Insulin is secreted by beta cells, which is 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 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, signals the liver to stop release of glucose, enhances

storage of dietary fat in adipose tissues, and accelerates transport of amino

acids into cells. Insulin also inhibits the breakdown of stored glucose, protein

and fat.

During fasting periods, the pancreas continuously releases a small amount of

insulin; another pancreatic hormone called glucagon is released when blood

glucose levels decrease and stimulates the liver to release stored glucose.

The insulin and the glucagon in the blood by stimulating the release of

glucose from the liver.

Initially, the liver produces glucose through the breakdown of glycogen. After

8-12 hours without food, the liver forms glucose from the breakdown of non-

carbohydrate substances, including amino acids.

In type II diabetes, the two main problems are insulin resistance and

impaired insulin secretion. Insulin resistance refers to a decreased tissue

sensitivity to insulin. Normally, insulin binds to special receptors on cell

surfaces and initiates a series of reactions involved in glucose metabolism. In

type II diabetes, these intracellular reactions are diminished, making insulin

less effective at stimulating glucose uptake by the liver. The exact

mechanisms that lead to insulin resistance and impaired insulin secretion in

type II diabetes are unknown, although genetic factors are ought to play a

role.

To overcome insulin resistance and prevent the buildup of glucose in the

blood, increased amounts of insulin must be secreted to maintain the

glucose level at a normal or slightly elevated level. However, if the beta cells

cannot keep up with the increased demand for insulin, the glucose level rises

and type II diabetes develops.

Despite the impaired secretion of insulin that is a characteristic of type II

diabetes, there is enough insulin present to prevent the breakdown of fat the

accompanying production of ketone bodies. Therefore, DKA does not

typically occur in type II diabetes. However, uncontrolled type II diabetes

may lead to another acute problem.

Because type II diabetes is associated with a slow, progressive glucose

intolerance, its onset may go undetected for many years. If the patient

experiences symptoms, they are frequently mild and may include fatigue,

irritability, polyuria, polydipsia, poor healing skin wounds, vaginal infections

or blurred vision if glucose levels are very high.

A cerebrovascular accident (CVA), an ischemic stroke or brain attack, is

a sudden loss of brain function resulting from a disruption of the blood supply

to a part of the brain.

Description

Stroke is the primary cerebrovascular disorder in the United

States.

Strokes are usually hemorrhagic (15%) or

ischemic/nonhemorrhagic (85%).

Ischemic strokes are categorized according to their cause: large

artery thrombotic strokes (20%), small penetrating

artery thrombotic strokes (25%), cardiogenic embolic strokes

(20%), cryptogenic strokes (30%), and other (5%).

Cryptogenic strokes have no known cause, and other strokes result

from causes such as illicit drug use, coagulopathies, migraine, and

spontaneous dissection of the carotid or vertebral arteries.

 The result is an interruption in the blood supply to the brain,

causing temporary or permanent loss of movement, thought,

memory, speech, or sensation.

Risk Factors

Nonmodifiable

Advanced age (older than 55 years)

Gender (Male)

Race (African American)

Modifiable

Hypertension

Atrial brillation

Hyperlipidemia

Obesity

Smoking

Diabetes

Asymptomatic carotid stenosis and valvular heart disease (eg,

endocarditis, prosthetic heart valves)

 Periodontal disease

Pathophysiology

Cerebrovascular accident (CVA, stroke or brain attack) is injury or death

to parts of the brain caused by an interruption in the blood supply to that

area causing dis- ability, such as paralysis or speech impairment.

Statistics

Morbidity: In 2005, prevalence of stroke was estimated at 2.3

million males and 3.4 million females; many of the approximately

5.7 million U.S. stroke survivors have permanent stroke-related

disabilities.

Mortality: In 2004, stroke ranked fth as the cause of death for

those aged 45 to 64 years and third for those aged 65 years or

older (National Heart, Lung and Blood Institute [NHLBI], 2007),

with 150,000 deaths (American Heart Association and American

Stroke Association, 2008); hemorrhagic strokes are more severe,

and mortality rates are higher than ischemic strokes, with a 30-day

mortality rate of 40% to 80%.

 Cost: Estimated direct and indirect cost for 2008 was $65.5 billion

(American Heart Association and American Stroke Association,

2008).

Clinical Manifestations

General signs and symptoms include numbness or weakness of face, arm, or

leg (especially on one side of body); confusion or change in mental status;

trouble speaking or understanding speech; visual disturbances; loss of

balance, dizziness, difculty walking; or sudden severe headache.

Motor Loss

Hemiplegia, hemiparesis

Flaccid paralysis and loss of or decrease in the deep

tendon reexes (initial clinical feature) followed by (after 48

hours) reappearance of deep reexes and abnormally increased

muscle tone (spasticity)

Communication Loss

Dysarthria (difculty speaking)

 Dysphasia (impaired speech) or aphasia (loss of speech)

Apraxia (inability to perform a previously learned action)

Perceptual Disturbances and Sensory Loss

Visual-perceptual dysfunctions (homonymous hemianopia [loss of

half of the visual eld])

Disturbances in visual spatial relations (perceiving the relation of

two or more objects in spatial areas), frequently seen in patients

with right hemispheric damage

Sensory losses: slight impairment of touch or more severe with

loss of proprioception; difculty in interrupting visual, tactile, and

auditory stimuli

Impaired Cognitive and Psychological Effects

Frontal lobe damage: Learning capacity, memory, or other higher

cortical intellectual functions may be impaired. Such dysfunction

may be reected in a limited attention span, difculties in

comprehension, forgetfulness, and lack of motivation.

Depression, other psychological problems: emotional

lability, hostility, frustration, resentment, and lack of cooperation.

Diagnostic Studies

CT scan taken some time after a large stroke.

The black area is where the stroke was and now the brain tissue has died and
left a large hole. Photo via: emedicinehealth.com

CT scan (with/without enhancement): Demonstrates structural

abnormalities, edema, hematomas, ischemia, and

infarctions. Note: May not immediately reveal all changes, e.g.,

ischemic infarcts are not evident on CT for 812 hr; however,

intracerebral hemorrhage is immediately apparent; therefore,

emergency CT is always done before administering tissue

plasminogen activator (t-PA). In addition, patients with TIA

commonly have a normal CT scan.

PET scan: Provides data on cerebral metabolism and blood ow

changes, especially in ischemic stroke.

 MRI: Shows areas of infarction, hemorrhage, AV malformations;

and areas of ischemia.

Cerebral angiography: Helps determine specic cause of stroke,

e.g., hemorrhage or obstructed artery, pinpoints site of occlusion

or rupture. Digital subtraction angiography evaluates patency of

cerebral vessels, identies their position in head and neck, and

detects/evaluates lesions and vascular abnormalities.

Lumbar puncture (LP): Pressure is usually normal and CSF is clear

in cerebral thrombosis, embolism, and TIA. Pressure elevation and

grossly bloody uid suggest subarachnoid and intracerebral

hemorrhage. CSF total protein level may be elevated in cases of

thrombosis because of inammatory process. LP should be

performed if septic embolism from bacterial endocarditis is

suspected.

Transcranial Doppler ultrasonography: Evaluates the velocity of

blood ow through major intracranial vessels; identies AV

disease, e.g., problems with carotid system (blood ow/presence of

atherosclerotic plaques).

EEG: Identies problems based on reduced electrical activity in

specic areas of infarction; and can differentiate seizure activity

from CVA damage.

 X-rays (skull): May show shift of pineal gland to the opposite side

from an expanding mass; calcications of the internal carotid may

be visible in cerebral thrombosis; partial calcication of walls of an

aneurysm may be noted in subarachnoid hemorrhage.

Laboratory studies to rule out systemic causes: CBC, platelet and

clotting studies, VDRL/RPR, erythrocyte sedimentation rate (ESR),

chemistries (glucose, sodium).

ECG, chest x-ray, and echocardiography: To rule out cardiac origin

as source of embolus (20% of strokes are the result of blood or

vegetative emboli associated with valvular disease, dysrhythmias,

or endocarditis).

Prevention

Help patients alter risk factors for stroke; encourage patient to quit

smoking, maintain a healthy weight, follow a healthy diet

(including modest alcohol consumption), and exercise daily.

Prepare and support patient through carotid endarterectomy.

Administer anticoagulant agents as prescribed (eg, low

dose aspirin therapy).

6 ways to reduce your stroke risk. Photo via: HuffingtonPost.com

Medical Management

Recombinant tissue plasminogen activator (tPA),

unless contraindicated; monitor for bleeding

Anticoagulation therapy

Management of increased intracranial pressure (ICP): osmotic

diuretics, maintain PaCO2 at 30 to 35 mm Hg, position to avoid

hypoxia (elevate the head of bed to promote venous drainage and

to lower increased ICP)

Possible hemicraniectomy for increased ICP from brain edema in a

very large stroke

 Intubation with an endotracheal tube to establish a patent airway,

if necessary

Continuous hemodynamic monitoring (the goals for blood pressure

remain controversial for a patient who has not received

thrombolytic therapy; antihypertensive treatment may be withheld

unless the systolic blood pressure exceeds mm Hg or the diastolic

blood pressure exceeds 120 mm Hg)

Neurologic assessment to determine if the stroke is evolving and if

other acute complications are developing

Management of Complications

Decreased cerebral blood ow: Pulmonary care, maintenance of a

patent airway, and administration of supplemental oxygen as

needed.

Monitor for UTIs, cardiac dysrhythmias, and complications of

immobility.
Bibliography

http://nurseslabs.com/8-cerebrovascular-accident-stroke-nursing-
care-plans/

http://nurseslabs.com/diabetes