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Mononucleosis

What is mononucleosis
Infectious mononucleosis sometimes called "mono" or "the kissing disease," is an infection usually caused by the Epstein-Barr virus (EBV). EBV is very common, and many people have been exposed to the virus at some time in childhood.

EBV infectious mononucleosis (also known

as Pfeiffer's disease, colloquially as the kissing disease, or as mono in Northern America and more commonly known as glandular fever in other English-speaking countries) is an infectious, viral disease which most commonly occurs in adolescents and young adults often in 15- to 17-year-olds, the infection may occur at any age

How it is transmitted?
often transmitted by saliva by kissing someone

who has been infected direct contact with saliva (spit) from someone infected with EBV, such as by sharing a straw, a toothbrush, or an eating utensil. occurring most often in 15- to 17-year-olds, the infection may occur at any age.

Symptoms usually begin to appear 4 to 7 weeks

after infection with the virus


constant fatigue fever loss of appetite sore muscles /stiffness skin rash abdominal pain

swollen lymph nodes (commonly called glands, located in your neck, underarms, and groin )

Less frequently occurring symptoms include: Jaundice (yellow cast to skin) Headache Neck stiffness Sensitivity to light Cough Shortness of breath Chest pain Rapid heart rate Fatigue Nosebleed Hives

symptoms of mono gradually go away on their own over a period of weeks to months.

Pathophysiology
EBV oral secretions ( saliva) up to 8 weeks incubation period replication of virus within epithelial cells in the pharynx within B cells ( invaded via their CD21)

immune response SORE THROAT IgM Ab

cytotoxic (CD 8 +) T cells

infected by B lymphocytes

Heterphite Ab production

ATYPICAL LYMPHOCYTES ( Downey Cells)

The most commonly used diagnostic criteria is the

presence of 50% lymphocytes with at least 10% atypical lymphocytes (large, irregular nuclei whilst the person also has fever, pharyngitis and adenopathy.
Physical exam - swollen lymph nodes, tonsils,

liver or spleen
Blood tests -

confirms mononucleosis Antibody tests (monospot test ) Epstein-Barr virus antigen by immunofluorescence (positive for EBV) Epstein-Barr virus antibody titers to help distinguish acute infection from past infection with EBV White blood cell count - elevated number of white blood cells (lymphocytes) or abnormallooking lymphocytes.(unusual-appearing white blood cells )

Susceptibility

If antibodies to the viral capsid antigen are not detected (IgM & IgG), the patient is susceptible to EBV infection Primary Infection is indicated if IgM antibody to the viral capsid antigen is present and antibody to EBV nuclear antigen, or EBNA, is absent rising or high IgG antibody to the viral capsid antigen and negative antibody to EBNA after at least 4 weeks of illness is also strongly suggestive of primary infection

Past Infection

antibodies to both the viral capsid antigen and EBNA are present (from 4 to 6 months to years earlier) Reactivation presence of antibodies to EBNA an elevation of antibodies to early antigengen Chronic EBV Infection illness lasts more than 6 months, investigate other causes of chronic illness

acute cytomegalovirus and Toxoplasma gondii

infections Acute HIV infection Leukemia Diphtheria common cold influenza (the flu)

is generally self-limiting and only symptomatic

and/or supportive treatments are used


Most patients recover within 2-4 weeks

without medication
Rest is recommended during the acute phase of

the infection, but activity should be resumed once acute symptoms have resolved heavy physical activity and contact sports should be avoided to abrogate the risk of splenic rupture, for at least one month following initial infection and until splenomegaly has resolved, as determined by ultrasound scan

Treatment
acetaminophen/paracetamol or non-steroidal anti-

inflammatory drugs (NSAIDs) to reduce fever and pain Intravenous corticosteroids, usually hydrocortisone or dexamethasone, are not recommended for routine use[15] but may be useful if there is a risk of airway obstruction, severe thrombocytopenia, or hemolytic anemia aciclovir, may reduce initial viral shedding antiviral drug valacyclovir has recently been shown to lower or eliminate the presence of the EpsteinBarr virus in subjects afflicted with acute mononucleosis, leading to a significant decrease in the severity of symptoms.

Antibiotics are not used as they are ineffective

against viral infections. amoxicillin and ampicillin are relatively contraindicated in the case of any coinciding bacterial infections during mononucleosis because their use can frequently precipitate a nonallergic rash. In a small percentage of cases, mononucleosis infection is complicated by co-infection with streptococcal infection in the throat and tonsils (strep throat). Penicillin or other antibiotics (with the exception of the two mentioned above) should be administered to treat the strep throat. Opioid analgesics are also relatively contraindicated due to risk of respiratory depression.

Complications
Enlargement of the spleen

significant complications of mononucleosis In extreme cases, spleen may rupture, causing sharp, sudden pain in the left side of your upper abdomen. If such pain occurs, seek medical attention immediately you may need surgery. Hepatitis Jaundice

Prevention
Mononucleosis is spread through saliva. If you're

infected, you can help prevent spreading the virus to others by not kissing them and by not sharing food, dishes, glasses and utensils until several days after your fever has subsided and even longer, if possible. The Epstein-Barr virus may persist in your saliva for months after the infection. There's no vaccine to prevent mononucleosis.

Fatigue R/T the infectious process

Hyperthermia R/T the infectious process


Acute pain R/T throat inflammation &

swelling

Administer medications to treat symptoms ,

as needed Provide warm saline gargles for symptomatic relief of sorethroat Provide adequate fluids and nutrition Plan care to provide frequent rest periods Check the patients temperature regularly Monitor patients response to analgesics, antipyretics, & other supportive measures

Explain that convalescence may take several

weeks, usually until the patients WBC count returns to normal Stress the need for bed rest during acute illness Warn patient to avoid excessive activity, which could lead to splenic rupture To minimize throat discomfort, encourage patient to drink milk shakes, fruit juices, and broths and to eat cool, bland foods

Rheumatic Heart Disease

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And this!!!

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Stick around for this.

Streptococcal (strep) infections are communicable diseases that develop when Streptococcus bacteria normally found on the skin or in the intestines, mouth, nose, reproductive tract, or urinary tract invade other parts of the body and contaminate blood or tissue.

Rheumatic Fever
Rf is a diffuse, inflammatory disease caused

by a delayed exaggerated immune response to infection by the group A B-hemolytic streptococcus in genetically predisposed individuals. - Is a febrile illness - If untreated, can cause scarring and deformity of cardiac structures - RHD Streptococci are a part of normal animal flora! It is believed to be caused by antibody crossreactivity and can involve the heart, joints, skin, and brain

Epidemiology
2 3 % of people with untreated Group A

beta-hemolytic streptococcal infection. 470,000 new cases and 233,000 deaths each year. Mostly in developing countries, among indigenous groups. over 15 million people are estimated to have rheumatic heart disease. In the US and other developed countries the incidence is low (hygiene and routine antibiotic use)

Predisposing Factors
AGE 90% occur between the ages of 5 15 y.o.

- Also the AGED, severe cardiac disability and death. SOCIOECONOMIC FACTORS slum, city dweller more than the farmer. GENETICS may appear to develop in household members.

Etiology
Exact cause remains uncertain!

- bacteria do not grow within the heart and joints 2 Theories:


The body undergoes an allergic response to invading

streptococci. The host develop an autoimmune response in which streptococcal antibodies attack the host tissue. Basis of the theories: 1. RF develops following an URTI by streptococci 2. The devlp of RF is between 1 - 5weeks, with an average of 18 days. The time our body needs to sensitized an organism and undergo immune response. 3. Since only 2 -3 % devlp RF after strep. throat, it has been hypothesized that these people have a greater immunological reaction.

Pathophysiology
Predisposing Factors Invasion of streptococcus from normal flora Pharyngitis Treatment initiated If untreated macrophages presents bacterial antigen to lymphocyte
Activation of B-cells

Activation of T-cells
T- Suppressor T-Killer Failure of Suppressor cell

T- Helper

Antibody Prodxn. *Cross reactn with cardiac myofiber myosin, and smooth muscle of arteries

*Cytokine release *Inflammatory process away from primary site of Strep. Infxn.

*Joint
Smooth muscle of

CNS

HEART
arteries

*Chorea
Polyarthritis

Skin
*Erythema marginatum

Endocardial inflammation Swelling of the valve leaflets

Erosion along the leaflets


*Deposition of platelets and fibrin on eroded valvular tissue BD Become progressively adherent scarring and shortening of leaflets

Valves becomes narrowed blood

Regurgitation of

Increase cardiac workload HEART FAILURE

Myocardium
*Aschoff bodies

C Valve loose its elasticity Mitral, aortic, tricuspid valve dysfunction murmur

D
Pericardial Inflammation

Chest pain effusion

serofibrinous

Audible friction
rub

Assessment
Almost always follows a streptococcal infection of the

nasopharynx.

Did you experience sore throat lately? How often?


Signs and Symptoms: 1. Polyarthritis prominent finding; last hours to days 2. Carditis common manifestation 3. Relapsing fever 38o C and episode of normal temp. 4. Subcutaneous nodules small, painless firm nodules (knees, knuckles, and elbows); usually in children; only in first week. 5. Erythema Marginatum crescent shape lesion with clear centers chicken-wire rash 6. Abdominal pain may be related to liver engorgement 7. Sydenhams chorea St. Vitus dance; late stages, usually in girls; Involuntary grimacing and jerky, purposeless movements. 8. Malaise, weakness, weight loss, and anorexia As

Erythema Marginatum

Subcutaneous nodules

Diagnostic Measures
There is no single diagnostic feature identifies

rheumatic fever. JONES CRITERIA - gauges the probability of the presence of rheumatic fever in an individual. Premise: 1. Diagnosis requires two major manifestation 2. One major manifestation and two minor manifestation

Medical Intervention
Control and alleviate infecting streptococci if still

present. Protect the heart against the damaging effects of carditis. Relieve joint pain, fever, and other symptoms. Typical intervention: 1. Chemotherapy with penicillin, salicylates, and steriods 2. Bed rest 3. Proper diet

Diagnosis
Rheumatic fever is mainly a clinical diagnosis No single diagnostic sign or specific laboratory

test available for diagnosis physical exam may include: 1. Checking the joints for pain and inflammation 2. Examining the skin for rashes or lumps 3. Listening to the heart for abnormal rhythms or murmurs 4. Doing a neurological exam to check for abnormal movements

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To diagnose rheumatic fever, doctors generally look for evidence of a preceding strep throat infection, which is characterized by:
Sore throat Red and swollen tonsils Fever Fatigue Abdominal pain (in younger children) Tender lymph nodes in the front of the neck Headache Muscle aches
45
Norimel Andrea A. Labarda,RN,MAN

11/27/08

Diagnosis based on MODIFIED JONES CRITERIA

46

Norimel Andrea A.Labarda,RN,MAN

11/27/08

Jones Criteria (Revised) for Guidance in the Diagnosis of Rheumatic Fever*


Major Manifestation
Carditis Polyarthritis Chorea Erythema Marginatum Subcutaneous Nodules

Minor Manifestations
Clinical Previous rheumatic fever or rheumatic heart disease Arthralgia Fever Laboratory Acute phase reactants: Erythrocyte sedimentation rate, C-reactive protein, leukocytosis Prolonged PR interval

Supporting Evidence of Streptococal Infection


Increased Titer of AntiStreptococcal Antibodies ASO (anti-streptolysin O),

others
Positive Throat Culture for Group A Streptococcus Recent Scarlet Fever

*The presence of two major criteria, or of one major and two minor criteria, indicates a high probability of acute rheumatic fever, if supported by evidence of Group A streptococcal nfection.

Exceptions to Jones Criteria


Chorea

alone, if other causes have been excluded Insidious or late-onset carditis with no other explanation Patients with documented RHD or prior rheumatic fever,one major criterion,or of fever,arthralgia or high CRP suggests recurrence
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Goals of Treatment Are to relieve symptoms, destroy the group A streptococcus and prevent future infection.
49
Norimel Andrea A. Labarda, RN,MAN 11/27/08

Treatment
Step I - primary prevention

(eradication of streptococci) Step II - anti inflammatory treatment (aspirin,steroids) Step III- supportive management & management of complications Step IV- secondary prevention (prevention of recurrent attacks)
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STEP I: Primary Prevention of Rheumatic Fever

(Treatment
Mode Duration Once

of Streptococcal Tonsillopharyngitis)
Agent Benzathine penicillin G Dose 600 000 U for patients Intramuscular 27 kg (60 lb) 1 200 000 U for patients >27 kg

or
Penicillin V Children: 250 mg 2-3 times daily Oral (phenoxymethyl penicillin) Adolescents and adults: 500 mg 2-3 times daily For individuals allergic to penicillin Erythromycin: Estolate 20-40 mg/kg/d 2-4 times daily (maximum 1 g/d) Oral 10 d 10 d

or
Ethylsuccinate 40 mg/kg/d 2-4 times daily (maximum 1 g/d) Oral 10 d

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Recommendations of American Heart Association

Step II: Anti inflammatory treatment


Clinical condition Drugs

Arthritis only

Aspirin 75-100 mg/kg/day give as 4 divided doses for 6 weeks (Attain a blood level of 20-30mg/dl)

Carditis

Prednisolone 2-2.5 mg/kg/day Give as 2 divided doses for 2 weeks Taper over 2 weeks while tapering give aspirin 75mg/kg/day for 2 weeks Continue aspirin alone 100mg/kg/day for another 4 weeks

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3.Step III: Supportive management & management of complications


Bed rest Treatment of congestive cardiac failure:

digitalis,diuretics Treatment of chorea: -diazepam or haloperidol Rest to joints & supportive splinting

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STEP IV : Secondary Prevention of Rheumatic Fever (Prevention of Recurrent Attacks) Agent


Benzathine penicillin G

Dose
1 200 000 U every 4 weeks*

Mode
Intramuscular

or
Penicillin V 250 mg twice daily Oral

or
Sulfadiazine 0.5 g once daily for patients 27 kg (60 lb Oral 1.0 g once daily for patients >27 kg (60 lb)

For individuals allergic to penicillin and sulfadiazine


Erythromycin 250 mg twice daily Oral

*In high-risk situations, administration every 3 weeks is justified and recommended


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Recommendations of American Heart Association

Pharmacologic Intervention
PENICILLIN for 10 days ff. the onset of rheumatic fever. ERYTHROMYCIN if allergic to penicillin Prophylactic doses of same med is given to prevent further attacks Monthly injections of Longacting Penicillin must be given for a period of 5 years in patients having one attack of Rheumatic fever SALICYLATES to control fever and to relieve joint pain. Aspirin give with food to reduce gastric irritation STERIODS relieve inflammatory symptoms; prevent further scarring of tissue and may prevent development of sequelae such as Mitral stenosis CARDIAC GLYCOSIDES (digitalis) and DIURETICS

Nursing Management
NURSING ASSESSMENT * Cardiac function * Tolerance to activity and feelings towards restriction * Support Systems * Coping Strategies * Nutritional Status * Level of Discomfort * Knowledge with RF NURSING GOALS 1. Person will demonstrate progression toward an optimal level of physical activity tolerance. 2. Person will use adaptive coping strategies. 3. Person will experience increased comfort. 4. Person will show fewer behavioral and physical symptoms of anxiety. 5. Person will maintain or restore proper nutritional balance. 6. The person will restore or maintain hemodynamic status lungs, Urine output, weight,

Nursing Dx and Interaction


Alteration in Comfort Activity Intolerance Bed rest (reduces strain on the heart and

reduces metabolic needs)

* Temp is normal without salicylates * Resting pulse (adults) < 100 * ECG shows no signs of myocardial damage * ESR rate returns to normal
Alteration in Nutrition: Less than Body Requirements Knowledge Deficit Regarding Preventive Measures Against

Initial and Recurring Attacks of Rheumatic Fever

pharyngitis

* Continue prophylactic medication for five years. * Prophylactic medication before and after surgery or dental procedure. (for bacterial endocarditis) * Advise patient that they have to adhere this permanently. * Proper dental hygiene and prompt dental care. * Avoid people who had recent streptococcal infection. * It is very important to begin antibiotic therapy after
has developed.

Prognosis and Complication


With antibiotic therapy, the prognosis is generally

good. (only 1 2 % die from initial attack; acute myocarditis) Laboratory and clinical signs subsides within one to two months following therapy. Some develop residual heart damage: MITRAL REGURGITATION and/or STENOSIS AORTIC REGURGITATION

Prognosis
Rheumatic fever can recur whenever the

individual experience new GABH streptococcal infection,if not on prophylactic medicines Good prognosis for older age group & if no carditis during the initial attack Bad prognosis for younger children & those with carditis with valvar lesions

59

Hypertension:
- Persistent elevation of systolic blood pressure of

140mmHg or above and a diastolic pressure of 90mmHg or above.(JNC) Etiology/Risk Factors: - Age - Gender - Genetic - Lifestyle: Increased Na intake, excessive alcohol consumption, Increased fat intake, cigarette smoking - Obesity - Prolonged or recurrent stress - DM

Classification
A. Primary Hypertension also known as

essential or idiopathic hypertension B. Secondary Hypertension hypertension secondary to (caused by) a specific disorder of a particular organ or blood vessel, such as the kidney, adrenal gland, or aortic artery. Isolated systolic hypertension - is defined as a systolic pressure that is above 140 mm Hg with a diastolic pressure that still is below 90. This disorder primarily affects older people and is characterized by an increased (wide) pulse pressure.

White coat hypertension is defined as hypertension

in persons who are actually normotensive except when their blood pressure is measured by a healthcare professional.

ANS imbalance
Increase SNS stimulation Adrenal medulla Cathecholamines NEP bind Adrenergic receptor alpha vasoconstriction Inc. systemic vascular resistance Inc. HR beta EP

Inc. myocardial contraction

Dec. blood flow to the kidneys


Release renin from juxtraglomerular cells
Catalyzed angiotensinogen

Inc. cardiac workload Inc afterload

Angiotensin 1 Angiotensin 2 Inc. Na absorption Inc. H2O absorption

Inc Blood pressure

Manifestations:
No clinical manifestations other than elevated BP

NO signs and symptoms for individual to seek

health care Most clinical manifestations of HPN is caused by complications that damage the organs and tissues outside the vascular system

Evaluation
Diagnosis requires the measurement of blood

pressure on at least 2 separate occassions averaging two readings at least 2 minutes apart (140mmHg for SBP and 90mmHg for DBP), with the patient seated, the arm supported at heart level, after 5 minutes rest with no smoking or caffeine intake in the previous 30 mins.
24 hour blood pessure monitoring

CBC
Urinalysis Blood chem ECG

Stages
BP classification Normal Prehypertension SBP DBP Without compelling indication

<120 120-139mmHg

<80 80-89 mmHg No antihypertensive drugs Thiazide diuretics, may consider ACE, CCB, BB or combination 2 drugs combination for most

Stage 1

140-159mmHg

90-99mmHg

Stage 2

160mmHg

100mmHg

Complications

Treatment
Lifestyle Changes

Follow a Healthy Eating Plan


Therapeutic Lifestyle Changes (TLC). Dietary Approaches to Stop

Hypertension (DASH) eating plan Increase Physical Activity Maintain a Healthy Weight Medications:

Diuretics - Thiazide Blood Pressure Lowering Drugs

-Beta-blockers (such as acebutolol, atenolol, metoprolol, nadolol, and propranolol) -Angiotensin-converting enzyme (ACE) inhibitors (such as benazepril, captopril, enalapril, lisinopril, and ramipril) -Calcium-channel blockers (such as amlodipine, felodipine, nifedipine, nicardipine, and verapamil) -Alpha/beta blockers (such as labetalol)

Cholesterol-Lowering Drugs

-Statins (such as lovastatin, pravastatin, simvastatin, atorvastatin, and fluvastatin)


Blood Thinning Drugs, Platelet Inhibitors

Aspirinfirst choice platelet inhibitor for

preventing and treating atherosclerosis; reduces risk of transient ischemic attack (TIA), stroke, and heart attacks Ticlodipinefor individuals who can not take aspirin (due to allergies, for example) or do not improve from aspirin; has more side effects than aspirin Dipyridamolenot as effective as aspirin when used alone but may be used in combination with aspirin or warfarin (another blood thinner); often used after bypass surgery

Clopidogrelreduces risk of heart attacks


Glycoprotein IIb/IIIa receptor agonists (such as

abciximab, eptifibatide, lamifiban, and tirofiban)used when awaiting or just following an angioplasty

Blood Thinning Drugs, Anticoagulants

Heparinused intravenously in the hospital

following a TIA, stroke, or heart attack Low molecular weight heparinadministered by self-injection following a stroke or for coronary artery disease Warfarinused to prevent stroke in individuals who have irregular heart rhythms

Blood Thinning Drugs, Thrombolytics The following medications are used in the

hospital just after a heart attack. They are most effective when used within three hours of a stroke or heart attack. Recombinant Tissue Plasminogen Activator (rTPA) Streptokinase Urokinase Other Medications Nitratesused to relax the vessels that supply the heart with blood; these medications reduce chest pain

Non-surgical techniques

The following nonoperative techniques may be

performed on individuals with coronary and peripheral artery disease: Angioplastya procedure used to widen narrowed arteries. A surgeon inserts a catheter with a deflated balloon into the narrowed part of the artery. The balloon is inflated, widening the inner diameter of the blood vessel so blood can flow more easily. The balloon is then deflated and the catheter is removed. This procedure may also include the placement of a permanent stent (wire mesh) that holds the artery open and improves blood flow. Angioplasty with stent placement is considered the safest and most effective procedure for atherosclerosis.

Atherectomya procedure to remove plaque

from the arteries using a laser catheter or a rotating shaver Laser revascularizationa procedure in which a laser creates multiple channels through the heart muscle into the main pumping chamber of the heart. These channels fill with blood from the pumping chamber which then supplies oxygen and needed nutrients to the heart muscle. It is used to relieve severe chest pain in individuals who have no other treatment options.

Surgical Procedures
Bypass surgerya procedure that reroutes or

bypasses blood around clogged arteries to improve blood supply to affected areas such as the heart or the lower extremities Minimally invasive bypass surgerythis procedure creates a small incision rather than the broad opening in the chest wall created during regular bypass surgery Endarterectomya procedure primarily used to remove plaque in the carotid (a major artery located in the front of the neck) or peripheral arteries

Peripheral Vascular Disease


Refers to any abnormality in the arteries and

veins outside the heart. Most common sites of atheromas in the peripheral circulation are the abdominal aorta, femoral and iliac arteries Partial Occlusion impair both muscle activity and sensory function in the legs Total Occlusion Loss of blood supply, necrosis, ulcers and gangrene

Signs and symptoms


Increasing weakness and fatigue in the legs

Intermittent claudication or leg pain associated


with exercise or walking due to muscle ischemia Sensory impairment may also be noted as paresthesia tingling or burning and numbness. Peripheral pulses distal to the occlusion become weak or absent Appearance of the skin of the feet and legs changes with marked pallor or cyanosis Skin is dry and hairless

Toenails are thick and hard

Feel feel cold

Diagnostic test: Doopler studies Arteriography Plethysmography

Treatment
Reduction of serum cholesterol levels is

recommended Administration of anticoagulants: Aspirin and Heparin Cessation of smoking Exercise Maintaining a dependent position for the legs an improve arterial perfusion Care should be taken to avoid trauma and regular exam of the feet is very important to avoid pressure from shoes

Surgical Treatment:

a. bypass graft using a vein or synthetic material


b. Angioplasty c. Endarterectomy Gangrenous feet antibiotics and debridement Amputation

Thromboangiitis Obliterans (Buergers Dse) -An inflammatory condition of medium-sized and small arteries in the legs and arms -Thrombus forms easily and firosis leads to vascular occlusion -Common in young men before age 35 -Aggravated by cigarette smoking -Genetic common in jewish, japanese and indian origin -*Intermittent caludication -Ulcerations and gangrene -Amputation

Raynaud Syndrome(Idiopathic)

-An example of vasospastic condition in which periodic temporary vasoconstriction occurs in the arterioles and small arteries in the superficial tissues of the fingers. -Common in young women -Triggered by exposure to cold

-Ischemia with pallor, numbness and cyanosis followed by vasoconstriction -Redness and throbbing pain -Instruct patient to protect hands from touching cold objects.

Aneurysms
Localized dilatation in an arterial wall Most common site is the abdominal aorta 3 forms of aneurysms: A. Saccular projects from one side of the vessel

only B. Fusiform Develops if an entire arterial segment becomes dilated C. Dissecting Happens when there is a tear in the intima, allowing blood to flow along the length of the vessel between the layers of the arterial wall. -serious bec they can rupture leading to hemorrhage and death.

Etiology
Atherosclerosis most common cause

Hypertension
Other infection that affect the arterial wall

Signs and symptoms


Asymptomatic for a long period of time until they

become large or rupture. Once ruptured may cause severe hemorrhage: pain and indications of shock
Treatment: Surgical repair with resection and replacement with a synthetic graft can prevent rupture

Venous Disorder
1. Varicose Veins Are irregular, dilated and tortuous areas of the superficial or deep veins Most common location is the legs but they are also found in the esophagus and rectum. Varicose vein develops from a defect or weakness in the vein walls or in the valves.

Signs and symptoms


Superficial varicosities

Edema
Shiny

Thrombophlebitis and Phlebothrombosis


Often used interchangeably

It is difficult to differentiate the two conditions but

sometimes there is a significant difference in the predisposing factors Thrombophlebitis refers to the development of a thrombus in a vein in which inflammation is present. Phlebothrombosis a thrombus forms spontaneously in a vein without prior inflammation, although inflammation may develop secondarily in response to thrombosis

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