Debre Brehan University School of Health Science Program of Nursing Medical-Surgical Nursing I

Peripheral Vascular disorder Prepared by Tesfa D. (B.Sc. In Nursing)

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Hypertension

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Learning objectives
On completion of this chapter, the learner will be able to: 1. Define blood pressure and identify risk factors for hypertension. 2. Explain the difference between normal blood pressure and hypertension and discuss the significance of hypertension. 3. Describe the treatment approach for hypertension, including lifestyle changes and medication therapy. 4. Use the nursing process as a framework for care of the patient with hypertension. 5. Describe the necessity for immediate treatment of hypertensive crisis.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Definition of terms
Dyslipidemia: abnormally high or low blood lipid levels. Hypertensive emergency: a situation in which blood pressure must be lowered immediately to prevent damage to target organs Hypertensive urgency: a situation in which blood pressure must be lowered within a few hours to prevent damage to target organs. JNC VI: Sixth Joint National Committee on the Prevention, Detection, Evaluation and Treatment of High Blood Pressure; committee established to study and make recommendations about hypertension in the United States. Findings and recommendations of JNC VI are contained in an extensive report published in 1997.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
Monotherapy: medication therapy with a single medication. Primary hypertension: also called essential hypertension; denotes high blood pressure from an unidentified cause. Rebound hypertension: pressure that is controlled with therapy and that becomes uncontrolled (abnormally high) with the discontinuation of therapy Secondary hypertension: high blood pressure from an identified cause, such as renal disease.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Introduction 
Blood pressure is the product of cardiac
output multiplied by peripheral resistance.
(BP=CO x PR) 

Cardiac output is the product of the
heart rate multiplied by the stroke volume.
(CO=HR x SV) 

In normal circulation, pressure is exerted by the flow of blood through the heart and blood vessels.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d 
High blood pressure, known as hypertension, can result from a change in; 

Cardiac output, Peripheral resistance, or Both.
The medications used for treating hypertension decrease peripheral resistance, blood volume, or the strength and rate of myocardial contraction.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Hypertension 
Hypertension is a systolic blood pressure
greater than 140 mm Hg and a diastolic pressure greater than 90 mm Hg over a sustained period, based on the average of two or more blood pressure measurements taken in two or more contacts with the health care provider after an initial screening.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Classification of Hypertension
1. Based on the responsible cause. A. Primary Hypertension meaning that the reason for the elevation in blood pressure cannot be identified. B. Secondary hypertension is the term used to signify high blood pressure from an identified cause (such narrowing of the renal arteries, renal parenchymal disease, hyperaldosteronism (mineralocorticoid hypertension), certain medications, pregnancy, and coarctation of the aorta).

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Based on the Measured BP
2. Based on the measured blood pressure.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d 
To say normal the measurement is done while the individual not taking antihypertensive drugs and not acutely ill. When systolic and diastolic blood pressures fall into different categories, the higher category should be selected to classify the individual·s blood pressure status. For example, 160/92 mm Hg should be classified as stage 2 hypertension, and 174/120 mm Hg should be classified as stage 3 hypertension. In addition to classifying stages of hypertension on the basis of average blood pressure levels, clinicians should specify presence or absence of target organ disease and additional risk factors. This specificity is important for risk classification and treatment.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
´The classification shows the direct relation between the risk of morbidity and mortality from hypertension and the level of systolic and diastolic blood pressures. ´The higher the systolic or diastolic pressure, the greater the risk. ´The JNC VI also developed recommendations for follow-up monitoring according to initial blood pressure readings at the time of diagnosis.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Recommendations for Follow-up Based on Initial Blood Pressure Measurements for Adults

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
*If systolic and diastolic categories are different, follow recommendations for shorter follow-up time (eg, 160/86 mm Hg, evaluate or refer to source of care within 1 month). ‚Modify the scheduling of follow-up according to reliable information about past blood pressure measurements, other cardiovascular risk factors, or target organ disease. ÂProvide advice about lifestyle modifications.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
Hypertension is sometimes called ´the silent killerµ because people who have it are often symptom free. In a national survey (1991 to 1994), 32% of people who had pressures exceeding 140/90 mm Hg were unaware of their elevated blood pressure (Burt et al., 1995a). Once identified, elevated blood pressure should be monitored at regular intervals because hypertension is a lifelong condition. Hypertension often accompanies risk factors for atherosclerotic heart disease, such as dyslipidemia and diabetes mellitus.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
High blood pressure can be viewed in three ways:

As a sign:- nurses and other health care
professionals use blood pressure to monitor a patient·s clinical status. A risk factor:- hypertension contributes to the rate at which atherosclerotic plaque accumulates within arterial walls.

A disease:-hypertension is a major contributor
to death from cardiac, renal, and peripheral vascular disease.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d 
Prolonged blood pressure elevation eventually damages blood vessels throughout the body, particularly in target organs such as the heart, kidneys, brain, and eyes.  The usual consequences of prolonged, uncontrolled hypertension are;

myocardial infarction,  heart failure,  renal failure,  strokes,  impaired vision, and  left ventricular hypertrophy (echocardiogram). 

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Risk factor 
Smoking. Dyslipidemia (elevated LDL cholesterol and /or low HDL cholesterol). DM. Impaired renal function (GFR <60ml/min and/or microalbuminuria).

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d 
Obesity. Physical inactivity. Age (older than 55years for men, 65 years for women). Family Hx of CVD (in female relative younger than 65 years or male relative younger than 55 years).

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cause and Pathophysiology 
Several hypotheses about the pathophysiologic bases of elevated blood pressure are associated with the concept of hypertension as a multifactorial condition. Hypertension may be caused by one or more of the following: 

Increased sympathetic nervous system activity.  Increased renal reabsorption of sodium, chloride, and water.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d 
Increased activity of the renin-angiotensinaldosterone system.  Decreased vasodilation of the arterioles. Resistance to insulin action. Hypertriglyceridemia. Obesity. Glucose intolerance.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Gerontologic considerations
‡ Structural and functional changes in the heart and blood vessels contribute to increases in blood pressure that occur with age. ‡ The changes include;
´ accumulation of atherosclerotic plaque, ´fragmentation of arterial elastins, ´ increased collagen deposits, and ´impaired vasodilation.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
The result of these changes is a decrease in the elasticity of the major blood vessels. Consequently, the aorta and large arteries are less able to accommodate the volume of blood pumped out by the heart (stroke volume), and the energy that would have stretched the vessels instead elevates the systolic blood pressure with out the change of diastolic pressure called Isolated systolic hypertension. Isolated systolic hypertension is more common in older adults.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Clinical manifestations
People with hypertension can be asymptomatic and remain so for many years. However, when specific signs and symptoms appear, they usually indicate vascular damage, with specific manifestations related to the organs served by the involved vessels. Physical examination may reveal no abnormalities other than high blood pressure.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
The manifestation is categorized based on the target organs of HTN
Eye;
Retinal hemorrhages, exudates (fluid accumulation), arteriolar narrowing, cottonwool spots (small infarctions), and papilledema (swelling of the optic disc) may be seen.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
Heart
Coronary artery disease (angina or myocardial infarction) Left ventricular hypertrophy heart failure.

Kidney
increased blood urea nitrogen [BUN] and creatinine levels) may manifest as nocturia.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
Cerebrovascular
stroke or transient ischemic attack (TIA), manifested by; alterations in vision or speech, dizziness, weakness, a sudden fall, or temporary paralysis on one side (hemiplegia).

o o o o o

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Assessment and diagnostic evaluation 
Health history. A risk factor assessment. Physical examination (Comprehensive). Laboratory studies; 
Urinalysis (BUN, creatinine, albumin, protein, renin). Blood chemistry (i.e., analysis of sodium, potassium, creatinine, fasting glucose, and total and high-density lipoprotein [HDL] cholesterol levels). Electrocardiogram (ECG).

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Medical management
‡ The goal of hypertension treatment is to;
´ Prevent death and complications by achieving and maintaining the arterial blood pressure at 140/90 mm Hg or lower. ´The JNC VI specified a lower goal pressure of 130/85 mm Hg for people with diabetes mellitus or with proteinuria greater than 1 g per 24 hours ( JNC VI, 1997).

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Algorithm of hypertension treatment

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Pharmacologic therapy

For patients with uncomplicated hypertension and no specific indications for another medication, the recommended initial medications include;
Diuretics, Beta-blockers, or Both.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
Patients are first given low doses of medication. If blood pressure does not fall to less than 140/90 mm Hg, the dose is increased gradually, and additional medications are included as necessary to achieve control. When the blood pressure has been less than 140/90 mm Hg for at least 1 year, gradual reduction of the types and doses of medication is recommended. To promote compliance, clinicians try to prescribe the simplest treatment schedule possible, ideally one pill once each day.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Preferred medication
1. Diuretics
A. Thiazide Diuretics (e.g. chlorothiazide (Diuril), hydrochlorothiazide (Esidrix;HydroDIURIL). B. Loop Diuretics (e.g. furosemide (Lasix)). C. Potassium-Sparing Diuretics (e.g. spironolactone (Aldactone)).

2. Adrenergic Agents
A. Peripheral Agents (e.g. reserpine (Serpasil)).

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
‡ B. Central Alpha Agonists (e.g. methyldopa (Aldomet)). Its site of action appears to be in the brain rather than in the periphery. C. Beta-Blockers (e.g. propranolol (Inderal)). D. Alpha Blocker (e.g. prazosin hydrochloride (Minipress)).

3. Vasodilators (e.g. hydralazine hydrochloride
(Apresoline), sodium nitroprusside (Nipride, Nitropress), nitroglycerin diazoxide (Hyperstat, NitroBid IV Tridil)). ,

4. Angiotensin-Converting Enzyme Inhibitors
(e.g. captopril (Capoten) enalapril (Vasotec), lisinopril (Prinivil, Zestril), ramipril (Altace)).

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d 5. Calcium Antagonists
A. Nondihydropyridines (e.g. verapamil) B. Dihydropyridines (e.g.nifedipine (Procardia Adalat CC), felodipine (Plendil), nicardipine (Cardene), nisoldipine (Sular)).

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Lifestyle modifications for hypertension prevention and management
Lose weight if overweight. Limit alcohol intake Increase aerobic physical activity. Reduce sodium intake. Maintain adequate intake of dietary potassium. Maintain adequate intake of dietary calcium and magnesium for general health. Stop smoking and reduce intake of dietary saturated fat and cholesterol for overall cardiovascular health.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
The DASH (Dietary Approaches to Stop Hypertension) Diet (Based on 2000 calories per day).

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Hypertensive crises 
There are two hypertensive crises that require nursing intervention: These are; 

Hypertensive emergency.  Hypertensive urgency. 
Hypertensive emergencies and urgencies may occur in patients whose hypertension has been poorly controlled or in those who have abruptly discontinued their medications.  Once the hypertensive crisis has been managed, a complete evaluation is performed to review the patient·s ongoing treatment plan and strategies to minimize the occurrence of subsequent hypertensive crises.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Hypertensive emergency
Hypertensive emergency is a situation in which blood pressure must be lowered immediately (not necessarily to less than 140/90 mm Hg) to halt or prevent damage to the target organs. Conditions associated with hypertensive emergency include acute myocardial infarction, dissecting aortic aneurysm, and intracranial hemorrhage. ´Hypertensive emergencies are acute, life threatening blood pressure elevations that require prompt treatment in an intensive care setting because of the serious target organ damage that may occur.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
´The medications of choice in hypertensive emergencies are those that have an immediate effect.
´Intravenous vasodilators, including; ´ Sodium nitroprusside (Nipride, Nitropress), ´Nicardipine hydrochloride (Cardene), ´Fenoldopam mesylate (Corlopam), ´Enalaprilat (Vasotec I.V.), and ´Nitroglycerin (Nitro-Bid IV, Tridil), have an immediate
action that is short lived (minutes to 4 hours), and they are therefore used as the initial treatment.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Hypertensive urgency
‡ Hypertensive urgency is a situation in which blood pressure must be lowered within a few hours. ‡ Severe perioperative hypertension is considered a hypertensive urgency.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d 
Hypertensive urgencies are managed with oral doses of fast-acting agents such as; 
loop diuretics (bumetanide [Bumex], furosemide [Lasix]). beta-blockers (propranolol (Inderal), metoprolol (Lopressor), nadolol (Corgard)). 

angiotensin-converting enzyme inhibitors

(benazepril [Lotensin], captopril [Capoten], enalapril [Vasotec]), calcium antagonists (diltiazem [Cardizem], verapamil [Isoptin SR, Calan SR, Covera HS]), or alpha2-agonists (Clonidine (Catapres) and guanfacine (Tenex)).

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Disorder of

Arteries

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Arteriosclerosis and Atherosclerosis 
Arteriosclerosis is the most common disease of the arteries, means hardening of the arteries. 
It is a diffuse process where by the muscle fibers and the endothelial lining of the walls of small arteries and arterioles become thickened. 

Atherosclerosis involves a different process, affecting the intima of the large and medium sized arteries. 
Atherosclerosis is usually present elsewhere in the body. These changes consist of the accumulation of lipids, calcium, blood components, carbohydrates, and fibrous tissue on the intimal layer of the artery. These accumulations are referred to as atheromas or plaques.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d 
Both occur together and used interchangeably. Atherosclerosis can develop at any point in the body, but certain sites are more vulnerable, typically bifurcation or branch areas. 
In the proximal lower extremity, these include the distal abdominal aorta, the common iliac arteries, the orifice of the superficial femoral and profunda femoris arteries, and the superficial femoral artery in the adductor canal. Distal to the knee, atherosclerosis occurs anywhere along the artery. There are no specific areas, such as arterial bifurcations, that are more vulnerable for atherosclerosis.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
Risk Factors
Modifiable
x x x x x x Nicotine use (i.e., tobacco smoking, chewing) Diet (contributing to hyperlipidemin) Hypertension Diabetes Stress Sedentary lifestyle

Non-modifiable
x Age x Gender

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
Clinical Manifestations The clinical signs and symptoms resulting from atherosclerosis depend on the organ or tissue affected.

Heart;
Coronary atherosclerosis (heart disease). Angina. Acute myocardial infarction.

Brain;
Cerebral ischemic attacks. Stroke.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
Aorta;
Aneurysm.

Extremities
Atherosclerotic lesions.

Kidney;
Renal artery stenosis. End-stage renal disease. Hypertension.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
Medical Management
Modification of risk factors. Controlled exercise program to improve circulation and increase the functioning capacity of the circulation. Medication. Interventional or surgical graft procedures.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
Prevention
Healthy diet (substituting unsaturated fats for saturated fats, and decreasing cholesterol intake). Exercise. Several classes of medication are used to prevent atherosclerosis: bile acid sequestrants (cholestyramine [Questran, Prevalite] or colestipol [Colestid]), nicotinic acid (niacin, B , Niacor; Niaspan), statins (atorvastatin [Lipitor], lovastatin [Mevacor], pravastatin [Pravachol], simvastatin [Zocor]), fibric acids (gemfibrozil [Lopid]), and lipophilic substances (probucol). Elimination of all controllable risk factors, particularly tobacco use, is strongly recommended.
3

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Aneurysm 
An aneurysm is a localized sac or dilation formed at a weak point in the wall of the aorta. It may be classified by its shape or form. The most common forms of aneurysms are; 
Saccular: aneurysm projects from one side of the vessel only. Fusiform: entire arterial segment becomes dilated. 

Very small aneurysms due to localized infection are called mycotic aneurysms.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d

(A) Normal artery. (B) False aneurysm. (C) True aneurysm. (D) Fusiform aneurysm. (E) Saccular aneurysm. (F) Dissecting aneurysm.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d

Causes
‡ Congenital:
Primary connective tissue disorders (Marfan·s syndrome, Ehlers-Danlos syndrome) and other diseases (tuberous sclerosis, Turner·s syndrome, Menkes· syndrome).

‡ Mechanical (hemodynamic):
Poststenotic and arteriovenous fistula and amputationrelated.

‡ Traumatic (pseudoaneurysms):
Penetrating arterial injuries. Blunt arterial injuries. Pseudoaneurysms.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
‡ Inflammatory (noninfectious):
Associated with arteritis (Takayasu·s disease, giant cell arteritis, systemic lupus erythematosus, Behçet·s syndrome, Kawasaki·s disease) and periarterial inflammation (i.e., pancreatitis)

‡ Infectious (mycotic):
Bacterial. Fungal. Spirochetal infections.

‡ Pregnancy-related degenerative:
Nonspecific, inflammatory variant.

‡ Anastomotic (postarteriotomy) and graft aneurysms:
Infection. Arterial wall failure, suture failure, graft failure.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Thoracic aortic aneurysm
‡ Approximately 85% of all cases of thoracic aortic aneurysm are caused by atherosclerosis. ‡ They occur most frequently in men between the ages 40 and 70 years. ‡ The thoracic area is the most common site for a dissecting aneurysm. ‡ About one third of patients with thoracic aneurysms die of rupture of the aneurysm.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
Clinical Manifestations
Pain (constant and boring occur in supine). Dyspnea. Cough(paroxysmal and with a brassy quality). Hoarseness. Stridor. Weakness or complete loss of the voice (aphonia). Dysphagia.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
Assessment and Diagnostic Findings
Hx. P/E.
x Superficial veins of the chest, neck, or arms become dilated. x Edematous areas on the chest wall and cyanosis. x Unequal pupils.

Chest x-ray. Transesophageal echocardiography. CT.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
Medical Management
Controlling blood pressure (Systolic pressure is maintained at about 100 to 120 mm Hg) with antihypertensive medications Correcting risk factors. Surgical repair.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Abdominal aortic aneurysm
The most common cause of abdominal aortic aneurysm is atherosclerosis. Most of these aneurysms occur below the renal arteries (infrarenal aneurysms).

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
Clinical Manifestations
Feeling their heart beating in their abdomen when lying down. Feel an abdominal mass or abdominal throbbing. Blue toes.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
Assessment and Diagnostic Findings
Hx. P/E.
x a pulsatile mass in the middle and upper abdomen. x A systolic bruit may be heard over the mass.

Ultrasonography or CT is used to determine the size, length, and location of the aneurysm.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
Medical Management 
Surgical graft.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Arterial embolism and arterial thrombosis 
Acute vascular occlusion may be caused by an embolus or acute thrombosis. Cause 
Iatrogenic injury (during insertion of invasive catheters such as those used for arteriography, or an intra-aortic balloon pump).  Fracture.  Crush injury.  Penetrating wounds.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
Pathophysiology o Arterial emboli arise most commonly from thrombi that develop in the chambers of the heart (as a result of atrial fibrillation, myocardial infarction, infective endocarditis, or chronic heart failure). o These thrombi become detached and are carried from the left side of the heart into the arterial system, where they lodge in and obstruct an artery that is smaller than the embolus.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
Clinical Manifestations  The six P·s associated with acute arterial embolism are; 

Pain.  Pallor.  Pulselessness.  Paresthesia.  Poikilothermia (coldness).  Paralysis.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
Assessment and Diagnostic Findings
Hx. P/E. Echocardiography. Chest x-ray. Electrocardiography. Ultrasonography. Arteriography.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
Medical Management Management of arterial thrombosis depends on its cause. Management of acute embolic occlusion usually requires surgery because time is of the essence. Heparin therapy (an initial bolus of 5,000 to 10,000 units) is administered intravenously, followed by a continuous infusion of 1,000 units per hour until the patient is able to undergo surgery.

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Cont«d
Surgical management
Emergency embolectomy.

Nursing Management 
Preoperative care.  Postoperative care.

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Disorder of Veins

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Phlebitis 
Is inflammation of a vein related to both a chemical and mechanical irritation. 

Common complication of intravenous therapy. The incidence depends on with; Length of the therapy, 
Cannula size, Medication type.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d Clinical Manifestation
Redness. Warm area along the vein or localized. Pain, tenderness at the site. Swelling.

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Cont«d Managements
D/C (Discharge) IV fluid. Restart in another site. Applying a warm moist compress.

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Cont«d
Prevention Use aseptic technique. Use appropriates size cannula. Consider the compositions of fluids and medications when selecting a site. Observe the site for any complications every hour.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Thrombophlebitis and Phlebothrombosis 

Thrombophlebitis is inflammation of
the walls of the veins and frequently accompanied by the formation of a clot. 

Phlebothrombosis is when a clot
develops initially in the veins as a result of stasis or hypercoagulablity, but with out inflammation.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
Venous thrombosis can occur in any vein but occurs most frequently in the veins of the lower extremities. Both the superficial and deep veins of the legs may be affected. Of the superficial veins, the saphenous vein is mostly frequently affected. Of the deep leg veins, the iliofemoral, popliteal, and small calf veins are most often involved.

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Cont«d

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Cont«d
Exact cause of venous thrombosis remains unclear, but three factors are believed to play a significant role in its development:

1. Stasis of blood. 2. Vessel wall injury. 3. Altered blood coagulation. The presence of at least two factors appears to be necessary for thrombosis to occur.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
1. Stasis of blood. 
Venous stasis occurs; 
When blood flow is retarded (i.e. heart failure or shock).  When veins are dilated, as a result of medication therapy.  When skeletal muscle contraction is reduced, as with immobility, extremity paralysis, or anesthesia.  Bed rest has been shown to reduce blood flow in the legs by at least 50%.

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Cont«d
2. Vessel wall injury 
Damage to the intimal lining of blood vessels, creates a site for clot formation.  Direct trauma to the vessels, such as occurs following a fracture or dislocation, diseases of the veins, and chemical irritation of veins from intravenous medication. All surgical patients are at risk for deep vein thrombosis (DVT).

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Cont«d
Clinical Manifestations As many as 50% of all patients with venous thrombosis of the lower extremities have no symptom. In others symptoms are variable and not usually specific for thrombophlebitis.

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Cont«d ‡ Deep Veins;
Tenderness . Heaviness· on standing position. Cramping leg pain. Swelling.
Pain on the calf (not specific to DVT). Sign of pulmonary embolus.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Cont«d
‡ Superficial veins (dissolve spontaneously so risk of dislodge or fragmenting is low). Pain or tenderness. Redness and warmth in the involved area. Local swelling: bumpy and knotty. Red tender, local indurations on saphenous vein.

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Cont«d 
Diagnostic evaluation

For superficial x Venography. x Venous scanning.

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Cont«d Management
Bed rest. Elevation of leg. Analgesics. Anti-inflammatory medication.

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Lecture Note for Second Year Regular Nursing Student, November 2003/2010.

Varicose veins 
Varicose veins (varicosities) are abnormally
dilated, tortuous, superficial veins caused by incompetent venous valves. Most commonly, this condition occurs in the lower extremities, the saphenous veins, or lower trunk. However, it can occur elsewhere in the body (e.g. esophageal varices).

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Cont«d
Pathophysiology  It can be; Primary varicose veins (which is not involving the deep veins). Secondary varicose veins (resulting from obstruction of deep veins).

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Cont«d
C/F For superficial vein involvement no symptoms
x Dilated vein make trouble by the cosmetic appearance.

If symptoms occurs
x x x x x Dull aching pain. Cramp. Increased muscle fatigue in the lower leg. Ankle edema. Felling heaviness of the legs.

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Cont«d
Deep vein involvement;
x x x x x Edema. Pain. Pigmentation. Ulceration. Susceptibility to injury and infection is increased.

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Cont«d
Diagnostic evaluation Brodie- tendelenburg test. Perthe·s test. Additional diagnosis veins.

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Cont«d
‡ Prevention Avoid venous stasis by wearing tight. Elevating the leg. Change position frequently. Elastic stoking (knee- high). Weight reduction. Walking up the stairs.

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Cont«d
‡ Management Surgery. Sclerotherapy.

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Varicose Ulcer
Varicose ulcers: A condition which is characterized by an ulcer due varicose veins. Cause
Varicose veins. Phlebitis. Deep vein thromobosis. Leg trauma. Rheumatoid arthritis. Osteoarthritis Septic arthritis. Patellar tendonitis. Compartment syndrome.

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Cont«d
C/M  Localized destruction of tissue - usually on the skin of lower legs.  Localized swelling.  Brownish discoloration.

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Disorder of Lymphatic System

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The lymphatic system consists of a set of vessels that spread throughout most of the body. These vessels start as lymph capillaries that drain unabsorbed plasma from the interstitial spaces (spaces between the cells). The lymphatic capillaries unite to form the lymph vessels, which pass through the lymph nodes and then empty into the large thoracic duct that joins the jugular vein on the left side of the neck. The fluid drained from the interstitial space by the lymphatic system is called lymph. The flow of lymph depends on the intrinsic contractions of the lymph vessels, the contraction of muscles, respiratory movements, and gravity.

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Lymphangitis 
It is a spread of infection from a cellulitis or abscess to the lymphatic system. Lymphangits is an acute inflammation of the lymphatic channels. It arises most commonly from a focus of infection in an extremity.

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Cont«d
Cause Cellulitis. Hemolytic streptococcus. C/F Red streaks that extend up the arm or the leg from an infected wound outline the course of the lymphatic vessels as they drain. Rx Antibiotic.

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lymphadenitis 
The lymph nodes located along the course of the lymphatic channels also become enlarged, red, and tender (acute lymphadenitis). They can also become necrotic and form an abscess (suppurative lymphadenitis). The nodes involved most often are those in the groin, axilla, or cervical region.

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Cont«d
Rx 

An elastic compression stocking or sleeve should be worn on the affected extremity for several months to prevent long-term edema. Antibiotics.

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Lymphedema 
Tissue swelling occurs in the extremities because of an increased quantity of lymph that results from obstruction of lymphatic vessels.  It is especially marked when the extremity is in a dependent position.  Lymphedemas are classified as; Primary (congenital malformations)  The most common type is congenital lymphedema (lymphedema praecox), which is caused by hypoplasia of the lymphatic system of the lower extremity.  This disorder is usually seen in women and first appears between ages 15 and 25.

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Cont«d
Secondary (acquired obstructions)  The obstruction may be in the lymph nodes and the lymphatic vessels.  Sometimes, it is seen in the arm after an axillary node dissection (eg, for breast cancer) and in the leg in association with varicose veins or chronic thrombophlebitis. C/M  Initially, the edema is soft, pitting, and relieved by treatment.  As the condition progresses, the edema becomes firm, nonpitting, and unresponsive to treatment.

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Cont«d
Medical Management ‡ The goal of therapy is to reduce and control the edema and prevent infection. ‡ It includes; ‡ Active and passive exercises. ‡ External compression (custom-fitted elastic compression stockings or sleeves are worn; those with the highest compression strength (exceeding 40 mm Hg). ‡ Strict bed rest with the leg elevated. ‡ Medication (diuretic furosemide (Lasix), antibiotic).

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Cont«d
Surgical management
‡ Surgery is performed if the edema is severe and uncontrolled by medical therapy, if mobility is severely compromised, or if infection persists. ‡ One surgical approach involves the excision of the affected subcutaneous tissue and fascia, with skin grafting to cover the defect. ‡ Another procedure involves the surgical relocation of superficial lymphatic vessels into the deep lymphatic system by means of a buried dermal flap to provide a conduit for lymphatic drainage.

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Cont«d
Nursing Management ‡ Prophylactic antibiotics may be prescribed for 5 to 7 days. ‡ Constant elevation of the affected extremity and observations for complications. ‡ The nurse instructs the patient or caregiver to inspect the dressing daily. ‡ The patient is informed that there may be a loss of sensation in the skin graft area. ‡ The patient is also instructed to avoid the application of heating pads or exposure to sun to prevent burns or trauma to the area.

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Elephantiasis 
Elephantiasis is lymphatic obstruction caused by a parasite (filaria) is seen frequently in the tropics. Pathophysiology  When chronic swelling is present, there may be frequent bouts of acute infection characterized by high fever and chills and increased residual edema after the inflammation has resolved.

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Cont«d 
These lead to chronic fibrosis, thickening of the subcutaneous tissues, and hypertrophy of the skin.  This condition, in which chronic swelling of the extremity recedes only slightly with elevation. C/M  Elephant like skin (rough). Rx  Minimize the risk of exposure to filaria.

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Lymphoma 
The lymphomas are neoplasms of cells of lymphoid origin.  These tumors usually start in lymph nodes but can involve lymphoid tissue in the spleen, the gastrointestinal tract (eg, the wall of the stomach), the liver, or the bone marrow.  They are often classified according to the degree of cell differentiation and the origin of the predominant malignant cell.  Lymphomas can be broadly classified into two categories: Hodgkin·s disease (HL) and non-Hodgkin·s lymphoma (NHL).

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Hodgkin·s disease
‡ Hodgkin·s disease is a relatively rare malignancy that has an impressive cure rate. ‡ It is somewhat more common in men than women and has two peaks of incidence: one in the early 20s and the other after 50 years of age. ‡ It is unicentric in origin in that it initiates in a single node. ‡ The disease spreads by contiguous extension along the lymphatic system.

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Cont«d
‡ The malignant cell of Hodgkin·s disease is the Reed-Sternberg cell, a gigantic tumor cell that is morphologically unique and is thought to be of immature lymphoid origin. Cause 
It is unknown, but a viral etiology (Epstein-Barr virus) is suspected. Heredity (first degree relatives).

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Cont«d
Clinical Manifestations
‡ Lymphadenopathy (a painless, firm but not hard enlargement of one or more lymph nodes on one side of the neck). ‡ The most common sites for are the cervical, supraclavicular, and mediastinal nodes. ‡ Pruritus. ‡ Severe pain after drinking alcohol.

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Cont«d
Assessment and Diagnostic Findings 
Health history.  Physical examination.  Lymph node biopsy and the finding of the Reed-Sternberg cell.  A chest x-ray and a CT scan of the chest, abdomen, and pelvis are crucial to identify the extent of lymphadenopathy within these regions.  Laboratory tests include CBC, platelet count, ESR, and liver and renal function studies.  A bone marrow biopsy is performed if there are signs of marrow involvement.  Bone scans may be performed to identify any involvement in these areas.  A staging laparotomy and lymphangiography.

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Cont«d
Medical Management ‡ Early Hodgkin·s disease was treated by a staging laparotomy followed by radiation therapy. ‡ A short course (2 to 4 months) of chemotherapy followed by radiation therapy in certain subsets of early-stage disease (IA and IIA). ‡ Combination chemotherapy, for example with doxorubicin (Adriamycin), bleomycin (Blenoxane), vinblastine (Velban), and dacarbazine (DTIC), referred to as ABVD, is now the standard treatment for more advanced disease (stages III and IV and all B stages).

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Cont«d
Potential Long-Term Complications of Therapy for Hodgkin·s Disease 
       

Immune dysfunction. Herpes infections (zoster and varicella) Pneumococcal sepsis. Acute myeloid leukemia (AML) Non-Hodgkin·s lymphoma Solid tumors Thyroid cancer Thymic hyperplasia Hypothyroidism

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Cont«d 
       

Pericarditis (acute or chronic) Cardiomyopathy Pneumonitis (acute or chronic) Avascular necrosis Growth retardation Infertility Impotence Myelodysplastic syndromes (MDS) Dental caries

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Non-hodgkin·s lymphomas (NHLs)
‡ The NHLs are a heterogeneous group of cancers that originate from the neoplastic growth of lymphoid tissue. ‡ Most NHLs involve malignant B lymphocytes; only 5% involve T lymphocytes. ‡ In contrast to Hodgkin·s disease, the lymphoid tissues involved are largely infiltrated with malignant cells.

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Cont«d
‡ Lymph nodes from multiple sites may be infiltrated, as may sites outside the lymphoid system (extranodal tissue). ‡ The incidence increases with each decade of life; the average age at diagnosis is 50 to 60 years. ‡ Although no common etiologic factor has been identified, there is an increased incidence of NHL in people with; 
Immuno-deficiencies or autoimmune disorders.  Viral infections (including Epstein-Barr virus and HIV).  Exposure to pesticides, solvents, or dyes.

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Cont«d
Clinical Manifestations ‡ The pt develop manifestation at these stages (III or IV). ‡ Lymphadenopathy. ‡ Recurrent fever. ‡ Drenching night sweats. ‡ Unintentional weight loss of 10% or more.

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Cont«d
Assessment and Diagnostic Findings ‡ CT scans. ‡ Bone marrow biopsies. ‡ Occasionally cerebrospinal fluid analysis.

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Cont«d
Medical Management ‡ Treatment is based on the actual classification of disease, the stage of disease, prior treatment (if any), and the patient·s ability to tolerate therapy. ‡ More intermediate forms are commonly treated with combination chemotherapy and radiation therapy for stage I and II disease.

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Cont«d

Hematologic Disorder

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1. Anemia 
Anemia is a term that indicates a low red cell count and a below ±normal hemoglobin or hematocrit level. It is not a disease but rather reflects a disease state or altered body function. There are different kinds of anemia's;
Due to inadequate production of red blood cells secondary to chronic diseases (aplastic anemia). Premature or excessive destruction of red blood cells (hemolytic anemia). Due to excessive blood loss (iron deficiency anemia). Deficits in nutrients ,such as vit B12, folic acid (megaloblastic anemia).

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Classification of Anemia A. Aplasitc anemia 
Aplastic anemia occurs when the bone marrow produces too few of all types of blood cells: red cells, white cells, and platelets. A reduced number of red blood cells causes the hemoglobin (a type of protein in the red blood cells that carries oxygen to the tissues of the body) to drop. A reduced number of white blood cells causes the patient to be susceptible to infection. A reduced number of platelets can cause the blood not to clot as easily.

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Cont«d
Risk factors ‡ Treatment with high-dose radiation or chemotherapy for cancer ‡ Exposure to toxic chemicals ‡ Use of some prescription drugs ² such as chloramphenicol, which is used to treat bacterial infections, and gold compounds used to treat rheumatoid arthritis ² that are known to rarely induce aplastic anemia ‡ Certain blood diseases, autoimmune disorders and serious infections ‡ Pregnancy, rarely.

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Cont«d
Causes High-dose radiation and chemotherapy treatments. Exposure to toxic chemicals (e.g. exposure to benzene). Use of certain drugs (medications used to treat rheumatoid arthritis). Autoimmune disorders (e.g. lupus). A viral infection (e.g. hepatitis, Epstein-Barr, cytomegalovirus, parvovirus B-19 and HIV). Pregnancy. Unknown factors/idiopathic.

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Cont«d
C/F ‡ Fatigue ‡ Shortness of breath with exertion ‡ Rapid or irregular heart rate ‡ Pale skin ‡ Frequent or prolonged infections ‡ Unexplained or easy bruising ‡ Nosebleeds and bleeding gums ‡ Prolonged bleeding from cuts ‡ Skin rash ‡ Dizziness ‡ Headache

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Cont«d
Dx ‡ Blood tests. ‡ Bone marrow biopsy.

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Cont«d
Treatments  Blood transfusions.  Bone marrow transplantation.  Immuno suppressants (such as cyclosporine and anti-thymocyte globulin (Thymoglobulin).  Corticosteroids (such as methylprednisolone).  Bone marrow stimulants (such as sargramostim (Leukine), filgrastim (Neupogen)).  Antibiotics, anti-virals.

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B. Iron²deficiency anemia 
Iron deficiency anemia is a specific type of anemia that is usually caused by blood loss or decreased absorption of iron from foods. Iron deficiency anemia can be mild or severe, and can be temporary or chronic. The condition is common in the United States, affecting 1 to 2 percent of adults. It is even more common in developing countries, primarily due to differences in diet.

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Cont«d
Causes
‡ Two common causes of iron deficiency anemia are blood loss (most common) and decreased absorption of iron from food. 1. Blood loss :² The source of blood loss may be obvious, such as repeated blood donations, trauma, surgery, heavy menstrual bleeding, bleeding in digestive tract. 2. Decreased iron absorption:² If the GI tract is not functioning correctly, as in people with certain conditions (eg, celiac disease, gastritis, ulcer, H. pylori infection), an inadequate amount of iron may be absorbed. 3. Other causes ² A common cause of iron deficiency anemia in developing countries is a lack of foods that contain iron.
1. 2. Vegetarians are at increased risk for developing iron deficiency anemia because iron from plant sources is not absorbed as readily as iron from meat sources. Pregnant women often develop iron deficiency anemia because of the increased iron requirements of the growing fetus and placenta, and the increased volume of blood circulating in the woman's body during pregnancy.

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Cont«d
C/M  Weakness  Headache  Irritability  Fatigue  Difficulty exercising (due to shortness of breath, rapid heart beat) ‡ Less common symptoms; 
brittle nails,  sore tongue,  restless legs syndrome,  Pica (it is an abnormal craving to eat non-food items, such as clay or dirt, paper products, or starch (eg, cornstarch)).  Pagophagia (It is an abnormal craving to eat ice).

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Cont«d
Diagnosis ‡ Medical history. ‡ Physical examination. ‡ Blood tests.
Complete blood count
x It includes a red blood cell count, Hgb, and Hct-low. x It also includes the mean corpuscular volume (MCV, referring to the cell size-microcytic), mean corpuscular hemoglobin (MCH, referring to the cell colorhypochromic), and others.

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Cont«d
Further testing includes measure of;  Serum iron.  Total iron binding capacity (TIBC or transferrin).  Transferrin saturation.  Ferritin.

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Cont«d
Mgx ‡ Search for cause of iron deficiency. ‡ Ferrous sulfate, ferrous gluconate, ferrous fumarate most effective less expensive. ‡ Blood transfusion (their hemoglobin or hematocrit level is very low (eg, hemoglobin less than 7 g/dL or hematocrit less than 20 percent)). ‡ Rx continued for years. Nursing intervention ‡ Pt education food source high in iron include organ meats (liver, cow, chicken leafy vegetables ‡ Vitamin C enhance absorption. ‡ Avoid antacid.

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Megaloblastic anemia·s
‡ Megaloblastic anemia is the end-product of deficiencies in the B vitamins folate or vitamin B12 (also called cobalamin), or both. Such deficiencies produce abnormally large red blood cells (megaloblastic) that have a shortened lifespan.

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Cont«d
Causes (Vitamin B12 deficiency) ‡ Vitamin B12 deficiency from diet. ‡ Pernicious anemia. ‡ Complications of gastrointestinal surgery. ‡ Overgrowth of intestinal bacteria. ‡ Tropical sprue (an acquired malabsorption disease occurring in tropical climates).

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Cont«d
Causes (folate deficiency) ‡ Poor diet coupled with alcoholism. ‡ Any condition that disturbs the small intestine and impairs its absorption ability (inflammatory bowel disease). ‡ Parasitic diseases, such as giardiasis. ‡ Short bowel syndrome. ‡ High demand for folic acid caused by conditions such as cancer, pregnancy, severe psoriasis, severe hyperthyroidism, and hemolytic anemia. ‡ Some drugs, including phenytoin, methotrexate, trimethoprim, and triamterene.

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Cont«d
C/M ‡ Skin Color (pale all over the body). ‡ lack of appetite. ‡ weight loss. ‡ Mouth and Tongue soreness. ‡ Numbness in the hands and the feet. ‡ Nausea ‡ vomiting.

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Cont«d
Dx  Complete blood count (shows anemia with large red blood cells).  Bone marrow examination (can help show whether your bone marrow is healthy and making enough red blood cells).  Serum B12 (can help show vitamin B12 blood level).  Schilling test (detect vitamin B12 absorption).  Serum folate (can help show whether you have pernicious anemia or another type of anemia).

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Cont«d
Rx ‡ Preventing or treating the anemia and its signs and symptoms. ‡ Controlling complications, such as heart and nerve damage. ‡ The treatment depends on the cause. ‡ Usually treatment may include vitamin B12 injections and folic acid supplement. ‡ A well-balanced diet is essential to provide other elements for healthy blood cell development, such as folic acid, iron, and vitamin b12. ‡ Which foods are contain rich folic acid and vitamin B12: eggs meat poultry milk shellfish

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Hemolytic anemia
‡ Hemolytic anemia is a blood disorder in which the red blood cells are destroyed prematurely. ‡ The cells are broken down at a faster rate than the bone marrow can produce new cells. ‡ The term for destruction of red blood cells is hemolysis. ‡ Hemolysis may occur by two mechanisms:
Extravascular (most common): red cells are removed from the circulation by the mononuclear-phagocytic system either because they are intrinsically defective or because of the presence of bound immunoglobulins to their surfaces. Intravascular: due to complement fixation, trauma, or other extrinsic factors. Examples are prosthetic cardiac valves, glucose-6-phosphate dehydrogenase deficiency, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation and paroxysmal nocturnal hemoglobinuria.

‡ Hemolytic anemias, which result from the increased destruction of red blood cells, are less common than anemias caused by excessive blood loss or lack of red blood cell production, or high rates of red blood cell destruction.

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Cont«d
Types of Hemolytic anemia 1. Inherited Hemolytic Anemia 
One or more of the genes that control red blood cell production are faulty.  The defects may involve the hemoglobin, cell membrane, or enzymes that maintain healthy red blood cells.  The abnormal cells may be fragile and break down while moving through the bloodstream. If this happens, an organ called the spleen may remove the cell debris from the bloodstream.  Inherited hemolytic anemias are often inherited, such as sickle cell anemia, thalassemia and hereditary spherocytosis, in addition to include G6PD Deficiency.

2. Acquired Hemolytic Anemia 
your red blood cells may be normal.  However, some other disease or factor causes the body to destroy red blood cells and remove them from the bloodstream.  Acquired Hemolytic anemias, such as Autoimmune hemolytic anemia.

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Cont«d
Causes 
The immediate cause is the early destruction of red blood cells.  A number of diseases, conditions, and factors can cause the body to destroy its red blood cells.  Inherited hemolytic anemias are caused by; 
inborn defects in components of the red blood cells, the cell membrane, the enzymes, or the hemoglobin. 

Acquired hemolytic anemias cuased by; 
Infections, such as hepatitis, cytomegalovirus, typhoid fever, escherichia coli, or streptococcus.  Medications, such as penicillin, antimalaria medications, sulfa medications, acetaminophen.  Autoimmune disease, such as systemic lupus erythematous (SLE, or lupus), rheumatoid arthritis, Wiskott-Aldrich syndrome, or ulcerative colitis.  Lymphocytic leukemia or lymphoma.

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Cont«d
C/M ‡ abnormal paleness or lack of color of the skin ‡ jaundice, or yellowing of the skin, eyes, and mouth ‡ dark color to urine ‡ fever ‡ weakness ‡ dizziness ‡ confusion ‡ intolerance to physical activity ‡ enlargement of the spleen and liver ‡ increased heart rate (tachycardia) ‡ heart murmur

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Cont«d
Dx Blood tests.  Reticulocyte count. Peripheral smear. Haptoglobin. Bilirubin test. Hemoglobin electrophoresis. Urine test. Urobilinogen in the urine. Bone marrow aspiration and biopsy.

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Cont«d
Mgx Treat the underlying course. Blood transfusion.

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Leukemias
‡ Leukemias is a malignant disorder of the hematopoietic system involving the bone marrow and lymph nodes. ‡ It is characterized by;
Uncontrolled proliferations of leukocytes, myelocytes and their precursors. Enlargement of organ of hematopoiesis. Thrombocytopenia. Anemia due to immature WBCs.
x Decreased immunocompetence. x Increased suseptabity to infection.

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Cont«d
Classification ‡ The leukemias are classified as acute or chronic and are further subdivided according to cell type or maturity. 1. Acute leukemias
Rapid on set. Short course ending in death if un treated.

2. Chronic leukemias
Insidious onset

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Cont«d
‡ ‡ ‡ ‡ Acute lymphocytic leukemia It is a malignant disorder arising from lymphoid stem cell. Cause is unknown. Affect age b/n 2 to 4 years and incidence decrease after 10 years of age. It is a malignant disorder arising from a single lymphoid stem cell with impaired maturation and accumulation of malignant cell in the bone marrow.

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Cont«d
Signs and symptoms
Anemia Bleeding Lymphadenopathy Predisposition to infection

Diagnosis
Blood smear may show immature lymphoblast. Platelet count and HCT level are reduced in most patients.

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Cont«d
Nursing intervention Family education. High protein fiber, and fluid diet. Avoid infection (hand washing, avoid crowds). Report injury, any sign of bleeding and infection. Avoid spicy, hot food. Acute myelogenous leukemia ‡ AML arises from a single myeloid stem cell and is characterized by the development of immature myeloblasts in the bone marrow.

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Cont«d
Chronic lymphocytic leukemia ‡ CLL is characterized by a proliferation of small, abnormal, mature lymphocytes after leading to decreased synthesis of immunoglobulins and depressed antibody response. Chronic myelogenous leukemia
Onset is 4th and 3rd decade.

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Cont«d
‡ Uncontrolled proliferation of the granulocytosis cell;
Basophils Esnophils Neutrophils Circulating granulocytes increase. Polycythemia Hemocytoblast stem cell.

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Cont«d

Hemorrhagic disorder

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Thrombcytosis 
It is the presence of abnormally high number of circulating platelets Mild bleeding syndromes may be caused by quantitatively normal but functionally defective platelets.

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Thrombocytopenia
‡ Thrombocytopenia is defined as a lower than normal number of circulating platelets. ‡ Normal range 150,000 to 400,000/mm3. Cause ‡ Decreased platelet production. ‡ Decreased platelet survival. ‡ Increased platelet destruction (common cause drug induced). ‡ Sequestration of blood in the spleen (splenomegaly). ‡ Loss from hemorrhage.

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Cont«d
C/F
P/E
x Petechiae ± skin spot, purple hemorrhagic spot. x Only in platelet disorder. x Ecchymosis ± blue ±black larger in diameter irregular. x Purpura.

Hx
x Menorrhagia. x Epistaxis. x Gingival bleeding.

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Cont«d
Dx ‡ Platelet count. ‡ Peripheral blood smear. ‡ Bleeding time. ‡ Bone marrow examination.

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Cont«d
Treatment
Corticosteroid (most common treatment ). Immununoglobulin. Splenectomy . Danazol and immunosuppressive drug. Platelet transfusion.

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Cont«d
Nursing care ‡ Avoiding trauma ‡ Bleeding associated with trauma is likely with a platelet count less than 60,000/mm3 . ‡ Spontaneous hemorrhage may be a life ²threatening possibility when the platelet count is be low 20, 000/mm3 . ‡ Be alert for an increase in ecchymosis or petechiae, and bleeding from other sites and change in mental status. ‡ Pt with platelet count below 20,000mm3 have bleeding precaution;
Test all urine and stools for blood. Do not take temperature rectally. Do not administer intramuscular injections. Apply pressure to all venus puncture site for 5 minutes and 10 arterial puncture site for 10min.

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Hemophilia
‡ Hemophilia is a hereditary coagulation disorder. ‡ Factors:-deficiency, inherited as sex linked recessive disorders and are exclusively limited to males. C/F ‡ Hx of excessive bleeding after circumcision or dental extractions. ‡ Lifelong bleeding. ‡ Bleeding can be spontaneous or after trauma. Dx ‡ Specific assays for factors VIII, lX, Xl. ‡ Partial thromboplastin time (PTT).

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Cont«d
Complication
Joint deformity Retroperitoneal bleeding. Intracranial, paratracheal soft tissue hemorrhages.

Mgx
Replacement of the deficient coagulation factor where bleeding episodes do not respond to local treatment.

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Vitamin K deficiency
‡ Vitamin K, a fat ² soluble vitamin, is a cofactor in the synthesis of clotting factors II, VII, lX, and X, obtained from diet, and by intestinal bacteria. Cause ‡ Decreased intake. ‡ Broad ² spectrum antibiotics. ‡ Absorption problem i.e. ulcerative colitis. ‡ Drugs interfere with vitamin K function
x Salicylates x Guanine x Bribitureates

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Cont«d
C/F ‡ Bleeding of mucous membranes and into the tissues. ‡ Post operative hemorrhage. ‡ In severe case measure GI bleeding. Dx ‡ Prolonged PTT. ‡ Decreased in the level of vitamin K dependent clotting factors. Rx ‡ Vitamin K parenteral and oral preparation.

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³Education is Enabling an individual to win victory over the five victory's; lust, anger, greed, infatuation and ego.´ (Nanak, Gruru)

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