medical surgical nursing:periphero vascular disorder

8/6/2019 Medical Surgical Nursing:Periphero Vascular Disorder.

1/165

Peripheral Vascular disorderPrepared by Tesfa D.

(B.Sc. In Nursing)

Debre Brehan University

School of Health ScienceProgram of Nursing

Medical-Surgical Nursing I


2/165

Hypertension

Lecture Note for Second

Year Regular Nursing

Student, November

2003/2010.

2


3/165

Learning objectivesOn 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 ofhypertension.

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.



Student, November

2003/2010.

3


4/165

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 targetorgansHypertensive urgency: a situation in which blood pressure

must be lowered within a few hours to prevent damage totarget organs.

JNC VI: Sixth Joint National Committee on the Prevention,Detection, Evaluation and Treatment of High BloodPressure; committee established to study and makerecommendations about hypertension in the United States.Findings and recommendations of JNC VI are contained inan extensive report published in 1997.



Student, November

2003/2010.

4


5/165

Contd

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.



Student, November

2003/2010.

5


6/165

Introduction

Blood pressure is the product of cardiac

output multiplied by peripheral resistance.(BP=CO x PR)

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

In normal circulation, pressure is exertedby the flow of blood through the heart and

blood vessels.



Student, November

2003/2010.

6


7/165

Contd

High blood pressure, known as hypertension, canresult from a change in;

Cardiac output,Peripheral resistance, orBoth.

The medications used for treatinghypertension decrease peripheral resistance,blood volume, or the strength and rate ofmyocardial contraction.



Student, November

2003/2010.

7


8/165

Hypertension

Hypertension is a systolic blood pressuregreater than 140 mm Hg and a diastolic pressuregreater 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.



Student, November

2003/2010.

8


9/165

Classification ofHypertension

1. Based on the responsible cause.

A. Primary Hypertension meaning that the reason forthe elevation in blood pressure cannot beidentified.

B. Secondary hypertension is the term used to signifyhigh blood pressure from an identified cause (such

narrowing of the renal arteries, renal parenchymaldisease, hyperaldosteronism (mineralocorticoidhypertension), certain medications, pregnancy, andcoarctation of the aorta).



Student, November

2003/2010.

9


10/165

Based on the Measured BP

2. Based on the measured blood pressure.



Student, November

2003/2010.

10


11/165

Contd

To say normal the measurement is done while the individualnot taking antihypertensive drugs and not acutely ill.

When systolic and diastolic blood pressures fall intodifferent categories, the higher category should be selected toclassify the individuals 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 3hypertension.

In addition to classifying stages of hypertension on thebasis of average blood pressure levels, clinicians shouldspecify presence or absence of target organ disease andadditional risk factors. This specificity is important for riskclassification and treatment.



Student, November

2003/2010.

11


12/165

Contd

The classification shows the direct relation between

the risk of morbidity and mortality fromhypertension 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.



Student, November

2003/2010.

12


13/165

Recommendations for Follow-up Based on Initial

Blood Pressure Measurements for Adults



Student, November

2003/2010.

13


14/165

Contd

*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 pressuremeasurements, other cardiovascular risk factors, or

target organ disease.

Provide advice about lifestyle modifications.



Student, November

2003/2010.

14


15/165


16/165

Contd

High blood pressure can be viewed in three ways:

As a sign:- nurses and other health careprofessionals use blood pressure to monitor apatients clinical status.

A risk factor:- hypertension contributes to therate at which atherosclerotic plaque accumulateswithin arterial walls.

A disease:-hypertension is a major contributorto death from cardiac, renal, and peripheral vasculardisease.



Student, November

2003/2010.

16


17/165

Contd

Prolonged blood pressure elevation eventually damagesblood 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).



Student, November

2003/2010.

17


18/165

Risk factor

Smoking.

Dyslipidemia (elevated LDL cholesterol and /or lowHDL cholesterol).

DM.

Impaired renal function (GFR


19/165

Contd

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).



Student, November

2003/2010.

19


20/165


21/165

Contd

Increased activity of the renin-angiotensin-

aldosterone system. Decreased vasodilation of the arterioles.

Resistance to insulin action.

Hypertriglyceridemia.

Obesity.

Glucose intolerance.



Student, November

2003/2010.

21


22/165

Gerontologic considerations

Structural and functional changes in the heart and

blood vessels contribute to increases in bloodpressure that occur with age.

The changes include;

accumulation of atherosclerotic plaque,

fragmentation of arterial elastins,

increased collagen deposits, and

impaired vasodilation.



Student, November

2003/2010.

22


23/165

Contd

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 systolichypertension.

Isolated systolic hypertension is more common in older

adults.



Student, November

2003/2010.

23


24/165

Clinical manifestations

People with hypertension can be asymptomatic

and remain so for many years. However, whenspecific 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.



Student, November

2003/2010.

24


25/165

Contd

The manifestation is categorized based on the

target organs of HTNEye;Retinal hemorrhages,

exudates (fluid accumulation),

arteriolar narrowing,

cottonwool spots (small infarctions), and

papilledema (swelling of the optic disc) may be seen.



Student, November

2003/2010.

25


26/165


27/165

Contd

Cerebrovascular

stroke or transient ischemic attack (TIA),manifested by;

o alterations in vision or speech,

o dizziness,

o weakness,o a sudden fall, or

o temporary paralysis on one side (hemiplegia).



Student, November

2003/2010.

27


28/165

Assessment and diagnosticevaluation

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).



Student, November

2003/2010.

28


29/165

Medical management

The goal of hypertension treatment is to;

Prevent death and complicationsby 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).



Student, November

2003/2010.

29


30/165

Algorithm of hypertension treatment



Student, November

2003/2010.

30


31/165

Contd



Student, November

2003/2010.

31


32/165

Pharmacologic therapy

For patients with uncomplicated

hypertension and no specificindications for another medication,the recommended initial

medications include;Diuretics,

Beta-blockers, or

Both.



Student, November

2003/2010.

32


33/165

Contd

Patients are first given low doses of medication. Ifblood pressure does not fall to less than 140/90 mm Hg,

the dose is increased gradually, and additionalmedications are included as necessary to achievecontrol.

When the blood pressure has been less than 140/90 mmHg for at least 1 year, gradual reduction of the typesand doses of medication is recommended.

To promote compliance, clinicians try to prescribe thesimplest treatment schedule possible, ideally one pillonce each day.



Student, November

2003/2010.

33


34/165

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 AgentsA. Peripheral Agents (e.g. reserpine (Serpasil)).



Student, November

2003/2010.

34


35/165

Contd

B. Central Alpha Agonists (e.g. methyldopa (Aldomet)). Itssite 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)).



Student, November

2003/2010.

35


36/165

Contd

5. Calcium Antagonists

A. Nondihydropyridines (e.g. verapamil)B. Dihydropyridines (e.g.nifedipine (Procardia Adalat

CC), felodipine (Plendil), nicardipine (Cardene),

nisoldipine (Sular)).



Student, November

2003/2010.

36


37/165

Lifestyle modifications for hypertensionprevention 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 andmagnesium for general health.

Stop smoking and reduce intake of dietarysaturated fat and cholesterol for overallcardiovascular health.



Student, November

2003/2010.

37


38/165

Contd

The DASH (Dietary Approaches to Stop

Hypertension) Diet (Based on 2000 calories per

day).



Student, November

2003/2010.

38


39/165


40/165

Hypertensive emergency

Hypertensive emergency is a situation in which bloodpressure must be lowered immediately (not necessarily

to less than 140/90 mm Hg) to halt or prevent damageto the target organs.

Conditions associated with hypertensive emergencyinclude acute myocardial infarction, dissecting aorticaneurysm, and intracranial hemorrhage.

Hypertensive emergencies are acute, life threateningblood pressure elevations that require prompttreatment in an intensive care setting because of theserious target organ damage that may occur.



Student, November

2003/2010.

40


41/165

Contd

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 immediateaction that is short lived (minutes to 4 hours), and they are

therefore used as the initial treatment.



Student, November

2003/2010.

41


42/165

Hypertensive urgency

Hypertensive urgency is a situation in which bloodpressure must be lowered within a few hours.

Severe perioperative hypertension is considered ahypertensive urgency.



Student, November

2003/2010.

42


43/165

Contd

Hypertensive urgencies are managed with oral doses offast-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)).



Student, November

2003/2010.

43

44


44/165

Disorder of Arteries



Student, November

2003/2010.

44

45


45/165

Arteriosclerosis and Atherosclerosis

Arteriosclerosis is the most common disease of thearteries, means hardening of the arteries.

It is a diffuse process where by the muscle fibers and theendothelial lining of the walls of small arteries andarterioles become thickened.

Atherosclerosis involves a different process, affectingthe 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 fibroustissue on the intimal layer of the artery. Theseaccumulations are referred to as atheromas or plaques.



Student, November

2003/2010.

45

46


46/165

Contd

Both occur together and used interchangeably.

Atherosclerosis can develop at any point in the body,

but certain sites are more vulnerable, typicallybifurcation or branch areas.In the proximal lower extremity, these include the distal

abdominal aorta, the common iliac arteries, the orifice ofthe 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 arterialbifurcations, that are more vulnerable for atherosclerosis.



Student, November

2003/2010.

46

47


47/165

Contd

Risk Factors Modifiablex Nicotine use (i.e., tobacco smoking, chewing)

x Diet (contributing to hyperlipidemin)

x Hypertension

x Diabetes

x Stress

x Sedentary lifestyle

Non-modifiablex Age

x Gender



Student, November

2003/2010.

47

48


48/165

Contd

Clinical ManifestationsThe 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.



Student, November

2003/2010.

48

49


49/165

Contd

Aorta;

Aneurysm.

Extremities

Atherosclerotic lesions.

Kidney;

Renal artery stenosis.

End-stage renal disease.

Hypertension.



Student, November

2003/2010.

49

50


50/165

Contd

Medical Management

Modification of risk factors.

Controlled exercise program to improve circulationand increase the functioning capacity of the

circulation.

Medication.

Interventional or surgical graft procedures.



Student, November

2003/2010.

50

51


51/165

Contd

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]), nicotinicacid (niacin, B3, 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, particularlytobacco use, is strongly recommended.



Student, November

2003/2010.

51

52


52/165

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.



Student, November

2003/2010.

52

53


53/165

Contd

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

aneurysm.



Student, November

2003/2010.

53

54


54/165

Contd

Causes Congenital:

Primary connective tissue disorders (Marfans syndrome,Ehlers-Danlos syndrome) and other diseases (tuberoussclerosis, Turners syndrome, Menkes syndrome).

Mechanical (hemodynamic): Poststenotic and arteriovenous fistula and amputation-

related. Traumatic (pseudoaneurysms):

Penetrating arterial injuries. Blunt arterial injuries. Pseudoaneurysms.



Student, November

2003/2010.

54

55


55/165

Contd Inflammatory (noninfectious):

Associated with arteritis (Takayasus disease, giant cell arteritis,systemic lupus erythematosus, Behets syndrome, Kawasakisdisease) 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.



Student, November

2003/2010.

55

56


56/165

Thoracic aortic aneurysm

Approximately 85% of all cases of thoracic aorticaneurysm are caused by atherosclerosis.

They occur most frequently in men between theages 40 and 70 years.

The thoracic area is the most common site for a

dissecting aneurysm. About one third of patients with thoracicaneurysms die of rupture of the aneurysm.



Student, November

2003/2010.

56

57


57/165

Contd

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.



Student, November

2003/2010.

57

58


58/165

Contd

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.



Student, November

2003/2010.

58

59


59/165

Contd

Medical Management

Controlling blood pressure (Systolic pressure ismaintained at about 100 to 120 mm Hg) with

antihypertensive medications

Correcting risk factors.

Surgical repair.



Student, November

2003/2010.

59

60


60/165

Abdominal aortic aneurysm

The most common cause of abdominal aortic

aneurysm is atherosclerosis.

Most of these aneurysms occur below the renal

arteries (infrarenal aneurysms).



Student, November

2003/2010.

60

61


61/165

Contd


Feeling their heart beating in their abdomen whenlying down.

Feel an abdominal mass or abdominal throbbing.

Blue toes.



Student, November

2003/2010.

61

62


62/165

Contd


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.



Student, November

2003/2010.

63


63/165

Contd

Medical Management

Surgical graft.



Student, November

2003/2010.

64


64/165

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.



Student, November

2003/2010.

65


65/165

Contd

Pathophysiology

oArterial 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 carriedfrom the left side of the heart into the arterial

system, where they lodge in and obstruct an artery

that is smaller than the embolus.



Student, November

2003/2010.

66


66/165

Contd


The six Ps associated with acute arterial embolismare; Pain.

Pallor.

Pulselessness.

Paresthesia.

Poikilothermia (coldness).

Paralysis.



Student, November

2003/2010.

67


67/165

Contd


Hx.

P/E.

Echocardiography.

Chest x-ray.

Electrocardiography.

Ultrasonography.

Arteriography.



Student, November

2003/2010.

68


68/165

Contd

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 10,000units) is administered intravenously, followed by a

continuous infusion of 1,000 units per hour until

the patient is able to undergo surgery.



Student, November

2003/2010.

69


69/165

Contd

Surgical management

Emergency embolectomy.

Nursing Management

Preoperative care.

Postoperative care.



Student, November

2003/2010.

70


70/165

Disorder of Veins



Student, November

2003/2010.

71


71/165

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.



Student, November

2003/2010.

72


72/165

Contd

Clinical Manifestation

Redness. Warm area along the vein or localized.

Pain, tenderness at the site.

Swelling.



Student, November

2003/2010.

73


73/165

Contd

Managements

D/C (Discharge) IV fluid. Restart in another site.

Applying a warm moist compress.



Student, November

2003/2010.

74


74/165

Contd

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.



Student, November

2003/2010.

75


75/165

Thrombophlebitis and Phlebothrombosis

Thrombophlebitis is inflammation of

the walls of the veins and frequentlyaccompanied by the formation of a clot.

Phlebothrombosis is when a clot

develops initially in the veins as a result ofstasis or hypercoagulablity, but with out

inflammation.



Student, November

2003/2010.

76


76/165

Contd

Venous thrombosis can occur in any vein butoccurs most frequently in the veins of the lower

extremities.Both the superficial and deep veins of the legsmay 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 ofteninvolved.



Student, November

2003/2010.

77


77/165

Contd



Student, November

2003/2010.

78


78/165

Contd

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.



Student, November

2003/2010.

79


79/165

Contd

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 withimmobility, extremity paralysis, or anesthesia.

Bed rest has been shown to reduce blood flow in the legs

by at least 50%.



Student, November

2003/2010.

80


80/165

Contd

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 fromintravenous medication.

All surgical patients are at risk for deep vein

thrombosis (DVT).



Student, November

2003/2010.

81


81/165

Contd


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.



Student, November

2003/2010.

82


82/165

Contd

Deep Veins;

Tenderness . Heaviness on standing position.

Cramping leg pain.

Swelling.

Pain on the calf (not specific to DVT). Sign of pulmonary embolus.



Student, November

2003/2010.

83


83/165

Contd

Superficial veins (dissolve spontaneouslyso risk of dislodge or fragmenting is low).

Pain or tenderness.

Redness and warmth in the involvedarea.

Local swelling: bumpy and knotty. Red tender, local indurations onsaphenous vein.



Student, November

2003/2010.

84


84/165

Contd

Diagnostic evaluation

For superficialxVenography.

xVenous scanning.



Student, November

2003/2010.

85


85/165

Contd

Management

Bed rest. Elevation of leg.

Analgesics.

Anti-inflammatory medication.



Student, November

2003/2010.


86/165

87


87/165

Contd

Pathophysiology

It can be;

Primary varicose veins (which is not involving thedeep veins).

Secondary varicose veins (resulting from

obstruction of deep veins).



Student, November

2003/2010.

88


88/165

Contd

C/F

For superficial vein involvement no symptomsx Dilated vein make trouble by the cosmetic appearance.

If symptoms occursx Dull aching pain.

x Cramp.

x Increased muscle fatigue in the lower leg.

x Ankle edema.

x Felling heaviness of the legs.



Student, November

2003/2010.

89


89/165

Contd

Deep vein involvement;x Edema.

x Pain.

x Pigmentation.

x Ulceration.

x Susceptibility to injury and infection is increased.



Student, November

2003/2010.

90


90/165

Contd

Diagnostic evaluation

Brodie- tendelenburg test.

Perthes test.

Additional diagnosis veins.



Student, November

2003/2010.

91


91/165

Contd

Prevention

Avoid venous stasis by wearing tight.

Elevating the leg.

Change position frequently.

Elastic stoking (knee- high).

W

eight reduction. Walking up the stairs.



Student, November

2003/2010.

92


92/165

Contd

Management

Surgery.

Sclerotherapy.



Student, November

2003/2010.

93


93/165

Varicose UlcerVaricose ulcers: Acondition 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.



Student, November

2003/2010.


94/165


95/165

96


96/165

The lymphatic system consists of a set of vessels thatspread throughout most of the body.These vessels start as lymph capillaries that drainunabsorbed plasma from the interstitial spaces (spacesbetween the cells).

The lymphatic capillaries unite to form the lymphvessels, which pass through the lymph nodes and thenempty 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 thelymphatic system is called lymph.The flow of lymph depends on the intrinsiccontractions of the lymph vessels, the contraction ofmuscles, respiratory movements, and gravity.



Student, November

2003/2010.

97


97/165

Lymphangitis

It is a spread of infection from a

cellulitis or abscess to the lymphaticsystem.

Lymphangits is an acute inflammation

of the lymphatic channels.It arises most commonly from a focus

of infection in an extremity.



Student, November

2003/2010.

98


98/165

ContdCause

Cellulitis.

Hemolytic streptococcus.C/F

Red streaks that extend up the arm or the legfrom an infected wound outline the course ofthe lymphatic vessels as they drain.

Rx

Antibiotic.



Student, November

2003/2010.

99


99/165

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.



Student, November

2003/2010.

100


100/165

Contd

Rx

An elastic compression stocking or sleeve

should be worn on the affected extremity for

several months to prevent long-term edema.

Antibiotics.



Student, November

2003/2010.

101


101/165

LymphedemaTissue swelling occurs in the extremities because of an

increased quantity of lymph that results from obstruction oflymphatic vessels.

It is especially marked when the extremity is in a dependentposition.

Lymphedemas are classified as;

Primary (congenital malformations)

The most common type is congenital lymphedema(lymphedema praecox), which is caused by hypoplasiaof the lymphatic system of the lower extremity.

This disorder is usually seen in women and firstappears between ages 15 and 25.



Student, November

2003/2010.


102/165

103


103/165

ContdMedical 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; thosewith the highest compression strength (exceeding 40mm Hg).

Strict bed rest with the leg elevated. Medication (diuretic furosemide (Lasix), antibiotic).



Student, November

2003/2010.

104


104/165

ContdSurgical management

Surgery is performed if the edema is severe and

uncontrolled by medical therapy, if mobility is severelycompromised, or if infection persists.

One surgical approach involves the excision of theaffected subcutaneous tissue and fascia, with skingrafting to cover the defect.

Another procedure involves the surgical relocation ofsuperficial lymphatic vessels into the deep lymphaticsystem by means of a buried dermal flap to provide aconduit for lymphatic drainage.



Student, November

2003/2010.


105/165

L t N t f S d

106


106/165

ElephantiasisElephantiasis 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.



Student, November

2003/2010.

L t N t f S d

107


107/165

Contd These lead to chronic fibrosis, thickening of the

subcutaneous tissues, and hypertrophy of the skin.

This condition, in which chronic swelling of theextremity recedes only slightly with elevation.

C/M

Elephant like skin (rough).

Rx

Minimize the risk of exposure to filaria.



Student, November

2003/2010.


108/165


109/165


110


110/165

Contd The malignant cell of Hodgkins disease is the

Reed-Sternberg cell, a gigantic tumor cell that is

morphologically unique and is thought to be ofimmature lymphoid origin.

Cause

It is unknown, but a viral etiology (Epstein-Barr

virus) is suspected.

Heredity (first degree relatives).



Student, November

2003/2010.


111


111/165

ContdClinical Manifestations

Lymphadenopathy (a painless, firm but not hard

enlargement of one or more lymph nodes on one sideof the neck).

The most common sites for are the cervical,supraclavicular, and mediastinal nodes.

Pruritus. Severe pain after drinking alcohol.



Student, November

2003/2010.


112


112/165

ContdAssessment and Diagnostic FindingsHealth 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 withinthese regions.

Laboratory tests include CBC, platelet count, ESR, and liver andrenal function studies.

A bone marrow biopsy is performed if there are signs of marrowinvolvement.

Bone scans may be performed to identify any involvement inthese areas.

A staging laparotomy and lymphangiography.



Student, November

2003/2010.


113


113/165


Early Hodgkins 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 ofearly-stage disease (IA and IIA).

Combination chemotherapy, for example with

doxorubicin (Adriamycin), bleomycin (Blenoxane),vinblastine (Velban), and dacarbazine (DTIC), referredto as ABVD, is now the standard treatment for moreadvanced disease (stages III and IV and all B stages).

ectu e ote o Seco d


Student, November

2003/2010.


114/165


115


115/165

Contd Pericarditis (acute or chronic)

Cardiomyopathy

Pneumonitis (acute or chronic) Avascular necrosis

Growth retardation

Infertility

Impotence

Myelodysplastic syndromes (MDS)

Dental caries


Student, November

2003/2010.


116


116/165

Non-hodgkins 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 Hodgkins disease, the lymphoidtissues involved are largely infiltrated with

malignant cells.


Student, November

2003/2010.


117


117/165

Contd 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; theaverage age at diagnosis is 50 to 60 years.

Although no common etiologic factor has beenidentified, 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.


Student, November

2003/2010.


118


118/165

ContdClinical Manifestations

The pt develop manifestation at these stages (III or

IV). Lymphadenopathy.

Recurrent fever.

Drenching night sweats.

Unintentional weight loss of 10% or more.


Student, November

2003/2010.


Y R l N i

119


119/165

ContdAssessment and Diagnostic Findings

CT scans.

Bone marrow biopsies.

Occasionally cerebrospinal fluid analysis.


Student, November

2003/2010.


Y R l N i

120


120/165


Treatment is based on the actual classification of

disease, the stage of disease, prior treatment (ifany), and the patients ability to tolerate therapy.

More intermediate forms are commonly treatedwith combination chemotherapy and radiation

therapy for stage I and II disease.


Student, November

2003/2010.



121


121/165

Contd

Hematologic Disorder


Student, November

2003/2010.



122


122/165

1.AnemiaAnemia is a term that indicates a low red cell count

and a below normal hemoglobin or hematocritlevel.

It is not a disease but rather reflects a disease stateor 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).


Student, November

2003/2010.



123


123/165

Classification ofA

nemiaA.Aplasitc anemia

Aplastic anemia occurs when the bone marrowproduces too few of all types of blood cells: red cells,

white cells, and platelets. Areduced number of redblood cells causes the hemoglobin (a type of proteinin the red blood cells that carries oxygen to thetissues of the body) to drop.

Areduced number of white blood cells causes thepatient to be susceptible to infection.

Areduced number of platelets can cause the bloodnot to clot as easily.


Student, November

2003/2010.



124


124/165

ContdRisk factors Treatment with high-dose radiation or

chemotherapy for cancer Exposure to toxic chemicals Use of some prescription drugs such as

chloramphenicol, which is used to treat bacterialinfections, and gold compounds used to treatrheumatoid arthritis that are known to rarely

induce aplastic anemia Certain blood diseases, autoimmune disorders and

serious infections Pregnancy, rarely.


Student, November

2003/2010.



125


125/165

ContdCausesHigh-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.


Student, November

2003/2010.



126


126/165

ContdC/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

g g

Student, November

2003/2010.



127


127/165

ContdDx

Blood tests.

Bone marrow biopsy.

g g

Student, November

2003/2010.



128


128/165

ContdTreatments

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.

g g

Student, November

2003/2010.



129


129/165

B. Irondeficiency anemiaIron 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.

Student, November

2003/2010.



130


130/165

ContdCauses Two common causes of iron deficiency anemia are blood loss (most

common) and decreased absorption of iron from food.1. Blood loss : The source of blood loss may be obvious, such as repeated

blood donations, trauma, surgery, heavy menstrual bleeding, bleeding indigestive tract.

2. Decreased iron absorption: 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 Acommon cause of iron deficiency anemia in developingcountries is a lack of foods that contain iron.

1. Vegetarians are at increased risk for developing iron deficiency anemia becauseiron from plant sources is not absorbed as readily as iron from meat sources.

2. Pregnant women often develop iron deficiency anemia because of the increasediron requirements of the growing fetus and placenta, and the increased volumeof blood circulating in the woman's body during pregnancy.

Student, November

2003/2010.



131


131/165

ContdC/MWeaknessHeadache

IrritabilityFatigueDifficulty 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).

Student, November

2003/2010.



St d t N b

132


132/165

ContdDiagnosis

Medical history.

Physical examination. Blood tests.

Complete blood countx 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 corpuscularhemoglobin (MCH, referring to the cell color-hypochromic), and others.

Student, November

2003/2010.



St d t N b

133


133/165

ContdFurther testing includes measure of;

Serum iron.

Total iron binding capacity (TIBC ortransferrin).

Transferrin saturation.

Ferritin.

Student, November

2003/2010.



Student November

134


134/165

ContdMgx 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 orhematocrit less than 20 percent)).

Rx continued for years.

Nursing intervention Pt education food source high in iron include organmeats (liver, cow, chicken leafy vegetables

Vitamin C enhance absorption. Avoid antacid.

Student, November

2003/2010.



Student November

135


135/165

Megaloblastic anemias Megaloblastic anemia is the end-product of

deficiencies in the B vitamins folate or vitamin

B12 (also called cobalamin), or both. Suchdeficiencies produce abnormally large red bloodcells (megaloblastic) that have a shortenedlifespan.

Student, November

2003/2010.



Student November

136


136/165

ContdCauses (Vitamin B12 deficiency)

Vitamin B12 deficiency from diet.

Pernicious anemia. Complications of gastrointestinal surgery.

Overgrowth of intestinal bacteria.

Tropical sprue (an acquired malabsorptiondisease occurring in tropical climates).

Student, November

2003/2010.



Student November

137


137/165

ContdCauses (folate deficiency) Poor diet coupled with alcoholism. Any condition that disturbs the small intestine and

impairs its absorption ability (inflammatory boweldisease).

Parasitic diseases, such as giardiasis. Short bowel syndrome. High demand for folic acid caused by conditions

such as cancer, pregnancy, severe psoriasis, severehyperthyroidism, and hemolytic anemia.

Some drugs, including phenytoin, methotrexate,trimethoprim, and triamterene.

Student, November

2003/2010.



Student, November

138


138/165

ContdC/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.

Student, November

2003/2010.



Student, November

139


139/165

ContdDx

Complete blood count (shows anemia with large red

blood cells). Bone marrow examination (can help show whether

your bone marrow is healthy and making enoughred blood cells).

Serum B12 (can help show vitamin B12 blood level). Schilling test (detect vitamin B12 absorption).

Serum folate (can help show whether you havepernicious anemia or another type of anemia).

Student, November

2003/2010.



Student, November

140


140/165

ContdRx

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. Awell-balanced diet is essential to provide other elements for

healthy blood cell development, such as folic acid, iron, and vitaminb12.

Which foods are contain rich folic acid and vitamin B12:

eggsmeatpoultrymilkshellfish

,

2003/2010.



Student, November

141


141/165

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 bythe mononuclear-phagocytic system either because they are intrinsicallydefective or because of the presence of bound immunoglobulins to theirsurfaces.

Intravascular: due to complement fixation, trauma, or other extrinsic factors.

Examples are prosthetic cardiac valves, glucose-6-phosphate dehydrogenasedeficiency, thrombotic thrombocytopenic purpura, disseminatedintravascular coagulation and paroxysmal nocturnal hemoglobinuria.

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

2003/2010.



Student, November

142


142/165

ContdTypes ofHemolytic anemia

1. InheritedHemolytic Anemia One or more of the genes that control red blood cell production are

faulty.

The defects may involve the hemoglobin, cell membrane, or enzymesthat maintain healthy red blood cells.

The abnormal cells may be fragile and break down while moving throughthe bloodstream. If this happens, an organ called the spleen may removethe cell debris from the bloodstream.

Inherited hemolytic anemias are often inherited, such as sickle cellanemia, thalassemia and hereditary spherocytosis, in addition to include

G6PD Deficiency.2. AcquiredHemolytic Anemiayour 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.

2003/2010.



Student, November

143


143/165

ContdCauses The immediate cause is the early destruction of red blood cells. Anumber 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, sulfamedications, acetaminophen. Autoimmune disease, such as systemic lupus erythematous (SLE, or

lupus), rheumatoid arthritis, Wiskott-Aldrich syndrome, or ulcerativecolitis.

Lymphocytic leukemia or lymphoma.

2003/2010.


144/165


145/165



Student, November

2003/2010

146


146/165

ContdMgx

Treat the underlying course.

Blood transfusion.

2003/2010.



Student, November

2003/2010

147


147/165

Leukemias Leukemias is a malignant disorder of the

hematopoietic system involving the bone marrow andlymph 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.

2003/2010.



Student, November

2003/2010

148


148/165

ContdClassification

The leukemias are classified as acute or chronic and

are further subdivided according to cell type ormaturity.

1. Acute leukemias

Rapid on set.

Short course ending in death if un treated.

2. Chronic leukemias

Insidious onset

2003/2010.



Student, November

2003/2010

149


149/165

ContdAcute 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 singlelymphoid stem cell with impaired maturation andaccumulation of malignant cell in the bonemarrow.

2003/2010.



Student, November

2003/2010

150


150/165

ContdSigns 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.

2003/2010.



Student, November

2003/2010.

151


151/165

ContdNursing 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 immaturemyeloblasts in the bone marrow.

2003/2010.



Student, November

2003/2010.

152


152/165

ContdChronic lymphocytic leukemia

CLL is characterized by a proliferation of small,

abnormal, mature lymphocytes after leading todecreased synthesis of immunoglobulins and

depressed antibody response.

Chronic myelogenous leukemia

Onset is 4th and 3rd decade.

003/ 0 0



Student, November

2003/2010.

153


153/165

Contd Uncontrolled proliferation of the granulocytosis

cell;

Basophils Esnophils

Neutrophils

Circulating granulocytes increase.

Polycythemia Hemocytoblast stem cell.



Student, November

2003/2010.

154


154/165

Contd

Hemorrhagic disorder



Student, November

2003/2010.

155


155/165

ThrombcytosisIt is the presence of abnormally high number of

circulating platelets

Mild bleeding syndromes may be caused byquantitatively normal but functionally defective

platelets.



Student, November

2003/2010.

156


156/165

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 druginduced).

Sequestration of blood in the spleen (splenomegaly).

Loss from hemorrhage.



Student, November

2003/2010.

157


157/165

ContdC/F

P/Ex

Petechiae skin spot, purple hemorrhagic spot.x Only in platelet disorder.x Ecchymosis blue black larger in diameter

irregular.x Purpura.

Hxx Menorrhagia.x Epistaxis.x Gingival bleeding.



Student, November

2003/2010.

158


158/165

ContdDx

Platelet count.

Peripheral blood smear. Bleeding time.

Bone marrow examination.



Student, November

2003/2010.

159


159/165

ContdTreatment

Corticosteroid (most common treatment ).

Immununoglobulin. Splenectomy .

Danazol and immunosuppressive drug.

Platelet transfusion.



Student, November

2003/2010.

160


160/165

ContdNursing care Avoiding trauma Bleeding associated with trauma is likely with a platelet count less than

60,000/mm3 .

Spontaneous hemorrhage may be a life threatening possibility whenthe platelet count is be low 20, 000/mm3 .

Be alert for an increase in ecchymosis or petechiae, and bleeding fromother 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.



Student, November

2003/2010.

161


161/165

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 dentalextractions.

Lifelong bleeding.

Bleeding can be spontaneous or after trauma.Dx

Specific assays for factors VIII, lX, Xl. Partial thromboplastin time (PTT).



Student, November

2003/2010.

162


162/165

ContdComplication

Joint deformity

Retroperitoneal bleeding. Intracranial, paratracheal soft tissue hemorrhages.

Mgx

Replacement of the deficient coagulation factor

where bleeding episodes do not respond to localtreatment.



Student, November

2003/2010.

163


163/165

Vitamin K deficiency Vitamin K, a fat 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 spectrum antibiotics. Absorption problem i.e. ulcerative colitis.

Drugs interfere with vitamin K functionx Salicylates

x Guanine

x Bribitureates


164/165



Student, November

2003/2010.

165


165/165

Education is Enabling an

individual to win victoryover the five victory's; lust,

anger, greed, infatuation

medical surgical nursing:periphero vascular disorder

Documents