action against the client continues. Principles in nursing action
is an effective approach to the client, as well as communication techniques teraupetik
penjalasan for each action is given to the client.

In nursing action using three stages, independent, dependent, interdependent.

Independent nursing action is an action taken by perawatn without instructions and
orders doctors or other health professionals, and dependent are measures in
connection with the implementation of the plan of medical action. While interdependent
is keperawatn action that describes an activity that memerlukah a collaboration with
other health professionals. Eg social workers, nutritionists and doctors.
 Bibliography

Doengoes, M.E. (2000). Rencana Asuhan Keperawatan, Edisi 3, Jakarta : EGC.

Engram, B. (1999). Rencana Asuhan Keperawatan Medikal Bedah, Jakarta : EGC.
Brunner & Suddarth. (2002). Buku Ajar Keperawatan Medikal Bedah, Vol. 2. Jakarta :
EGC.
Price. S.A. (1995). Patofisiologi, Edisi Kedua, Jakarta : EGC.
Jan Tambayong, dr. (2000). Patofisiologi Untuk Keperawatan. Jakarta : EGC.