Lesson 8: Major chronic illness of older adult understanding the Pathophysiology and Nursing

Intervention

MAJOR CHRONIC ILLNESSES

1. Essential hypertension
2. Arthritis
3. Musculoskeletal impairments
4. Cancer
5. Heart disease
6. Diabetes
7. Chronic airway obstruction
8. Peripheral vascular disease.

RISK FACTORS
1. Family history
2. Marital status (adds 10 yrs in men; 4 yrs in women)
3. Economic status
4. Body weight
5. Exercise
6. Alcohol (add 2 years if drink 1-3 drinks/day)
7. Smoking
8. Disposition (add 2 yrs if reasoned, practical)
9. Education
10. Environment (add 4 yrs if rural)
11. Sleep (more than 9 hours subtract 5 years)
12. Temperature (add 2 yrs if thermostat is < 68)
13. Health care – regular check ups add 3 yrs

1. HEART DISEASE
 Heart failure (HF) is generally defined as the inability of the heart to supply sufficient blood
flow to meet the needs of the body.
 HF is a complex clinical syndrome that can result from any structural or functional cardiac
disorder that impairs the ability of the ventricle to fill with or eject blood.
 In systolic heart failure the dominant feature is a reduction in cardiac output
 In diastolic heart failure the dominant feature is impaired filling of the left ventricle.
 Heart Failure is Primarily a Condition of the Elderly

CHARACTER OF HEART FAILURE

 Signs and symptoms of intravascular and interstitial volume overload, including shortness
of breath, rales, and edema.
 Manifestations of inadequate tissue perfusion, such as impaired exercise tolerance,
fatigue, and renal dysfunction.

CLASSICAL SYMPTOMS OF HF
 Fatigue or inability to exercise well; having less energy, feeling mor tired than usual;
 Dyspnea at rest or exertion.
 Paroxysmal nocturnal dyspnea shortness of breath while sleeping or that wakes you at
night
 Orthopnea-Shortness of breath while lying down, gets worse when you lie flat
 Cough – can be wet or dry, with crackles, and usually worse with lying down.
  Weight gain
 Swelling in the feet or ankles, usually worse at the end of the day or after standing for long
periods; shoes may no longer fit.
 Sometimes edema is painful but usually pressure indents the skin
 Abdominal swelling with decreased appetite and decreased muscle strength (Cardiac
Cachectic)
 Abdominal distention (Ascites) usually a sign of right heart failure.
 Urination- frequent urination, usually at night. Increased urination (Due to high BNP)

Common causes of heart failure

 Myocardial infarction
 Ischemic heart disease- Ischemic Heart disease and Prior MI account for 2/3 of systolic
heart failure
 Hypertension- Essential Hypertension is a major cause of ischemic and non ischemic
systolic heart failure. Hypertension increases afterload and accelerates the progression of
heart failure. HTN causes chronic pressure overload.
 Valvular heart disease
 Cardiomyopathy
 Other causes of Non ischemic heart failure are genetic diseases, Toxic/drug induced,
Immune mediated, infiltrative process
 Metabolic disorders

 Heart failure is a common, costly, disabling, and potentially deadly condition.

 In developed countries, around 2% of adults suffer from heart failure, but in those over the
age of 65, this increases to 6–10%.

Functional classification Classes (I-IV)

 Class I: no limitation is experienced in any activities; there are no symptoms from ordinary
activities.
 Class II: slight, mild limitation of activity; the patient is comfortable at rest or with mild
exertion.
 Class III: marked limitation of any activity; the patient is comfortable only at rest.
 Class IV: any physical activity brings on discomfort and symptoms occur at rest.

ACC/AHA Classification of CHF

RIGHT-SIDED HEART FAILURE
 Backward failure of the right ventricle leads to congestion of systemic capillaries. This
generates excess fluid they have that accumulation in the body.

 S/SX
1. Peripheral edema
2. Foot and ankle Swelling
3. Sacral edema
4. Fluid retention without dyspnea or rales.
5. Often associated with weight gain, dilation of the right ventricle.

LEFT-SIDED HEART FAILURE

 Backward failure of the left ventricle causes congestion of the pulmonary vasculature,
and so the symptoms are predominantly respiratory in nature.
S/SX
1. Shortness of breath on exertion
2. Dyspnea at rest

TYPES OF LEFT-SIDED HF
 Systolic dysfunction- reduced LV ejection fraction.
 Diastolic dysfunction- increased ventricular stiffness or impaired myocardial relaxation.
Often with preserved LV ejection fraction.
 Physiologic states where the heart cannot compensate for increased circulation or
metabolic requirements. (Regurgitant valvular disease, intra cardiac shunts, disorders
of heart rate or rhythm.)
COMPLICATIONS OF CHRONIC HEART FAILURE
 An irregular heartbeat leading to death (VT)
 A stroke leading to death
 A heart attack leading to death
 Deep vein thrombosis
 Pulmonary embolism
 Anemia
 Cognitive impairment
 Mitral valve regurgitation
Specific assessment and focus and management of heart failure
 Left sided failure:
1. Chest x-ray shows increased pulmonary and left ventricular hypertrophy
 Right-sided failure:
2. Chest x-ray reveals pulmonary congestion, cardiomegaly, and pleural effusions

KEY TREATMENTS
 Angiotensin-converting enzymes(ACE) inhibitors: - ACE inhibitors relieve symptoms,
reduce hospitalizations and improve survival in patients with systolic and diastolic heart
failure and should be used regardless of the severity of CHF.
1. Captopril (Capoten)
2. Enalapril (Vasotec)
3. Lisinopril (Prinivil)
 Cardiac glycoside
4. Digoxin (lanoxin)
 Inotropic agents
5. Dopamine hydrochloride (Intropin)
6. Dobutamine hydrochloride (Dobutrex)
 Diuretics- Sodium and Water retention are the hallmark of CHF and diuretics are
mandatory treatment for patients with pulmonary or Peripheral edema.
1. Furosemide (lasix)
2. Bumetadine (Bumex)
3. Metolazone (zaroxolyn)
 Nitrates
4. Isosorbide dinitrate (Isordil)
5. Nitroglycerine (Nitro-bid)
 Vasodilator-
1. Nitroprusside sodium (Nitropress)

KEY INTERVENTIONS
 Assess cardiovascular status including vital signs and hemo dynamic variables
 Assess respiratory status
 Keep the patients in semi-fowler’s position
 Administer oxygen
 Weigh the patient daily

PROGNOSIS
 Class IV has 30 to 70% annual mortality.
 Class III has 10 to 20% annual mortality.
 Class II has 5 to 10% annual mortality.
2. COPD
 Chronic obstructive pulmonary disease, or COPD, refers to a group of diseases that cause
airflow blockage and breathing-related problems.
 It includes emphysema, chronic bronchitis, and in some cases asthma.
 The primary cause of COPD is
1. Tobacco smoke
Other risk factors include:
1. Indoor air pollution (such as biomass fuel used for cooking and heating)
2. Outdoor air pollution:(Occupational dusts and chemicals (vapors, irritants, and fumes)
3. Frequent lower respiratory infections during
 In the developing world, indoor air quality is thought to play a larger role in the development
and progression of COPD than it does in the developed world.
 WHO estimates that in 2005 5.4 million people died due to tobacco use.
 Tobacco-related deaths are projected to increase to 8.3 million deaths per year by 2030.

Signs and symptoms:

 Chronic cough
 Sputum production
 Dyspnea
 History of exposure to risk factors for the disease
 Confirmed by a simple test called:
 Spirometry (which measures how deeply a person can breathe and how fast air can move
into and out of the lungs)
 Should be considered in any patient who has symptoms of a chronic cough, sputum
production, dyspnea (difficult or labored breathing), and a history of exposure to risk
factors for the disease.
 Confirmed by a simple test called spirometry, which measures how deeply a person can
breathe and how fast air can move into and out of the lungs.
 A low peak flow is consistent with COPD but may not be specific to COPD because it can
be caused by other lung diseases and by poor performance during testing.
 Chronic cough and sputum production often precede the development of airflow limitation
by many years, although not all individuals with cough and sputum production go on to
develop COPD.

Three major types that affect older adults

 1. CHRONIC BRONCHITIS
 Assessment Findings:
1. Dyspnea
2. Airway mucosa edema
3. Copious sputum production with a tendency to airway closure on expiration
4. Productive cough
5. Prolonged expiration
6. Rhonchi,wheezes
7. Use of accessory muscles
8. Weigth gain, edema, jugular venous distention
 Key test results:
a. Chest X-ray shows hyperinflation and increased brochovascular markings
b. PFT’s may reveal increased residual volume, decreased vital capacity and forced
expiratory volumes, normal static compliance and diffusion.
 Treatment
a. Chest physiotherapy, postural drainage, and incentive spirometry
b. Dietary changes, including establishing a diet high in protein, vitamin C, calories,
and nitrogen
c. Fluid intake up to 3,000 ml/day, if not contraindicated
d. Intubation and mechanical ventilation if respiratory status deteriorates
e. O2 therapy or mechanical nebulizer treatments

 NURSING INTERVENTIONS
 1. Administer low-flow O2
 Rationales:
1. They have a hypoxic respiratory drive.
2. Higher flow rates may eliminate this hypoxic respiratory drive
 2. Administer medications, as prescribed, to relieve symptoms and prevent complication
 3. Allow activity, as tolerated, to avoid fatigue and reduce O2 demands
 4. Assess respiratory status, ABGs, and pulse oximetry to detect respiratory compromise,
severe hypoxemia, and hypercapnia
 5. Assist with turning, coughing, and deep breathing to mobilize secretions and facilitate
removal
 6. Keep patient in high-Fowler’s position to improve ventilation
 7. Monitor and record the color, amount, and consistency of sputum. Changes in sputum
characteristics may signal a respiratory infection
 8. Maintain the patient’s diet and administer small, frequent feedings to avoid fatigue when
eating and reduce pressure on the diaphragm from full stomach

 2. EMPYSEMA
 Is damage to the alveolar structures, causing them to enlarge and be damaged resulting
in reduction of the alveolar-capillary diffusion interface and airway closure caused by the
loss of support for the airway structures
 Abnormal permanent enlargement of the airspaces distal to the terminal bronchiole,
accompanied by destruction of their walls without fibrosis.
 Causes:
a. Deficiency of alpha1- antitrypsin: is a genetic disorder that may result in lung
disease or liver disease
b. Smoking
 Assessment findings
1. Anorexia, weight loss
2. Barrel chest
3. Decreased breath sounds
4. Dyspnea
5. Finger clubbing, late in the disease
6. Prolong expiration
7. Pursed-lip breathing
8. Use of accessory muscles for breathing
 Diagnostic Findings
1. Chest X-ray in advanced disease reveals a flattened diaphragm, reduced vascular
markings in the lung periphery, enlarged antero-posterior chest diameter, and a
vertical heart
2. CBC shows increased Hb late in disease when patient has severe persistent hypoxia
 3. PFT’s show increased residual volume, total lung capacity, diffusing capacity, and
expiratory volumes
 Nursing Interventions and Rationales
1. Administer low-flow O2 because emphysema patients have chronic hypercapnia, so
they have a hypoxic respiratory drive. Higher flow rates may eliminate this hypoxic
respiratory drive
2. Allow activity as tolerated to avoid fatigue and reduce O2 demands
3. Assist with turning, coughing, and deep breathing to mobilize secretions and facilitate
removal
4. Monitor laboratory studies. Follow drug levels for evidence of toxicity. Electrolytes
imbalances may occur with the use of diuretics. Reduced Hb and HCT affect the
oxygen-carrying capacity of the blood
5. Assist with diaphragmatic and pursed lip breathing to strengthen respiratory muscles.
6. Weigh the patient daily to detect edema caused by right-sided heart failure

 3. ASTHMA
 Is a form of COPD in which the bronchial linings overreact to various stimuli, causing
episodic spasms and inflammation that severely restrict the airways
 Types of asthma:
1. Extrinsic(atopic) is caused by sensitivity to specific external allergens
2. Intrinsic (nonatopic) is caused by a reaction to internal, nonallergic factors
 Causes of asthma
 Extrinsic asthma- Extrinsic asthma symptoms occur in response to allergens, such as dust
mites, pollen, and mold. It is also called allergic asthma and is the most common form of
asthma.
1. Allergens (pollen, dander, dust, sulphite food additives)
 Intrinsic asthma- Intrinsic asthma has a range of triggers, including weather conditions,
exercise, infections, and stress. People may call it nonallergic asthma.
1. Endocrine changes
2. Noxious fumes
3. Respiratory infection
4. Stress
5. Temperature and humidity
 Assessment Findings
1. Absent or diminished breath sounds during severe obstruction
2. Chest tightness
3. Dyspnea
4. Productive cough with thick mucous
5. Prolong expiration
6. Tachypnea, tachycardia
7. Use of accessory muscles
8. Usually asymptomatic between attacks
9. Wheezing, primarily on expiration but also sometimes on inspiration
 Treatment
1. Desensitization to allergens
2. Intubation and mechanical ventilation if respiratory status worsens
3. Oxygen therapy at 2L/minute
4. Fluids to 3,000 ml/day as tolerated
 Nursing Interventions
 1. Administer low-flow humidified O2 to reduce inflammation of the airways, ease
breathing and increase SaO2
2. Administer medications. As prescribed, to reduce inflammation and obstruction of
airways
3. Encourage patient to express feelings about fear of suffocation to reduce anxiety.
4. Keep patients in higher-fowler’s position to improve ventilation
5. Monitor and record vital signs. Tachycardia may indicate worsening asthma or drug
toxicity. Hypertension may indicate hypoxemia. Fever may signal infection
6. Provide chest physiotherapy, postural drainage, incentive spirometry, and suction to
aid in the removal of secretions

3. DIABETES MELLITUS
 Disease in which the body doesn’t produce or properly use insulin, leading to
hyperglycemia.
 In the writings of Aretaios (Aretaeus) of Cappadocia, a Greek physician who lived during
the period 120-200 A.D., there is a reference, probably to Diabetes. Amongst the disease
described, he mentioned a condition associated with unquenchable thirst, excessive
drinking of water and excessive passing of urine. The word "Diabetes" is perhaps derived
from a Greek word signifying a siphon, appropriately describing how in the disease the
fluid cannot be retained in the body. Greek physicians, like ancient Hindu physicians, used
to taste the patient's urine to detect abnormal constituents. This unpleasant practice
perhaps enabled them to detect diabetic patients.
Thomas Willis, in 1764, observed that the urine of a diabetic patient was sweet and he
surmised that it contained either sugar or honey.
 Diabetes mellitus comes from the Greek word "diabainein" meaning "to pass through,"
and the Latin word "mellitus" meaning "sweetened with honey." Put the two words together
and you have "to pass through sweetened with honey."
 Is highly prevalent and increasing in person over 65
 Poor glycemic controls synergistically interact with normal changes of aging and other
coexisting diseases to accelerate diabetes complications.
 About 41% of the population with diabetes is over the age of 65.
 Older people have higher rates than younger people (National Academy of an Aging
Society, 2000)
 Optimizing glucose control and decreasing risk factors for microvascular, macrovascular
and neurologic complications can improve the quality and quantity of life for patients of all
ages.
 The digestion of carbohydrate. The complex polysaccharide starch is broken down into
glucose by the enzyme’s amylase and maltase (secreted by the small intestine).
 Insulin Secretion- Panel 2. Insulin secretion - Insulin secretion in beta cells is triggered
by rising blood glucose levels. Starting with the uptake of glucose by the GLUT2
transporter, the glycolytic phosphorylation of glucose causes a rise in the ATP:ADP ratio.
This rise inactivates the potassium channel that depolarizes the membrane, causing the
calcium channel to open up allowing calcium ions to flow inward. The ensuing rise in levels
of calcium leads to the exocytotic release of insulin from their storage granule.
 The process by which insulin is released from beta cells, in response to changes in blood
glucose concentration, is a complex and interesting mechanism that illustrates the intricate
nature of insulin regulation. Type 2 glucose transporters (GLUT2) mediate the entry of
glucose into beta cells (see panel 2). As the raw fuel for glycolysis, the universal energy-
producing pathway, glucose is phosphorylated by the rate-limiting enzyme glucokinase.
This modified glucose becomes effectively trapped within the beta cells and is further
 metabolized to create ATP, the central energy molecule. The increased ATP:ADP ratio
causes the ATP-gated potassium channels in the cellular membrane to close up,
preventing potassium ions from being shunted across the cell membrane. The ensuing
rise in positive charge inside the cell, due to the increased concentration of potassium
ions, leads to depolarization of the cell. The net effect is the activation of voltage-gated
calcium channels, which transport calcium ions into the cell. The brisk increase in
intracellular calcium concentrations triggers export of the insulin-storing granules by a
process known as exocytosis. The ultimate result is the export of insulin from beta cells
and its diffusion into nearby blood vessels. Extensive vascular capacity of surrounding
pancreatic islets ensures the prompt diffusion of insulin (and glucose) between beta cells
and blood vessels.
 Insulin release is a biphasic process. The initial amount of insulin released upon glucose
absorption is dependent on the amounts available in storage. Once depleted, a second
phase of insulin release is initiated. This latter release is prolonged since insulin has to be
synthesized, processed, and secreted for the duration of the increase of blood glucose.
Furthermore, beta cells also must regenerate the stores of insulin initially depleted in the
fast response phase
 How insulin works
Insulin binding to the insulin receptor induces a signal transduction cascade which allows
the glucose transporter (GLUT4) to transport glucose into the cell.
Insulin molecules circulate throughout the blood stream until they bind to their associated
(insulin) receptors. The insulin receptors promote the uptake of glucose into various
tissues that contain type 4 glucose transporters (GLUT4). Such tissues include skeletal
muscles (which burn glucose for energy) and fat tissues (which convert glucose to
triglycerides for storage). The initial binding of insulin to its receptor initiates a signal
transduction cascade that communicates the message delivered by insulin: remove
glucose from blood plasma (see panel 3). Among the wide array of cellular responses
resulting from insulin ‘activation,’ the key step in glucose metabolism is the immediate
activation and increased levels of GLUT4 glucose transporters. By the facilitative transport
of glucose into the cells, the glucose transporters effectively remove glucose from the
blood stream. Insulin binding results in changes in the activities and concentrations of
intracellular enzymes such as GLUT4. These changes can last from minutes to hours.
 Insulin-mediated glucose uptake - Insulin binding to the insulin receptor induces a signal
transduction cascade which allows the glucose transporter (GLUT4) to transport glucose
into the cell.
 As important as insulin is to prevent too high of a blood glucose level, it is just as important
that there not be too much insulin and hypoglycemia. As one step in monitoring insulin
levels, the enzyme insulinase (found in the liver and kidneys) breaks down blood-
circulating insulin resulting in a half-life of about six minutes for the hormone. This
degradative process ensures that levels of circulating insulin are modulated, and that
blood glucose levels do not get dangerously low


 What goes wrong in diabetes?

 The body’s response to blood sugar requires the coordination of an array of mechanisms.
Failure of any one component involved in insulin regulation, secretion, uptake, or
breakdown can lead to the build-up of glucose in the blood. Likewise, any damage to the
beta cells, which produce insulin, will lead to increased levels of blood glucose. Diabetes
mellitus, commonly known as diabetes, is a metabolic disease that is characterized by
abnormally high levels of glucose in the blood. Whereas non-diabetics produce insulin to
reduce elevated blood glucose levels (i.e. after a meal), the blood glucose levels of
diabetics remain high. This can be due to insulin not being produced at all, or not in
quantities sufficient to be able to reduce the blood glucose level. The most common forms
of diabetes are Type 1 diabetes (juvenile onset, 5-10% of cases), which is an autoimmune
disease that destroys beta cells, and Type 2 diabetes (adult onset, 90-95% of cases),
which is associated with insufficient insulin. In either case, diabetes complications are
severe, and the disease can be fatal if left untreated.
 Insulin is the foundation for the management of insulin-dependent diabetes. Unfortunately,
the use of insulin is not a cure nor without side effects. In certain parts of the world, it is
not even available. Insulin is also not completely effective in preventing complications of
the disease such as blindness, heart disease, kidney failure, etc. While millions of men,
women, and children await a life without diabetes, let us hope that policy makers and the
scientific community can converge on strategies that promote discovery for a cure.
 Action of Insulin on the Cell Metabolism
 Insulin is a polypeptide hormone that travels around the bloodstream. Most of the cells in
the body carry receptors for the molecule in their cell membranes. Once the hormone has
become bound to one of these receptors, the receptor gives a signal to the cell's interior.
This signal leads to many enzyme-controlled reactions which, in turn lead to changes in
the metabolism of the cell.
 Many of the effects of insulin depend on the cell type in which it stimulates. However, in
nearly all the cells that have insulin receptors in their cell membrane, the binding of insulin
to the receptors leads to increased glucose uptake of the cell.
 The two types of cells that are the main exceptions are the brain and the liver. However,
this is only because these cells are readily permeable to glucose, even in the absence of
insulin. Liver cell membranes do contain insulin and glucagon receptors but binding of the
hormone to them affects cellular processes other than glucose permeability.
  The animation below illustrates the way insulin brings about the increase in glucose uptake
 Glucose enters the cells of the body through glucose transporter (GLUT) proteins which
are embedded within the cell membrane. This is a process called facilitated diffusion.
When insulin binds to its receptor, the intracellular domain of the receptor changes shape
slightly. This sets off a chain of reactions. These reactions serve to activate certain
enzymes.
 As a result, more glucose transporter proteins are released from intracellular stores and
move to the plasma membrane and become embedded within it.
 Action of Insulin on Carbohydrate, Protein and Fat Metabolism
 1. CARBOHYDRATE- In general we can say that insulin favors anabolic reactions;
glucagon, catabolic reactions. Put more simply, insulin favors storing energy and
production of proteins while glucagon activates release of stored energy in the form of
glucose or fatty acids. The actions of these two hormones on individual metabolic
processes are summarized:
1. Facilitates the transport of glucose into muscle and adipose cells
2. Facilitates the conversion of glucose to glycogen for storage in the liver and muscle.
3. Decreases the breakdown and release of glucose from glycogen by the liver.
 2. PROTEIN
 A protein-rich meal leads to release of both insulin and glucagon. The latter stimulates
gluconeogenesis and release of the newly formed glucose from the liver to the blood
stream. The very moderate rise in insulin associated with the protein meal stimulates
uptake of the sugar formed in the liver by muscle and fat tissue.
1. Stimulates protein synthesis
2. Inhibits protein breakdown; diminishes gluconeogenesis
 3. FATS
 One of the primary actions of insulin is to control movement of fatty acids in and out of
adipocytes. It does this through two mechanisms; regulation of hormone-sensitive lipase
and activation of glucose transport into the fat cell via recruitment of GLUT4.
 Storage of triglycerides after a meal is dependent upon insulin-stimulated glucose uptake
and glycolysis. Fat cells take up both fatty acids and glucose simultaneously. The fatty
acids come from the action of lipoprotein lipase at the capillary wall. Glucose uptake is
stimulated by insulin and occurs through the insulin-sensitive glucose transport protein
GLUT4. Thus, insulin increases glucose uptake and glycolysis in fat cells, inhibits
hormone-sensitive lipase and thereby increases storage of lipids as triglycerides in
adipocytes.
1. Stimulates lipogenesis- the transport of triglycerides to adipose tissue
2. Inhibits lipolysis – prevents excessive production of ketones or ketoacidosis

TYPE 1 DIABETES
 The total lack of insulin leads to two metabolic crises: a marked increase in the rate of
lipolysis in adipose tissue and activation of hepatic gluconeogenesis in spite of high
plasma glucose levels. The dramatically increased rate of lipolysis in adipose tissue
follows the lack of insulin inhibition of hormone-sensitive lipase. The increase in fatty acids
that results leads to a massive synthesis of ketone bodies in the liver. These then exceed
the buffer capacity of the blood, leading to ketoacidosis. Excess acid is a potent poison
for the brain. Coma and death follow ketoacidosis.
 Low or absent endogenous insulin
 Dependent on exogenous insulin for life
 Onset generally < 30 years
 5-10% of cases of diabetes
  Onset: sudden:
 Symptoms: 3 P’s: polyuria, polydipsia, polyphagia

TYPE II DIABETES
 Insulin levels may be normal, elevated or depressed
 Characterized by insulin resistance,
 diminished tissue sensitivity to insulin,
 and impaired beta cell function (delayed or inadequate insulin release)
 Often occurs >40 years
 Blood sugar levels are dependent upon glucose uptake after meals and hepatic release
of glucose between meals. The sugar released from the liver comes either from stored
glycogen or production of glucose from lactate and amino acids. This production of
glucose is largely responsible for stabilization of postprandial blood sugar levels. The
hyperglycemia noted in type 2 diabetes partially results from lack of control over hepatic
glucose formation due to resistance to insulin. It has recently become clear that part of
this insulin effect occurs indirectly through insulin-sensitive receptors in the brain (more
precisely, in the hypothalamus).
 Type 2 diabetes has a stronger genetic basis than type 1, yet it also depends more on
environmental factors. Sound confusing? What happens is that a family history of type 2
diabetes is one of the strongest risk factors for getting the disease but it only seems to
matter in people living a Western lifestyle.
 Americans and Europeans eat too much fat and too little carbohydrate and fiber, and they
get too little exercise. Type 2 diabetes is common in people with these habits. The ethnic
groups in the United States with the highest risk are African Americans, Mexican
Americans, and Pima Indians.
 In contrast, people who live in areas that have not become Westernized tend not to get
type 2 diabetes, no matter how high their genetic risk.
 Obesity is a strong risk factor for type 2 diabetes. Obesity is most risky for young people
and for people who have been obese for a long time.
 The insulin secretion is insufficient to compensate for the insulin resistance, which occurs
in response to decreased insulin effectiveness in stimulating glucose production.
 The body attempts to compensate for rising blood glucose levels by producing more
insulin
 90% of all diabetes usually females
 Often associated with obesity
 Strong inheritability
Signs and symptoms
1. Blurring of vision
2. Vulvovaginitis
3. Neuropathy
 RISK FACTORS
1. family history, sedentary lifestyle, obesity and aging
2. Controlled by weight loss, oral hypoglycemic agents and or insulin
 MANAGEMENT OF DM
1. Nutrition management
2. Blood glucose monitoring
3. Medications – insulin or oral hypoglycemic agents
4. Physical activity/exercise
5. Behavior modification
 MEDICAL NUTRITION THERAPY
 Balance food intake with insulin (or oral agents) and activity to achieve blood glucose
levels as near normal as possible.
 Achieve and maintain normal lipid (cholesterol) levels
1. Primary Goal – improve metabolic control
2. Blood glucose
3. Lipid (cholesterol) levels
4. Provide energy to reach and maintain short and long term body weight
5. Reach and maintain normal growth and development in children and adolescents
6. Prevent or treat complications
7. Improve and maintain nutritional status
8. Provide optimal nutrition for pregnancy
 Nutritional Management for Type I Diabetes
1. Consistency and timing of meals
2. Timing of meals and administration of insulin
3. Insulin plans should be designed to match the person’s eating pattern
4. Monitor blood glucose regularly
 Nutritional Management for Type I Diabetes
1. Weight loss
2. Smaller meals and snacks
3. Physical activity
4. Monitor blood glucose and medications
 NUTRITION RECOMMENDATION
 Carbohydrate
1. 60-70% calories from carbohydrates and monounsaturated fats
 Protein
1. 10-20% total calories
 Fat
1. <10% calories from saturated fat
2. 10% calories from PUFA
3. <300 mg cholesterol
 Fiber
1. 20-35 grams/day
 Alcohol
1. Type I – limit to 2 drinks/day, with meals
2. Type II – substitute for fat calories
 Type 1 and type 2 diabetes have different causes. Yet two factors are important in
both. First, you must inherit a predisposition to the disease. Second, something in your
environment must trigger diabetes.
 Genes alone are not enough. One proof of this is identical twins. Identical twins have
identical genes. Yet when one twin has type 1 diabetes, the other gets the disease at
most only half the time. When one twin has type 2 diabetes, the other's risk is at most 3
in 4.
 In most cases of type 1 diabetes, people need to inherit risk factors from both parents. We
think these factors must be more common in whites because whites have the highest rate
of type 1 diabetes. Because most people who are at risk do not get diabetes, researchers
want to find out what the environmental triggers are.
 One trigger might be related to cold weather. Type 1 diabetes develops more often in
winter than summer and is more common in places with cold climates. Another trigger
might be viruses. Perhaps a virus that has only mild effects on most people triggers type
1 diabetes in others.
  Early diet may also play a role. Type 1 diabetes is less common in people who were
breastfed and in those who first ate solid foods at later ages.
 In many people, the development of type 1 diabetes seems to take many years. In
experiments that followed relatives of people with type 1 diabetes, researchers found that
most of those who later got diabetes had certain autoantibodies in their blood for years
before. (Antibodies are proteins that destroy bacteria or viruses. Autoantibodies are
antibodies 'gone bad,' which attack the body's own tissues.)

 Complications that can develop due to poor glycemic control include the following:
 Eye disease leading to loss of vision or even blindness
 Kidney failure
 Heart disease
 Nerve damage that may cause a loss of feeling or pain in the hands, feet, legs or other
parts of the body (peripheral neuropathies)
 Stroke
 Poor wound healing due to impaired immune response and poor tissue perfusion in
peripheral vascular disease.

 Older patients with DM have higher rates of:

 Premature death
 Functional disability
 Coexisting illnesses, such as hypertensions, coronary heart disease and stroke than other
older adults.

 Goals of Management
 Older patients should be taught to perform blood glucose testing and to keep track of their
readings using a daily log.
 This log will provide feedback to the older patient and guide day-to-day choices regarding
exercise, food and medication.
 The normal readings and treatment goals should be clearly written in the log book for easy
referral.
 Oral Hypoglycemics
 Sulfonylureas
- promote insulin secretion by direct stimulation of B-cells
- reduction of serum glucagon
- increase binding of insulin to receptors
- Tolbutamide, Glipizide
 Biguanides
- reduces hepatic production of glucose by inhibiting glycogenolysis
- decrease intestinal absorption of glucose
- Metformin
 a-Glucosidase inhibitor
- decreases absorption of starch and disaccharides

4. CANCER
 Known as carcinoma or malignancy, is a tumor that invades the surrounding tissue with
the capability of spreading to other tissues at distant site.
 Physical changes result from the disease process, and the treatments have a great impact
on the patient’s quality and quantity of life.
 Cancer – just the word itself can send chills through a person. An actual diagnosis can
cause the patient and their family to go into a tailspin. However, modern medicine and
technology has come a long way in the diagnosis and treatment of cancer. It is not always
the death sentence it once was. Early detection and recognizing certain warning signs are
important factors one needs to be aware of when caring for the older adult.
 It is a leading cause of death in the elderly; the most common malignancies include
neoplasm of the lung, breast, and prostate, leukemia, lymphoma and colorectal
carcinoma.
 Progression from normal tissue to invasive cancer is 5 – 20 years
 Driven by a series of accumulative genetic changes
Risk factors for cancer development
 Chemical Factors
1. Organ-specific
2. Genotoxic (cause genetic damage)
3. Environmental exposures
4. Activation of endogenous mutagenic pathways (nitric oxide & oxy radicals)
5. Requires accumulated exposure
6. Gross chromosomal changes
7. Tobacco Smoke
8. Air Pollution
9. Diet
10. Alcohol
 Chemotherapy is one treatment of which side effects from the medication may not be
tolerated by the elderly patients because of the changes that occur with age, such as
poorer wound healing, comorbidities, and less organ reserve.
 Radiation therapy on the other hand can weaken bones and make them more susceptible
to fracture which is already a high risk for the elderly.
Aging and Cancer
 Age is the greatest risk factor for developing cancer. In fact, 60% of people who have
cancer are 65 or older. So are 60% of cancer survivors. If you are an older adult with
cancer, you are not alone. But you should know that age is just one factor in your cancer
and treatment. The best treatment plan for you depends on your general health, lifestyle,
wishes, and other factors.
 For adults in general, some of the most common cancers diagnosed at any age are the
following:
1. Lung Cancer
2. Bladder Cancer
3. Breast Cancer
4. Pancreatic Cancer
5. Kidney Cancer
6. Leukemia
7. Colon Cancer
 It is important to keep in mind that more than one-third of cancers occur in people over
the age of seventy-five. Unfortunately, older adults can be under-treated. Age should not
be a factor in cancer treatment. Instead, the older adult’s overall health should determine
the course of care. I
 t’s not just the risk of under-treatment that poses a concern for older adults. Even though
they account for the largest demographic among cancer cases in the U.S., adults over the
age of 65 are under-represented in clinical trials.
 The most common cancers in older adults are:
 1. Prostate Cancer – half of all cases are in men over the age of seventy-five
2. Bladder Cancer – 70% or more of all cases are in men between the ages of fifty and
eighty
3. Pancreatic Cancer – most cases are in adults over the age of sixty-five
4. Lung Cancer – 80% or more of all cases are in adults over the age of sixty
 The warning signs of cancer in older adults include:
1. Bladder Cancer – Elderly patients will see warning signs that include frequent
urination, blood in urine, a distended bladder and a burning sensation when urinating.
2. Lung Cancer – Elderly patients will see warning signs including chest pain caused by
coughing, intense or ongoing coughing, breathing difficulty, chronic pneumonia, and
coughing up blood.
3. Bone Cancer – Elderly patients will find that the most common warning sign is pain.
Swelling near a bone is also a symptom that needs to be checked out by a doctor.
4. Colon Cancer – Older patients may find that there are no warning signs during the
early stages. Later stages of colon cancer in elderly adults may include such
symptoms as blood in their stool, a change in bowel habits, vomiting, and stomach
pain.

5. DEMENTIA
 Is an acquired syndrome that causes progressive loss of intellectual abilities.
 Dementing disorders are characterized by gradual onset plus continuing decline that is
not due to other brain disease.
 Short term memory impairment is usually the first symptom of dementia. Clinical diagnosis
requires:
 Loss of an intellectual ability with impairment severe enough to interfere with social or
occupational functioning.
 Characterized by multiple cognitive deficits that include impairment of memory which
develops slowly
1. 80-90% irreversible
2. Reversible due to pathologic process
3. Most common: Alzheimer’s Dementia
 4 Symptoms of Dementia
1. Loss of memory
2. Deterioration of language function
3. Loss of ability of think abstractly, plan, initiate, sequence, monitor or stop complex
behavior
4. Loss of ability to perform ADLs
 Later changes in Dementia
1. Aphasia – speech
2. Apraxia – purposeful activity
3. Agnosia – sensory stimuli
4. Anomia – memory of items
5. Amnesia – loss of memory
 Prognosis: Irreversible
 Manifestations :
 Early: personality change, altered language pattern, neglect of personal appearance &
hygiene
 Progressive: Wandering, Incontinence, Sundowning, Confabulation
6. CEREBROVASCULAR ACCIDENT
 The medical term for a stroke. A stroke is when blood flow to a part of your brain is stopped
either by a blockage or the rupture of a blood vessel. There are important signs of a stroke
that you should be aware of and watch out for.
 May result from tumor, large blood clot, swollen brain tissue.
 The risk of stroke more than doubles for each decade after age 55. About 75% of new
strokes and 88% of stroke deaths occur in those ages 65 and older. About one third of all
initial stroke clients die within a year, with the percentage being higher in older adults.
About 2/3s of surviving stroke clients die within 12 years post stroke, although women
tend to out live men.
 The major issues for older persons who survive a stroke have:
1. activity limitations across multiple domains (basic and instrumental activities of daily
living)
2. psychological distress
3. communication difficulties.
 Stroke prevention are:
a. maintaining normal blood pressure
b. not smoking, exercising
c. maintaining normal weight.
 There are two main types of cerebrovascular accident, or stroke:
1. An ischemic stroke is caused by a blockage
2. A hemorrhagic stroke is caused by the rupture of a blood vessel. Both types of stroke
deprive part of the brain of blood and oxygen, causing brain cells to die.
 Ischemic stroke
 An ischemic stroke is the most common and occurs when a blood clot blocks a blood
vessel and prevents blood and oxygen from getting to a part of the brain. There are two
ways that this can happen. One way is an embolic stroke, which occurs when a clot forms
somewhere else in your body and gets lodged in a blood vessel in the brain. The other
way is a thrombotic stroke, which occurs when the clot forms in a blood vessel within the
brain.
 Hemorrhagic stroke
  A hemorrhagic stroke occurs when a blood vessel ruptures, or hemorrhages, and then
prevents blood from getting to part of the brain. The hemorrhage may occur in any blood
vessel in the brain, or it may occur in the membrane surrounding the brain.
 Symptoms of a cerebrovascular accident
 The quicker you can get a diagnosis and treatment for a stroke, the better your prognosis
will be. For this reason, it’s important to understand and recognize the symptoms of a
stroke.
 Stroke symptoms include:
1. difficulty walking
2. dizziness
3. loss of balance and coordination
4. difficulty speaking or understanding others who are speaking
5. numbness or paralysis in the face, leg, or arm, most likely on just one side of the body
6. blurred or darkened vision
7. a sudden headache, especially when accompanied by nausea, vomiting, or dizziness
 The symptoms of a stroke can vary depending on the individual and where in the brain it
has happened. Symptoms usually appear suddenly, even if they’re not very severe, and
they may become worse over time.
 Remembering the acronym “FAST” helps people recognize the most common symptoms
of stroke:
1. Face: Does one side of the face droop?
2. Arm: If a person holds both arms out, does one drift downward?
3. Speech: Is their speech abnormal or slurred?
4. Time: It’s time to call 911 and get to the hospital if any of these symptoms are present.

Assessment Findings During Stroke Progression

 When providing nursing care for people with strokes, it is important not only to understand
the cause of stroke but also to be able to recognize its precipitating & progressive
manifestations:
1. Headache, vomiting, seizures, coma, nuchal rigidity, fever, hypertension, ECG
abnormalities (prolonged ST segment), sclerosis of peripheral & retinal vessels,
confusion, disorientation, memory impairment, & other mental changes
 Focal warning signs:
1. hemiplegia, transient loss of speech, paresthesia involving half of the body
 General warning signs:
1. mental confusion, drowsiness, dizziness, headache
 Complete hemiplegia is common because the basal ganglia & adjacent internal capsule
are affected >2/3 of the time
 Speech center is usually located in the left side of the brain producing aphasia & right-
sided hemiplegia.
 Extensive cerebral lesions often produce conjugate deviation of the eyes or head or both
toward the lesion.
 Pupillary abnormalities may occur if the lesion produces edema pressing on the 3 rd cranial
nerve in the midbrain.
Intervention During Acute Phase Of Stroke
 First Aid
1. Maintain a patent airway
2. Loosen tight clothing to facilitate respiration & circulation to the head
3. Send for medical help & keep the person quiet
4. Position an unconscious patient on the side to facilitate drainage & prevent aspiration
 5. A conscious patient may be in the most comfortable position
6. Elevate patient’s head to avoid headache
7. If patient is cyanotic, administer O2 if available
8. Keep the patient warm
9. Offer assurance & explain procedures
 Treatment goals
1. Preserve life
2. Minimize residual disability
3. Prevent recurrence
 Nursing Intervention
 Assessment
1. Continuous NVS/GCS monitoring
2. Document changes in the level of consciousness, motor & sensory functions,
aphasia, respiratory difficulty, visual & perceptual defects
 Administer medications & fluids as prescribed
1. avoid sedatives, tranquilizers & opiates that depress the respiratory center
 Alteration in bowel elimination, constipation due to paralysis
1. encourage patient to avoid straining (increases intracranial & vascular pressures)
at bowel movement
2. bowel retraining as soon as possible
 Potential sleep pattern disturbance
1. create a restful, quiet atmosphere & planned periods of rest
2. don’t attempt to awake a lethargic patient

________________________________THE END ______________________________