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Assessment and Management of

patients with Diabetes Mellitus


Adult Health II
NUR315

Mr. Mahmoud Nasrallah


J.U.S.T
Fall 2009

Definition and Types of DM:

Def.: DM is a group of metabolic disease


characterized by elevated levels of glucose
in the blood (Hyperglycemia)

Resulting from
1.defects in insulin secretion,
2.Insulin action
3. or both

Affected about 15 million people

:Types of DM
1.

2.

3.

4.

Type I (Insulin dependent DM..IDDM): Absent of Insulin


Due to destroyed Beta-cells that produces insulin hormone
- Acute onset, before age 30, 5-10% of DM patients has
this type
Type II (Non-Insulin dependent DM.NIDDM): Decrease
sensitivity of insulin ( insulin resistance) or decrease
production of insulin
- represent 90-95% of Diabetic patients
Diabetes Mellitus associated with other conditions or
syndrome
Gestational diabetes mellitus (GDM)

( Impaired glucose tolerance, previous abnormality of glucose


tolerance, and potential abnormality of glucose tolerance)

Pathophysiology:

Type I: onset < 30 years, absent of Insulin

Causes:
1.
Genetic ( people Inherit genetic predisposing, or
tendency toward developing type I DM but do not
inherit Type I DM),
2.
Autoimmune response
3.
Environmental Factors

Insulin regulates the blood glucose levels by:


1.Inhibit glucogenolysis (Breakdown of stored glucose)
2. inhibit gluconeogenesis: production of glucose from
breaking down of amino acids and other substrates.
3.Stimulates up taking of glucose by body cells.

:Continue
Type II: Onset > 30 years
Causes:
1.
Insulin resistance due to obesity
2.
Impaired insulin secretion (but still there is insulin
secretion
3.
Hereditary

DKA does not occur in type II because there is


enough insulin to prevent breakdown of fat.

Detected incidentally

Gestational DM: Due to the secretion of placental


hormones.. Oral hypoglycemic agents are
contraindicated.

Pathogenesis of Type 2 Diabetes

Clinical manifestations:

Three ps (polyphagia, Polydepsia, Polyuria


Fatigue
Weakness
Sudden vision changes
Tinglings or numbness in the hands or feet
Dry skin
Sores that slow to heal and recurrent
infection
Type 1 may have sudden weight loss,
nausea, vomiting, and abdominal pain if DKA
has developed

Assessment and diagnostic


:tests

Fasting plasma glucose (FPG or FBS):


126mg/dl (7.0 mmol/L) or more
Random plasma glucose: more than
200mg/dl (11.1 mmol/L) plus the
Symptoms of DM
2-hour postload glucose: equal to or
more greater than 200 mg/dl during an oral
glucose tolerance test

Assessment Of Diabetic patients:

History: include history of hypo and hyperglycemia,


Glucose level, complications, Dietary compliance, and
exercise.

Physical examination: BP, WT, Check for the


complications

Laboratory Examination:
HgbA1c( every 3 months)
Microalbuminuria or 24-hour urine collection ( annually)
Fasting Lipids ( annually)

Referals: to opthalmology and podiatry.

Treatment Goal Is to Normalize


Blood Glucose Levels
Intensive control
dramatically
decreases vascular
and neuropathic
complications

Management:

Nutritional Management: See meal


planning
2.
Exercise:
- pt should use proper footwear
- Avoid exercise in extreme heat or cold
- inspect feet daily
3. Monitoring glucose and Ketones
4. Pharmacologic therapy
5. Education
1.

Dietary ManagementGoals

Provide optimal nutrition including all essential


food constituents

Meet energy needs

Achieve and maintain a reasonable weight

Prevent wide fluctuations of blood glucose levels

Decrease serum lipids, if elevated

Role of the Nurse

Be knowledgeable about dietary


management

Communicate important information to


the dietician or other management
specialists

Reinforce patient understanding

Support dietary and lifestyle changes

Meal Planning

Consider food preferences, lifestyle, usual eating


times, and cultural/ethnic background

Review diet history and need for weight loss, gain, or


maintenance

Consider caloric requirements and calorie distribution


throughout the day

Carbohydrates: 50% to 60% carbohydrates,


emphasize whole grains

Fat: 20% to 30%, with >10% from saturated fat and


>300 mg cholesterol

Fiber

Provide exchange lists

Glycemic Index

Describes how much a food increases blood glucose


Combining starchy food with protein- and fatcontaining food slows absorption and glycemic
response
Raw or whole foods tend to have lower response than
cooked, chopped, or pureed foods
Eating whole fruits rather than juices decreases the
glycemic response due to fiber-slowing absorption
Adding food with sugars may produce lower response
if eaten with foods that are more slowly absorbed

Other Dietary Concerns

Alcohol

Nutritive and non-nutritive


sweeteners

Reading labels

Exercise

Lowers blood sugar

Aids in weight loss

Lowers cardiovascular risk

Exercise Precautions

Exercise when blood sugar levels are elevated (above


250 mg/dL) and ketones are present in urine should
be avoided

Insulin normally decreases with exercise; patients on


exogenous insulin should eat a 15-g carbohydrate
snack before moderate exercise to prevent
hypoglycemia

If exercising to control or reduce weight, insulin must


be adjusted

Potential exists for post exercise hypoglycemia

Need to monitor blood glucose levels

Exercise Recommendations

Encourage regular daily exercise


Gradual increase in exercise period is encouraged
Modify exercise regimen to patient needs and
presence of diabetic complications or potential
cardiovascular problems
Conduct exercise stress test for patients older than
age 30 who have 2 or more risk factors is
recommended
Gerontologic considerations
See Chart 41-5

Monitoring:

1.

Self-Monitoring of blood glucose( SMBG): Enables


people with DM to adjust the treatment regimen to
obtain optimal blood glucose control. Allow early
detection of hypo and hyperglycemia and normalizing
blood glucose levels.
Disadvantages of SMBG are in the need for good visual
acuity, fine motor coordination, cognitive ability,
comfort with technology, willingness and cost
Candidates for SMBG:
- Unstable DM
- A tendency for sever ketosis and hypoglycemia
- Hypoglycemia without warning symptoms
- Abnormal renal glucose threshold
Frequency: 2-4 times per day is recommended (before
meals and bedtime)

Cont.

2.
3.
4.

Glucosylated Hemoglobin: HgbA1c (2-3 month)


Urine testing for glucose
Urine testing for Ketones (Ketonuria): should be
performed whenever patients with type 1 have
glucosuria or persistently elevated blood
glucose levels ( more than 240mg/dl for two
testing periods), and during illness and
pregnancy.

4. Pharmacological therapy:

I.

Insulin therapy: taken one or two times


per day( or even more often) to control
blood glucose. Accurate monitoring of blood
glucose levels is essential
Insulin preparations:
- Time course: onset, peak, and duration of action
( rapid acting (lispro), short acting (HR), intermediatacting (NPH or Lent), Long acting (Ultralent), and
Mixed (70% NPH and 30% R) (table 41-3)
Source: beef, pork, and Human insulin which is now
widly used

:Insulin regimens
1. Conventional regimen: is to simplify the
insulin regimen ( 1-2 injections/day). May
be appropriate for the terminally ill,
unwilling or unable to engage in the selfmanagement activities that are part of
amore complex insulin regimen
2. Intensive regimen: 3-4 injection/day to
achieve as much control over blood glucose
levels as is safe and practical and to
decrease complications

Teaching Patients Insulin


Self-Management

Use and action of insulin

Symptoms of hypoglycemia and hyperglycemia

Required actions

Blood glucose monitoring

Self-injection of insulin: see Charts 41-7 and 418

Insulin pump use

Insulin Pump

:Complications of insulin therapy

The most common complication of insulin


therapy is hypoglycemia.
Local allergic reaction: swelling, redness,
tenderness and induration 2-4 cm wheal
may appear in the sight of injection 1-2
hours after injection administered. (occur at
the beginning stage of therapy).
Systemic allergic reactions: Are rare. Can
treated with giving small doses of insulin
which gradually increased.
Insulin lipodystrophy: local reaction cause
either lipoatrophy or lipohypertrophy
(fibrofatty masses) at the site of injection.

Cont

Insulin resistance: due to obesity or


immune antibodies.
Morning Hyperglycemia: insufficient level of
insulin due to dawn phenomena
(normal glucose level up to 3 am when Bld
glucose start to rise) and Somogyi effect
(nocturnal hypoglycemia followed by
rebound hyperglycemia)
- Insulin waning: the progressive
increase in blood glucose from bed time to
morning and is prevented by moving the
evening dose of NPH insulin to bed time

Alternative Methods of insulin therapy:

Insulin pens
Jet injection: deliver insulin through skin under
pressure( absorbed faster)
Insulin pumps: continuous s/c insulin infusion
Implantable and inhalant insulin Delivery.
Transplantation.

II. Oral Antidiabetic Agents

Used for patients with type 2 diabetes who


cannot be treated with diet and exercise alone

Combinations of oral drugs may be used

Major side effects: hypoglycemia

Nursing interventions: monitor blood glucose and


assess for hypoglycemia and other potential side
effects

Patient teaching

See Table 41-6

Sites of Action of Oral Antidiabetic


Agents

II- Oral Antidiabetic Agents:

1.

Used for the treatment for type II Diabetic patients who cant
treated by diet and exercise alone
Cant be used during pregnancy
Are Five groups:
Sulfonylureas:
Action:
- Stimulating the pancreas to secret insulin. Cant be used with
Type I DM
- also improve insulin action at the cellular level.
- May directly decrease glucose production by the liver.
Side effects: GI symptoms, dermatology reactions and
hypoglycemia (most one) specially with delayed food intake or
exercise is increased.
2nd generation of this group have shorter half- life than 1 st
generation which make them safer to use in elderly and even in
adults in regards to hypoglycemia

2. Biguanides:

Metphormin (glucophage).
Action: Facilitating insulins action on peripheral receptors
sites.
Used in combination with Sulfonylureas agent
Side effects: Hypoglycemia, Lactic acidosis is a potential
serious side effect
Contraindicated in patient with renal impairment or at risk for
renal impairment
Nursing measures: renal function should be monitored,
should not be administered 2 days before any diagnostic test
requires use of contrast agent.

3. Oral Alpha Glucosidase inhibitors:

Acarbose (Precose)
Action: Delaying absorption of glucose from the intestinal system
resulting in a lower postprandial blood glucose level. Should be taken
immediately before meals.
They are not systemically absorbed.
Side effect: diarrhea and flatulence

4. Thiazolidinedions:

Troglitazone (Rezulin)

First line agent to treat type II DM, in conjunction of diet


Action: enhance insulin action at the receptor site without increasing
insulin secretion.
Side effect: can affect liver function, LFT showed be taken as base
line and monthly for 12 months
Can cause resumption of ovulation in perimenopausal women putting
them at risk for pregnancy.

Meglitinides:

Repaglinides (Prandin)
Action: stimulate the release of insulin from the pancreas
Has fast action and short duration and should be taken before
each meal.
Side effect: Hypoglycemia

5. Education:

the diabetic patient should be knowledgeable about


nutrition, medication effects and side effects, exercise,
disease progression, prevention strategies, monitoring
techniques, and medication adjustment.

:Acute complications of Diabetes

1.

Hypoglycemia (insulin reaction): when the blood


glucose falls to less than 50 to 60 mg/dl
- may caused by too much medication, too little food, or
excessive exercise.
Manifestation: Sweating, tremor, tachycardia,
palpitation, nervousness and hunger, inability to
concentrate, headache, lightheadedness, confusion,
numbness of the lips and tongue, slurred speech,
emotional changes, double vision. Sever
hypoglycemia lead to loss of consciousness.
Hypoglycemic unawareness.
Medical management: correction of hypoglycemia.

2. Diabetic ketoacidosis

Cause by an absence or markedly inadequate amount of insulin this


result in disorder in the metabolism of CHO, protein, and fat.
Main clinical features are:
1. hyperglycemia: decrease glucose uptake and glucose production by
liver increases.
2. Dehydration and electrolyte loss: Due to polyuria ( 6.5 L of water
and up to 400-500mEq of NA,K, CL may lost in 24 hours)
3. Acidosis: due to breakdown of fat into free fatty acid and glycerol.
Free fatty acids converted to ketones by the liver

Causes:

1. Decreased or missed dose of insulin.


2. illness (stress> which stimulate the secretion of certain
hormones such as glucagon, epinephrine and norepinephrine,
cortisol, and growth hormone.. Promote production of glucose from
liver and interfere glucose utilization
3. Undiagnosed and untreated diabetes

Cont

Clinical manifestations:

Polyuria and polydipsia

Blurred vision

Weakness and headache

Orthostatic hypotension due to dehydration

Gastrointestinal symptoms such as anorexia, nausea,


vomiting and abd pain and acetone breath

Hyperventilation to decrease the acidosis


Diagnostic Findings:

Glucose level vary from 300-800 mg/dl

Low serum bicarbonate and low PH (6.8 to 7.3)

Blood and urine ketone measurements

NA and K may be low, normal, or high.

Medical management:

Rehydration and correction of electrolyte


imbalance.
Treat acidosis: IVF (normal saline), Insulin
infusion ( 5unit/hr), Bicarbonate infusion is
contraindicated because causing sever sudden
hypokalemia
Nursing management:
- Monitoring

3. Hyperglycemic hyperosmolar Nonketotic Syndrom:

Hyperglycemia and hyperosmolarity predominate, with


alteration of awarness, with same time ketonsis is minimal
or absent
Cause: Lack of effective insulin ( insulin resistance).
Persistent of hyperglycemia causes osmotic diuresis,
resulting in losses of water and electrolyte.> water
shifts from intracellular fluid space to the Extracellular fluid
space
With glucosuria and dehydration, hypernatremia and
increased osmolarity occur.
Hyperglycemia and dehydration may be more sever.

Clinical manifestation: hypotension, profound dehydration,


tachycardia, alteration in awareness, hemiparesis.

Long-Term Complications of Diabetes:

1.

2.

Macrovascular disease: changes in the medium to large

blood vessels
Blood vessels walls thicken, sclerose, and become occluded by
plaque ( atherosclerosis).
May happened due to other diseases
Coronary artery disease, Cerebrovascular disease, and
peripheral vascular disease are the three main types of
Macrovascular.

Microvascula complications( Diabetic Retinopathy


and Nephropathy)

Unique to DM
Capillary basement membrane thickening of the retina
(microangiopathy) and kidneys (Nephropathy)
Proliferative retinopathy is characterized by the proliferation of
new blood vessel of new blood vessels growing out of the retina
into the vitreous which are prone to bleeding.

Cont.

Nephropathy: changes in the microvascular changes in the


kidney.
The kidneys filtration mechanism is stressed, allowing blood
protein to leak into the urine. As a result pressure in the
blood vessels of the kidney increased, this increases in the
pressure stimulate the development of Nephropathy.
Diagnostic findings: Microalbuminuria if present in two tests
ACE inhibitor should prescribed to lower pressure and reduce
microalbuminurea. Serum creatinine and BUN

3. Diabetic Neuropathies:

Group of disease that all types of nerves, including


peripheral (sensorimotor), autonomic, and spinal nerves
Causes: Vascular or a metabolic mechanism or both, and
demylinization of the nerves ( result in disruption of
conduction.
Most common types are:
1. sensorimotor polyneuropathy (peripheral neuropathy):
Clinical manifestation: parasthesias, burning sensations,
feet become numb, decrease awareness of position and
WT of objects, decrease sensation of light touch lead to an
unsteady gait,decrease sensation of pain and tempreture
2. autonomic neuropathy: Neuropathy of autonomic
nervous system.

Clinical manifestation:

1.

2.

3.

4.

5.

6.

Cardiovascular: Slight tachycardia, orthostatic hypotension, silent


or painless myocardial ischemia and infarction
Gastrointestinal: Delayed gastric emptying, bloating ,nausea, and
vomiting, Diabetic constipation or diarrhea may occur.
Urinary: Urinary retention, decreased sensation of bladder fullness,
increase risk of UTI.
Adrenal gland (Hypoglycemic Unawareness): Diminished or absent
of adrenegic symptoms of hypoglycemia
Sudomotor neuropathy: decrease or absence of sweating of the
extremities, with a compensatory increase in upper body sweating.
Dryness of feet increase the risk of foot ulcer
Sexual dysfunction: impotence in men ( This complication makes
the patients to seek health and mainly DM discovered after that).

Diabetic foot:

1.

2.

3.

Three diabetic complications increase risk of foot


infection:
Neuropathy: sensory neuropathy leads to loss of pain
and pressure sensation, autonomic neuropathy lead to
increase dryness and fissuring of the skin
Peripheral vascular disease: poor circulation. Poor
wound healing
Immunocompramise DM impairs the ability of
specialized WBCs to destroy bacteria.

Medical management: Control of Glucose level, bed rest,


antibiotic, debridement.
Nursing management:

Nursing diagnosis of newly diagnosed with DM

1.

2.

3.
4.

5.

Risk for fluid volume deficit related to polyuria and


dehydration
Altered nutrition related to imbalance of insulin, food and
physical activity
Knowledge deficit about diabetes self- care skills
Potential self-care deficit related to physical impairment or
social factors
Anxiety related to loss of control, fear of inability to manage
diabetes

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