Study Sheet

Patho Test #2 Study Sheet 1

Module 05: Upper and Lower Respiratory Tract DisordersRhinitis

A group of disorders characterized by inflammation and irritation of the mucous membranes of the nose. This condition may or may not be caused by allergies, and may be acute or chronic. Rhinitis may be caused by changes in temperature, odors, foods, infection, age, systemic disease, drugs (cocaine) or prescribed medicine, or presence of a foreign body. Signs and symptoms include rhinorrhea, (or excessive nasal drainage), congestion, itchiness or sneezing.

Viral Rhinitis (Common Cold): an afebrile, infectious, acute inflammation of the mucous

membranes of the nasal cavity. highly contagious because the virus is shed for about two

days before the symptoms appear and also during the first part of the symptomatic phase; Immunity and recovery is very individualized and depends on personal host resistance and the virus, which caused the cold.

There are five viruses known to be linked to viral rhinitis Each virus has multiple strains:

o Rhinovirus, o Parainfluenza viruso Coronavirus o Respiratory syncytical virus (RSV)o Influenza viruso Adenovirus

Clinical Manifestations of Viral Rhinitis: (Symptoms last 1-2 weeks)

runny nose sneezing sore throat malaise low grade fever chills, headache muscle aches. cough usually appears as the illness progresses.

Medical Management: The treatment for the common cold is symptomatic therapy.

This includes increasing fluid intake, encouraging rest, increasing intake of vitamin C, and use of expectorant as needed. Warm salt water gargles can sooth a sore throat. NSAIDs are used to relieve aches, pains, and fevers in adults. Antihistamines can be used to relieve sneezing, rhinorrhea, and nasal congestions. Some research suggests that zinc lozenges can reduce the duration of the cold if taken within the first 24 hours. Antibiotic use is not recommended because it does not affect the virus or reduce the incidence of bacterial complications.

Nurses can be instrumental in teaching patients (pts) about self care and treating the symptoms of their cold. Teaching about how to break the chain of infection is crucial because these viruses are transmitted by direct contact, and inhalation of particles. Proper hand washing is the best way to prevent the transmission of viruses that cause the common cold.

Otitis Media (OM)

Acute Otitis Media An acute infection of the middle ear caused by bacterial

infection related to upper respiratory infections, inflammation of surrounding areas, or allergic reactions. Bacteria enter from contaminated secretions in the nasopharynx and the middle ear from a tympanic

membrane perforation. Purulent exudate is usually present and can result in conductive hearing loss.

Symptoms vary with severity of the infection and include pain, drainage from the ear, fever and hearing loss. The tympanic membrane is erythematous and bulging upon otoscopic examination.

This condition is treated with oral antibiotics (or antibiotic otic preparation if drainage occurs). The outcome depends on efficacy of the therapy, virulence of the bacteria, and the patient’s physical status. The severity of the infection may call for an incision of the tympanic membrane (myringotomy or typmanotomy) to relieve pressure and drain fluid from the middle ear.

Serous Otitis Media: implies fluid, without evidence of infection and is

commonly found in children. Causes include Eustachian tube obstruction, radiation therapy, carcinoma, or barotraumas.

Typical symptoms include hearing loss, and congestion, or popping or crackling noises as the Eustachian tube attempts to open. The tympanic membrane is dull upon examination.

Treatment may not be necessary unless infection occurs. If hearing loss is caused by effusion in the middle ear, a myringotomy may be performed. Corticosteroids sometimes are used to decrease edema associated with barotraumas.

Chronic Otitis Media: The result of repeated acute otitis media causing

irreversible tissue pathology and damage. Clinical manifestations include degrees of hearing loss, and

sometimes a foul smelling otorhrea. Otoscopic evaluation may show tympanic perforation, or a cholesteatoma (in-growth of skin of the external layer of the eardrum into the middle ear). This creates high negative pressure in the middle ear and the skin creates sacs which collect degenerated skin and sebaceous materials. Surgery is usually recommended.

Treatment includes suctioning of the ear, and use of antibiotic drops or powders to treat purulent discharge. Systemic antibiotics are not prescribed unless acute infection is present. Surgical reconstruction of the tympanic membrane or middle ear bones may be necessary. Surgical removal of the cholesteatoma may increase access to diseased structures, and create a dry, healthy ear.

Acute Bronchitis

Acute Bronchitis: inflammation of the bronchi in the lower respiratory tract

due to infection. The most common cause is viral (influenza and rhinovirus). However, different strains of bacteria may cause acute bronchitis in both smokers and non-smokers.

Common symptoms: o persistent cough which follows an acute upper

respiratory infection, such as rhinitis or pharyngitis. Cough usually comes with the production of clear, mucoid sputum. Some patients however may produce purulent sputum.

o Fevero Headacheo Malaiseo SOBo May show a slightly elevated RR, HR, and

temperature.


Chest x-rays are used to differentiate acute bronchitis from pneumonia.

Treatment: generally includes fluids, rest, and anti-inflammatory medications. Cough suppressants and bronchodilators may be used to treat coughing or wheezing during the night. Antibiotics are usually only prescribed if a patient has a prolonged infection, or is a chronic smoker with COPD.

Chronic Obstructive Pulmonary Disease (COPD) defined as a disease state in which airflow is limited, and

which is not fully reversible. COPD is commonly linked to emphysema, chronic bronchitis. COPD is the fifth leading cause of death in the US for all ages and genders.

Pathophysiology: the key concept to understand with COPD is that the

airflow limitations are both progressive, and associated with the inflammatory response.

Over time the continuous injury-repair cycle causes scar tissue formation in the airways.

Chronic Bronchitis: the presence of cough and sputum production for three

months over two consecutive years. Constant irritation (smoke, or other environmental agents)

results in hyper secretion of mucous, and inflammation, and overall dysfunction of the airways.

Emphysema: An impaired gas exchange resulting from destruction of the

walls of over distended alveoli. The walls of the alveoli are destroyed over time from recurrent infections

Risk factors: Exposure to tobacco smoke accounts for 80-90% of COPD

cases. Passive smoking Occupational exposures Air pollution Genetic deficiency of alpha1-antitripsin (an enzyme

inhibitor which counteracts the destruction of lung tissue

Clinical Manifestations: The three main characterizations of COPD:

o Cougho Sputum production o Dyspnea on exertion

These often worsen over time, and affect a patient’s ADLs. Weight loss is common with dyspnea, as eating and the

work of breathing often drains the COPD patient of energy There is also an increase in the use of accessory muscles to

breathe as the disease progresses. The chronic hyperinflation of the chest (“barrel chest”) is

caused by emphysema.

Complications of COPD: Life threatening and include respiratory insufficiency or

failure. Pneumonia Atelectasis Pneumothorax Cor pulmonale.

Risk reduction: Smoking Cessation is the single most effective

intervention to prevent or slow the progression of COPD.

Bronchodilators may be used to relieve bronchospasms and reduce airflow obstruction.

Corticosteroids (inhaled or systemic) may also be used. COPD patients are strongly advised to get the flu shot every year as well.

Oxygen therapy can be used over a long course, during exercise, or to prevent acute dyspnea. In some cases, surgery may also be recommended (bullectomy, lung volume reduction surgery, or lung transplantation).

Pulmonary Edema abnormal accumulation of fluid in the lung tissue/ alveolar

space which is severe and life threatening. This condition usually occurs from increased microvascular

pressure from abnormal cardiac function. The backup of blood in the pulmonary vasculature is

caused by inadequate left ventricular function. Fluid then begins to leak into the interstitial space and

alveoli. Hypervolemia or sudden increased intravascular pressure in

the lung can also cause pulmonary edema. An example of this is a patient who has had one lung

removed, where all the cardiac output then goes to one lung.

Clinical Manifestations: increased respiratory distress in the patient, which includes

dyspnea, central cyanosis, anxiety and agitation. As fluid leaks into the alveolar space and mixes with air, a

froth or foam is formed. A nurse must look for these types of frothy and often blood

tinged secretions when suctioning, or if a patient is coughing up sputum.

If the patient is in acute respiratory distress, they may become confused or stuporous.

Assessment: Crackles in the lungs are due to movement of air through

the alveolar fluid. Chest x-rays will show increased interstitial markings. The patient may be tachycardic with their pulse oximetry

falling, and ABG values indicating hypoxemia.

Medical Management: Goal is to correct the underlying condition which is usually

improving left ventricular function. Vasodilators, contractility and other cardiac function

medications are often used. In some cases if the patient does not respond to these, an

intra-aortic balloon pump may be indicated. Fluid restriction and diuretics are used to reduce fluid

overload. Oxygen is administered to correct hypoxemia. Morphine can be administered to reduce anxiety and

control pain. Intubation and mechanical ventilation may be necessary in

extreme cases.

Nursing Management: Nurses are responsible for the administering of oxygen and

other medications, as well as monitoring the patient’s response.

A nurse may need to assist with intubation and mechanical ventilation if necessary.

The nurse must monitor the patient carefully for any changes and report them immediately.

Ventilated patients will be monitored in an ICU setting.


Pneumothorax Occurs when the pleural space (which is usually negative or

subatomic) is exposed to positive atmospheric pressure. Negative pressure is needed for proper lung function.

When air enters the pleural space, the lung, or a portion of it collapses.

Simple Pneumothorax: A spontaneous collapse usually due to a rupture of a bleb or

bronchopleural fistula, which allows air from the airways to enter the pleural cavity.

This type of pneumothorax may also be associated with interstitial lung disease or severe emphysema.

Traumatic Pneumothorax: Occurs when air escapes from a laceration in the lung itself

through a wound in the chest wall such as rib fractures, abdominal trauma (gunshot, stab wounds), invasive thoracic procedures, or barotrauma from mechanical ventilation.

Often accompanied by hemothorax (collection of blood in the pleural space from torn vessels, laceration of greater vessels or laceration to the lungs).

Clinical Manifestations: Pain is usually sudden. With simple or uncomplicated collapses, pts may only have

slight chest discomfort and tachypnea. When the pneumothorax is large or the lung collapses

completely, the patient is in acute respiratory distress, displaying high anxiety, dyspnea, increased use of accessory muscles, and may develop severe central cyanosis from hypoxemia.

Severe chest pain Tachypnea Decreased movement on affected side Tympanic sound on percussion of chest wall Decreased or absent breath sounds Tactile fremitus may occur.

Medical Management: The goal is to remove the blood or air from the pleural

space. Chest tubes and suctioning may be used to drain fluid or

air. Auto transfusion (taking the patient’s blood that is draining,

filtering it, then transfusing it back to their own vasculature) may be necessary.

Antibiotics are used to avoid infection.Tension Pneumothorax:

Occurs when air enters the lung but cannot leave the chest. As pressure increases, the heart, the great vessels, trachea

etc. are pushed to opposite side of the chest, which then compress the unaffected lung.

If this type of pneumothorax is suspected, high concentration of oxygen is given.

A large bore needle can be used on the affected side to relieve the pressure and vent the positive pressure to the external environment.

A chest tube is then used to re-establish the negative pressure.

If prolonged air leak continues, surgery may be necessary to close the leak.

Pulmonary Embolism (PE) obstruction of the pulmonary artery by a thrombus which

occurs somewhere in the venous system (right side of the heart).

Commonly associated with trauma, surgery, pregnancy, heart failure, age 50 and older, hypercoagulable states, and prolonged immobility.

Most thrombi originate in the deep veins of the legs. Atrial Fibrillation can cause blood to stagnate and clot. These clots are prone to travel in the pulmonary circulation.

Pathophysiology: A thrombus then completely or partially obstructs the

pulmonary artery, in turn there is little or no blood flow Substances are released from the clot and surrounding area

which cause blood vessels and bronchioles to constrict. This results in increased pulmonary arterial pressure, and

an increase in right ventricular work to maintain pulmonary blood flow.

Work requirements can lead to right ventricular failure, which decreases cardiac output, systemic pressure, and leads to shock.

Clinical Manifestations: Tachypnea is the most frequent sign. Chest pain is common and sudden, and sometimes mimics

angina or an MI. Anxiety Tachycardia Apprehension Cough Diaphoresis Hemoptysis Syncope.

Assessment/ Diagnostics: Death from PE can occur within an hour of symptoms, so

early detection and treatment is crucial. The nurse looks for signs of DVT which is commonly

associated with PE. Other diagnostic tools may include a chest x-ray or

ventilation-perfusion scan. A pulmonary angiography is considered the gold standard for the diagnosis of PE, but is very invasive.

Prevention: Active leg exercises Early ambulation Use of compression stockings Use of heparin Pneumatic leg compression devices

Medical Management: general measures to improve respiratory and venous status

(O2 therapy, elevating the leg) anticoagulant therapy (Heparin) Thrombolytic Therapy (clot busters) Surgical therapies (embolectomy).

Nursing management: Minimizing the risks for PE, Preventing thrombus formation Assessing for PE Monitoring thrombolytic therapy Managing pain and O2 therapy appropriately Relieving anxiety Monitoring for complications Providing post operative nursing care Teaching patients self care techniques.


Module 6: Cardiovascular DisordersIntroduction and Health History AssessmentThe nurse must understand the major function of the cardiovascular system that affects all body systems. The circulatory system is responsible for the transport of oxygen and nutrients for metabolic processes to the tissues, transport of wastes for elimination, and circulate electrolytes and hormones. The pulmonary circulation moves blood through the lungs and creates a link with gas exchange function of the respiratory system while the systemic circulation moves blood throughout all other tissues. Central circulation refers to blood in the heart and pulmonary circulation and that which is outside the circulation is called central circulation. Blood moves throughout circulation along a pressure gradient, moving from high-pressure arterial system to low pressure venous system.

For a review of cardiovascular function and assessment read [1] ch. 27 in addition to required readings and [2] ch. 17. Knowledge of the nursing implications related to diagnostic testing is essential in caring for persons with cardiovascular dysfunction. The nurse must have expert assessment and care planning skills for patients with s&s of cardiovascular dysfunction. This module will focus on the following disorders: Hypertension, Arrhythmias, MI complications, and HF.

Health History AssessmentThe nurse should include in the health history an evaluation of the following:

Patient’s general appearance Effectiveness of the heart as a pump Filling volumes, cardiac output Compensatory mechanisms How the patient is affected by any conditions.

Indications that the heart is not contracting sufficiently or functioning effectively as a pump include:

Reduced pulse pressure Cardiac enlargement Murmurs and gallop rhythms

Diagnostic tests include: cardiac enzyme analysis particularly in the event of an

MI lipid profiles Serum electrolytes BUN Serum glucose Coagulation studies Hematologic studies. Chest x-ray, fluoroscopy, EKG (ECG), continuous

electrocardiographic monitoring, and Echocardiography may be indicated.

Arrhythmias and Conduction Problems- Types and ManagementArrhythmias/Dysrhythmias disorders of formation/ conduction (or both) of the electrical impulse within the heart that disturb heart rate and/or rhythm.

Sites of Origin Mechanisms of Formation or Conduction

Sinus (SA) NodesAtriaAtria (AV)

Node/JunctionVentricles

*Named according to site and mechanism

Normal (idio) rhythmBradycardiaTachycardiaArrhythmiasFlutterFibrillationPremature ComplexesBlocks

Understanding Normal Electrical Conduction The electrical impulse begins in the SA node and travels to

the AV node, and stimulated muscle cells contract in the atria.

As the AV node slows the impulse, the ventricles fill with blood.

Electrical impulses then travel quickly to the Purkinje Fibers in the ventricles.

This electrical stimulation causes the ventricles to contract (systole). As the cells repolarize, the ventricles relax (diastole).

o Electrical stimulation = Depolarization (mechanical contraction is called systole)

o Electrical Relaxation = Repolarization (mechanical relaxation is called diastole)

Waves, Complexes, and Intervals*Shown and interpreted on an ECG/EKG shows each phase of cardiac cycle which is reflected on a piece of paper.

P Wave- represents electrical impulse starting at SA node and travelling through atria (atrial depolarization)

QRS Complex- part of the ECG that represents conduction of the electrical impulse through the ventricles (ventricular depolarization)

T Wave- part of the ECG that represents ventricular repolarization

U Wave- part of the ECG that represents Purkinje fibers (usually seen in pts with low serum potassium and may be mistaken for an extra P wave)

PR Interval- part of the ECG that represents the conduction of the electrical impulse from the SA node, through the SV node

ST Segment- part of the ECG that represents the end of ventricular depolarization (end of the QRS complex) through ventricular repolarization (end of the T wave)

QT Interval- part of the ECG that represents ventricular depolarization to repolarization

TP Interval- measured from end of the T wave until beginning of next P wave (isoelectric period)

PP Interval- measured from beginning of one P wave to the next P wave –used to determine atrial rhythm and rate

Normal Sinus Rhythm Ventricular and Atrial Rate: 60-100 in an adult Ventricular and Atrial Rhythm: Regular QRS shape and duration: usually normal but may be

regularly abnormal P wave: normal and consistent shape: always in front of

the QRS PR interval: consistent interval (0.12-0.2 seconds) P:QRS interval ratio: 1:1

Adjunctive Modalities and Management Depends whether arrhythmia is chronic/ acute, cause, and

what potential hemodynamic effects Treated with meds (listed on table 27-1) or external

electrical therapy Monitor pts response to meds-make sure pt has knowledge

to manage medication regimenPacemaker Therapy

Can be used in patients as a temporary or permanent way of managing conduction problems of the heart.

It provides a regulated electrical stimulus to the heart muscle to regulate the underlying problem.

This type of management is usually used for patients with slower- than- normal impulse formation or conduction problems that cause symptoms.


Other Therapies: Cardioversion Defibrillation Implantable Cardioverter Defibrillator Electrophysiologic Studies Cardiac Conduction Surgery

Hypertension (HTN)- Definitions, Risk Factors, Pathophysiology and Clinical Manifestations

Complex, chronic condition that is referred to the “silent killer” since the patient is often asymptomatic.

Detection and treatment delays result in target organs becoming damaged and other complications

Defined as blood pressure >140/90 mmHg HSFA (2005) in [3] pg 32 defines it: a medical condition in

which blood pressure is consistently above the normal range.

The pathophysiology of hypertension is complex. o Most hypertensive individuals have “essential”

hypertension, since they have no clear identifiable cause for their hypertension.

Research tells us that there are interrelated factors that contribute to elevated blood pressure: salt, obesity, insulin resistance, renin-angiotension system and the sympathetic nervous system.

Complications: [3] pg. 24:• Incidence of stroke increases approx. 8-fold• 40% of cases of acute MI or stroke are due to hypertension• Direct relationship to vascular mortality• Accelerates atherosclerosis and blood vessel injury

increasing the risk of vascular disease and subsequent organ damage (heart, brain, kidney, eye, or limbs)

• Due to poor adherence to anti-hypertensive treatment, approx. 75% of patients do not achieve optimal BP control

Diagnosis of Hypertension:• Nurses require knowledge of the process for establishing a

diagnosis of hypertension so that the nurse can expedite and

• support the client through the diagnosis phase. • CHEP (2005) in [3] pg 33 states that diagnosis of

hypertension can now be made in 1,2, or 3 visits based on an algorithm which now expedites the assessment and diagnosis of hypertension to enable more timely treatment.

• Summary of recommendations are:o For clients with high BP urgencies/emergencies a

diagnosis of treatment can be made on the first visit.

o If client has target organ damage, chronic kidney disease, diabetes, or BP = to or > than 180/110 a diagnosis can be made on the second visit made to assess blood pressure.

o For clients with BP= or > 160-179/100-109 (and not already diagnosed based on criteria outlined above), a diagnosis can be made at the third visit.

• CHEP (2005) in [3] pg 33 recommends all 3 validated BP monitoring technologies, office/clinic-based measurement, self/home and ambulatory BP monitoring (alone or in combination) to make diagnosis of hypertension. The most recent evidence suggests that when properly assessed, self/home and ABPM are as or more effective in facilitating diagnosis than office/clinic-based measurement.

• Health history further includes physical exam focusing on examination of retina, urinalysis increased BUN, CR, albuminuria, blood chemistry, EKG and Echo results, history of TIAs [1.

Treatment Hypertension Treatment Nursing best Practice Guidelines[3] pg.25-28.

Blood pressure control is one of several important components in an anti-atherosclerotic strategy.

Other factors important in a global CV risk management plan include:

o Lifestyle modifications (diet, wt loss, exercise, smoking cessation) is the cornerstone of global management of many atherosclerotic risk factors and may be enough to manage BP control

o Consideration of both statins and ASA as part of CV protection strategy for those with

Types of ArrhythmiasDescription AV Rate AV Rhythm

Sinus Bradycardia: SA node creates slower than normal rate (metabolic needs, vagal stimulation, meds, ICP, MI)

*Less than 60 in adults Normal

Sinus Tachycardia: SA node creates rate faster than normal (blood loss, shock, hypovolemia/hypervolemia, pain, anxiety, exercise)

*Greater than 100 in adults

Normal

Sinus Arrhythmias: SA node creates irregular rhythm; usually increases with inspiration, decreases with expiration (heart/ valvular diseases, respiratory related)

Normal Irregular

Atrial Flutter: impulses in atrium of 250-400, but AV node cannot conduct all impulses (therapeutic block at AV node: if ventricular rate was 250-400, possibly fatal)*causes chest pain, SOB, low BP

*A: 250-400*V: 75-150

*Atrial rhythm is regular; ventricular rhythm is usually regular but can be irregular due to change in AV conduction

Atrial Fibrillation: rapid, disorganized, uncoordinated twitching of atrial muscle; acute or chronic

*A: 300-600*V: 120- 200 (untreated)

*Highly irregular

Ventricular Tachycardia: 3 or more Premature Ventricular Complexes (PVC) (impulse that starts in ventricles and conducted before next sinus impulse) which exceed 100 BPM; associated with coronary artery disease; pt usually unresponsive and pulseless

*A- depends on underlying sinus rhythm*V- 100-200

*Usually normal

Ventricular Fibrillation: rapid, disorganized ventricular rhythm- quivering of the ventricles; no atrial activity seen on ECG

*V- 300 *Extremely irregular with no specific pattern


hypertensiono Angiotensin Converting Enzyme (ACE)

inhibitors for clients with established atherosclerotic disease

o ACE inhibitors or Angiotensin II Receptor Blockers (ARB) for those with diabetes and kidney disease

o Stable, normotensive persons should check their BP for a 1 week period every 3 months. BP should be checked more frequently if they have diabetes, or have difficulty following a treatment plan.

o Self/home BP values > or = 135/85 mmHg should be considered elevated and associated with increased overall mortality risk similar to clinic readings > 140/90 mmHg. In an asymptomatic person a BP of >200/130 mmHG is a medical emergency.

o The target BP for a person with diabetes or renal disease and a BP > or = 130/80 is to have BP < than 130/80. For the person with proteinuria >1gm/day the target is <125/75.

o See [3] pg 40 to appreciate how lifestyle therapies impact on BP in hypertensive adults

o Dietary Approaches to stop hypertension (DASH) includes fruits, vegetables, and low-fat dairy products and well as reduced sodium intake proves to significantly lower BP in persons with stage 1 (grade 1) hypertension, high normal BP, and isolated systolic hypertension.

o The CHEP (2005) recommends that sodium intake for hypertensive persons be limited to 65-100 mmol/day, which is equivalent of 1500-2400 milligrams or 2/3-1tsp of table salt.

o Keeping healthy BMI and waist circumference <102 cm for males, and 88 cm for females will reduce possibility of hypertension

There is rapid decline in CV risk up to 50% after 1 year for those who stop smoking. The nurse must be knowledgeable about the relationship between smoking and risk of CV disease and be able to implement Brief Tobacco Interventions after determining patient readiness. See [3] pg 45-56 for more on the effects of smoking, exercise, alcohol, and stress and hypertension.

Nurses must be able to educate clients regarding pharmacological management of hypertension in collaboration with physicians and pharmacists. One complication the nurse must advise on is the prevention of rebound hypertension with sudden cessation of antihypertensives. Another complication is the side effects of antihypertensive medication.

Nurses are in the best position to provide education about antihypertensive medications and monitor their therapeutic effectiveness. Hence nurses must be knowledgeable about classes of anti-hypertensive medication

Myocardial Infarction- Pathophysiology, Clinical Manifestations & AssessmentPathophysiology:Process in which areas of myocardial cells are permanently destroyed which is caused by reduced blood flow- atherosclerosis/ occlusion (embolus/thrombus). Other causes may be vasospasm, decreased O2 supply or increased demand for O2 (rapid heart rate/cocaine ingestion). When cells are deprived of O2, ischemia or cellular injury/death of cells (infarction) occurs. For further explanation of AMI please be familiar with Porth Ch.19.

Clinical Manifestations:Nurses should look for signs of chest pain possibly radiation to neck, jaw, left arm, especially any that continues with rest. Note that women experience atypical S&S and elderly more shortness of breath (SOB). SOB, anxiety, restlessness, cool/pale skin, increased HR and RR, indigestion, nausea and vomitting are other clinical manifestations which a nurse should be aware of. Symptoms often mirror those of unstable angina.Immediate Interventions:

Resting position, legs elevated and supine or semi-Fowler Oxygen 2L via nasal prongs Nitroglycerin sublingual 5 minutes apart x3 doses 12 lead ECG stat Transfer to critical care Thrombolytic therapy usually administered 20 minutes

later if unrelieved by nitro

Diagnostic Findings Diagnosis includes symptoms, 12 lead ECG and lab results. Patient History: presenting symptoms, previous illness,

family history ECG: monitors location, evolution and resolution of MI Classic ECG changes: T-wave inversion, ST-segment

elevation, abnormal Q wave. Laboratory Tests:

o Creatinekinase and its Isoenzymes: CK-MB is cardiac specific isoenzyme found in cardiac cells indicating damage to these cells.

o Myoglobin: heme-protein that helps transport O2-levels increase with onset of MI.

o Troponin: protein in myocardium responsible for contractile process- levels peak with CK-MB.

Myocardial Postinfarction Recovery Period Goal: prevent complications 3 zones of myocardial tissue damage, including inner zone

of necrosis with surrounding zone of cell injury, and outer zone of ischemia.

4-7 days post MI, rupture of the ventricle, interventricular septum, or the valve structures may occur. Replacement of necrotic myocardial tissue usually happens by the 7th week.

Fibrous scar tissue develops, which lacks the contractile, elastic, and conductive properties of normal myocardial cells.

An aneurism may develop due to scar tissue in ventricle, which can create thrombus formation and/ or increase workload of left side of heart causing left heart failure.

Stages of recovery related to size of infarct and changes and complications are determined by extent and location of the injury.

Complications include sudden death, heart failure and cardiogenic shock, pericarditis, and Dressler syndrome, thromboemboli, rupture of the heart, ventricular aneurisms, deep vein thrombosis.

Other Treatments Emergency Percutaneous Coronary Intervention (PCI)

includes Percutaneous Transluminal Coronary Angioplasty (PTCA)- Treats underlying sclerotic lesion and may be used to open occluded coronary artery-promote perfusion to area deprived of O2

Brachytherapy Coronary Artery Bypass Grafting (CABG)- for those with

significant CHD and who are not candidates for PCI

Pharmacologic Therapy Thrombolytics: usually IV- dissolve/lyse thrombus


(dissolve all clots: not to be used if pt has protective clot, after major surgery or hemorrhagic stroke)- best results if administered within 60-90 minutes of symptom onset, typically stretokinase is administered.

Analgesics: usually morphine (IV)- reduces pain/anxiety, reduces preload (less workload on heart), relaxes bronchioles (increase O2)

Angiotensin-Converting Enzyme Inhibitors (ACE-I): net result= decreased BP, diuresis, decreased O2 demand on heart- decreases mortality rate; ensure pt is not hypotensive, hypovolemic, hyponatremic or hyperkalemic; BP, urine output, electrolytes must be monitored.

B-Adrenergic-blocking drugs: may be used to reduce sympathetic stimulation of the heart after myocardial infarction. These drugs decrease myocardial contractility and cardiac workload, alter resting myocardial membrane potentials and decrease arrhythmia frequencies, may aid in redistributing coronary artery blood flow and improving myocardial blood flow.

Anti-arrhythmia medications: may be given to prevent or treat life-threatening arrhythmias that often occur with AMI.

Myocardial Infarction- The Nursing Process

The Nursing Process: Assessment:

o Establish baselineo Careful historyo Symptoms (time, duration, precipitating/relieving

factors, comparison to previous symptoms)o Physical assessment (detect

change/complications)o IV sites.

Diagnosis:o Nursing Diagnosis: based on clinical

manifestations, history, diagnostics (EX: ineffective tissue perfusion related to reduced coronary blood flow from coronary thrombus, anxiety related to fear of death etc.)

o Potential Complications: pulmonary edema, heart failure, cardiogenic shock, arrhythmias, cardiac arrest, myocardial rupture, deep vein thrombosis.

o Planning/Goals: relief of pain/ ischemic S&S, prevent further damage, decrease workload of heart, reduce anxiety

Nursing Interventions:o Immediate administration of oxygen and

nitroglycerino Relieving Pain/Ischemia: balance heart’s O2

supply/demand- meds (beta blocker, morphine, nitro, O2 therapy etc.), assess VS, promote physical rest (backrest elevated)

o Improving Respiratory Function: careful respiratory assessment, encourage pt to breathe deep/change positions (prevent fluid from pooling)

o Promote Tissue Perfusion: bed/chair rest, monitor temperature/peripheral pulses, teach dorsiflexion exercises and monitor Homan’s sign, admin. O2,

o Reduce Anxiety: create trust, provide info, quiet environment, using humor, support beliefs (praying etc.), music, address fears

o Monitor/Manage Potential Complications: close monitoring/ early ID-report changes promptly,

elastic stockings, ROM exercise, heparino Promoting Home/Community-Based Care: ID

priorities, educate, encourage involvement in rehab program

Evaluation:o Relief of anginao No respiratory difficultieso Adequate tissue perfusiono Decreased anxietyo Adherence to self-care programo Absence of complications

Chronic Heart Failure (CHF) CHF is the inability of the heart to fill (diastole) and/or

contract (systole) to pump sufficient blood to meet the needs of the tissues for oxygen and nutrients.

It is a clinical syndrome including fluid overload or inadequate tissue perfusion; however, many with Heart Failure (HF) do not manifest with pulmonary or systemic congestion.

Clinical Manifestations CHF produces S&S of failure of both ventricles. S&s tend to be differentiated based on the effect on the

ventricles. It is the nurse's role to monitor and manage potential

complications.

Left-sided Heart Failure: Increased L ventricular end-diastolic blood volume which

increase the L ventricular end-diastolic pressure, which decreases blood flow from L atrium to L ventricle, during diastole, resulting in pulmonary venous congestion backward failure.

Pulmonary congestion: dyspnea, cough, pulmonary crackles, lower O2 sat levels, possible S3 heard Dyspnea, DOE, orthopnea, PND

Bi-basilar crackles that do not clear with coughing, then all lobes affected

Cough-initially dry and unproductive mistaken for other disorder, eventually severe pulmonary edema.

Renal-oliguria, then release of renin then aldosterone, then Na+ and fluid retention intravascular volume. Nocturia due to ↑rest and therefore better perfusion.

Altered digestion Cerebral-e.g., dizziness, confusion, anxiety; Fatigue an

Insomnia Stimulation of SNS causes further vasoconstriction-cool

clammy skin, tachycardia, weak pulsesRight-Sided Heart Failure

Congestion of viscera and peripheral tissues since right ventricle can not accommodate venous return of blood

↑ JVP that is >3 cm above sternal angle Edema of lower extremities, beginning in ankles, then

upwards including sacrum if on bed rest, genitalia and abdomen, hands and arms may become edematous, also periorbital edema

Ascites Weakness, anorexia, nausea Fluid retention weight gain. Pitting edema with 4.5+L fluid

weight gain Hepatomegaly and RUQ tenderness, possible secondary

liver dysfunction, increased liver may exert pressure on other organs

Fatigue due to ↓ cardiac output, circulation, and inadequate removal of catabolic waste products from tissues.


DiagnosisS&s are common with other conditions like renal failure, liver failure, oncologic conditions, and COPD therefore, the patient risks being treated as if they have HF. Assessment of ventricular function is essential to diagnosis of HF.Diagnostics

Echocardiogram-identify cause, location, type, severity of HF

Radionuclide ventriculography Ventriculogram with cardiac catheterization Chest-ray and ECG Labs: lytes, BUN, TSH, CBC, urinalysis Patient risk should be determined following an MI

Interventions and TreatmentGoals:

Eliminate or reduce any etiologic contributory factors, especially those that may be reversible, such as A. Fibrillation or excessive ETOH ingestion and;

Reduce the workload on the heart by reducing afterload and preload

o Na+ (≤ 2-3g/day) and fluid restrictiono Monitor risk of hypokalemia-check labs and

increase K+ in dieto Monitor weight gain and I+O amounts dailyo Monitor oliguria or anuriao Monitor areas of edemao Monitor postural hypotensiono Monitor dehydration-skin turgor, mucous

membranes, BP etco Regular exerciseo ↓ETOH, smokingo O2 therapy-monitor O2 stats, orthopnea, PND,

DOE, lung and heart sounds, mental statuso PTCA may be necessary if CAD involved, also

mechanical assist devices and transplantationo Pacing device if electrical conduction defects-left

bundle branch block (LBBB) common

Pathophysiology Systolic HF decrease the amount of blood ejected from the

ventricle, which stimulates the sympathetic nervous system (sns) to release epinephrine and norepinephrine.

Continued release of these cause loss of beta1energic receptor sites and further damage the heart muscles.

The sympathetic stimulation and decrease renal perfusion cause release of renin from kidneys.

Renin promotes formation of angiotensin I which is converted to angiotensin II with production of ACE.

Angiotensin II, a vasoconstrictor promote Na+ and fluid retention, and thirst.

Aldosterone exacerbates myocardial fibrosis. Angiotensin, aldosterone, and other neurohormones lead to

an increase in preload and afterload, stressing the ventricular walls and workload of the heart.

As the heart's workload contractility of the myofibrils decreases.

Decreased contractility results in increased end-diastolic blood volume in the ventricle, stretching the myofibres and increasing the size of the ventricle that further stresses the ventricular wall.

To compensate the heart muscle thickens (ventricular hypertrophy); however, capillary blood supply cannot accommodate this growth, resulting in myocardial ischemia further complicated by sympathetic-induced coronary artery vasoconstriction, ↑ ventricular wall stress, and

decreased mitochondrial energy production. This scenario has been termed "vicious cycle of HF"

because the heart cannot pump sufficiently, yet is stimulated to work harder, and heart failure ensues. The dominant feature in HF is inadequate tissue perfusion.

Pharmacological Therapy Several meds for systolic HF Meds for diastolic failure depend on underlying condition

such as hypertension or valvular dysfunction -may include CA++ channel blockers

ACE inhibitor for mild HF If unable to continue ACE inhibitor due to renal

impairment (↑CR and ↑K+), then angiotensin II receptor blocker (ARB) or hydralazine and isosorbide dinitrate.

Diuretic- lasix, spironolactone Digitalis added to ACE inhibitor if symptoms continue Beta-blockers added to initial meds to improve mortality

and morbidity Possibly Anticaogulation NSAIDs should be avoided as ↑systemic vascular

resistance and renal perfusion Monitor complications of prolonged diuretic use

Heart Failure - A Case Study

The Case StudyA 78-year-old male is admitted to the hospital with the chief complaint of shortness of breath. He states the shortness of breath has been increasing over the past 2 months and is aggravated by exertion. He has found that he often awakens at night with a sensation of smothering that is partially relieved when he gets up and opens the window. He has not noted ankle swelling or edema.

Past medical history is only positive for myocardial infarction 8 years ago. He currently does not have complaints of chest pain.

Blood pressure is 140/98. When the nurse listens to his heart, she hears a normal S1 and S2 with a rate of 88. When listening to the lungs, the nurse notes bibasilar crackles. There is no peripheral edema.

The admission diagnosis for the patient was left-sided heart failure.

Question 1 - Describe the pathophysiology of left-sided heart failure.

The left side of the heart is responsible for pumping blood from the left ventricle to the systemic circulation. Blood flows from the pulmonary system to the left atrium into the left ventricle. Left ventricular failure occurs when the workload of the left ventricle increases and the muscle hypertrophies. Over time, the increased workload will increase the myocardial oxygen need of the left ventricle. Ventricular hypertrophy will cause a decreasing ability of left ventricular stretch to compensate for increasing end diastolic volume. The Frank-Starling mechanism in a normal heart is responsible for an increased stretch of the ventricular muscle, increasing contractility, when there is an increase in left ventricular end diastolic volume will increase stretch and increase cardiac output.

In the patient with hypertension, the afterload will increase secondary to increased peripheral vascular resistance. Increased afterload will increase the workload of the left ventricle. Progressive increased workload will cause the left ventricle to fail, decreasing cardiac output and increasing left ventricular end diastolic pressure. The increased end diastolic pressure will increase the workload of the left atrium. Increased workload will cause failure of the left atrium and increased pressure within the pulmonary system, which causes the


pulmonary crackles that are all commonly seen with increased pulmonary pressure.

Question 2 - Which of the clinical manifestations given in this case would be found in a patient with left-sided heart failure?

The increased pressure within the pulmonary system is responsible for the pulmonary symptoms seen in left ventricular failure. Increased pulmonary pressures lead to pulmonary congestion and decreased ability to oxygenate. Initially, as in this case, the individual will have complaints of increased shortness of breath with activity as exercise will increase oxygen needs. Further progression will lead to paroxysmal nocturnal dyspnea, a sensation of increased shortness of breath at night 1 to 2 hours after bedtime, which can be relieved with sitting or standing. On exam, the nurse will be able to hear pulmonary crackles that are a reflection of the fluid that has moved into the alveoli.Question 3 - How does left-sided heart failure impact preload, afterload, and contractility?Preload is a reflection of left ventricular end diastolic volume and pressure. Decreased ability to empty the left ventricle will decrease cardiac output and increase the amount of blood that is present in the left ventricle at the end of systole, which will increase preload.

Afterload is increased by both increased peripheral vascular resistance and changes in ventricular wall tension. Increased stretch of the left ventricle will be associated with increased ventricular wall tension and increased myocardial oxygen need. This can actually increase ischemia of the left ventricle and worsen failure.

Contractility actually is a measure of how well the left ventricle is able to mechanically perform its function. Increased contractility will improve cardiac output. Left ventricular failure will decrease contractility. Stretch of the ventricular muscle will decrease effectiveness of actin and myosin interactions.

Question 4 - Describe other clinical manifestations the nurse would monitor for in this patient. Which clinical manifestations would be seen in only left-sided failure? Which symptoms would occur if right-sided failure was present also?

Clinical manifestations of left ventricular failure will always include the pulmonary symptoms seen in this case. The most common symptoms are dyspnea on exertion (DOE), orthopnea, paroxysmal nocturnal dyspnea (PND), and pulmonary crackles.

The clinical manifestations of right-sided failure are related to increased pressure within the venous system. Remember that the superior and inferior vena cava empty into the right atrium, which then empties into the right ventricle. When the right ventricle fails, there is increased pressure within the right atrium that causes increased pressure in the venous system. This increased pressure will cause clinical manifestations of peripheral edema, hepatomegaly, and increased jugular venous distension.

Remember that many patients have biventricular failure, and in this case, the nurse would see a combination of the above symptoms.

Question 5 -What medications would you administer to a patient with CHF?Diuretics: diuretics are given to patient with congestive heart failure to decrease volume. In both left- and right-sided heart failure, there is associated fluid retention. Decreased cardiac output will stimulate the kidneys to decrease perfusion and retain fluid.

ACE inhibitors: an ACE inhibitor will decrease the release of aldosterone, which will decreased blood volume and preload. The

decreased formation of angiotensin will decrease peripheral vascular resistance and afterload.

Beta-blockers: Beta-blockers will decrease the workload of the heart and myocardial oxygen needs by decreasing cardiac output and contractility.

Pathophysiology of Ovarian CancerIn the adult female, the ovaries are flat, almond-shaped structures that measure 4 × 2.5 × 1.5 cm. They are located on either side of the uterus below the ends of the two fallopian tubes. The ovaries produce estrogens, progesterone, and androgens. In Canada, gynecologic tumors (cancers of the endometrium, ovaries, vulva, vagina, placenta, and adnexa) account for 11% of malignant tumors in women and 81% of genital cancers (Public Health Agency of Canada, 2003). Ovarian cancer causes more deaths than any other cancer of the female reproductive system. About 75% of cases are detected at a late stage (Duffy, 2001). The ovary is a common site of primary as well as metastatic lesions from other cancers. Most cases affect women ages 50 to 59.Cancer of the ovary is complex because of the diversity of tissue types that originate in the ovary. As a result of this diversity, there are several types of ovarian cancers: Malignant neoplasms of the ovary can be divided into three categories:

Epithelial tumors, Germ cell tumors, Gonadal stromal tumors.

About 90% of ovarian cancers derive from malignant transformation of the epithelium of the ovary, which is contiguous with the peritoneal mesothelium.

Risk Factors: A strong family history of cancer, particularly breast and

ovarian cancer is the most important risk factor. Nulliparity is also associated with increased risk, whereas

oral contraceptive use, pregnancy, and lactation are associated with decreased risk. These observations suggest that stimulation of the ovarian epithelium which occurs with nulliparity and uninterrupted ovulation may predispose to ovarian cancer.

A strong family history of breast and ovarian cancer, sometimes at an early age, may be related to the presence of an inherited mutation in one of two genes, known as BRCA1 and BRCA2. BRCA-1 is a genetic mutation that results in an increased risk for breast and ovarian cancer. BRCA-2 is another genetic mutation that may result in increased risk for both female and male breast cancers and for ovarian cancer

Older age is a major risk factor because the incidence of this disease peaks in the eighth decade of life.

High dietary fat intake, mumps before menarche, use of talc in the perineal area.

Multiparity, oral contraceptive use, breastfeeding, and anovulatory disorders may be protective.

Survival rates depend on the stage of the cancer at diagnosis.

Much more needs to be learned about the risks associated with some mutations, the reliability of testing, and the efficacy of follow-up.


Clinical Manifestations of Ovarian CancerSymptoms are nonspecific and include:

General abdominal discomfort Flatulence Indigestion Pressure Bloating Cramps Sense of pelvic heaviness Loss of appetite Feeling of fullness Changes in bowel habits

As the malignancy grows, a variety of manifestations such as: Increased abdominal girth Bowel and bladder dysfunction Persistent pelvic or abdominal pain Menstrual irregularities Leg pain Ascites

Symptoms are often vague, and many women ignore the symptoms. Ovarian cancer is often silent, but enlargement of the abdomen from an accumulation of fluid is the most common sign. Any woman with gastrointestinal symptoms and without a known diagnosis must be evaluated with ovarian cancer in mind. Flatulence, fullness after a light meal, and increasing abdominal girth are significant symptoms. An ovarian malignancy should be considered when abnormal vaginal bleeding occurs. Vague, undiagnosed, persistent gastrointestinal symptoms should alert the nurse to the possibility of an early ovarian malignancy. A palpable ovary in a woman who has gone through menopause is investigated because ovaries normally become smaller and less palpable after menopause.

Diagnostic Studies : No screening exists for ovarian cancer. Because early ovarian cancer is usually asymptomatic, yearly bimanual pelvic examinations should be performed to identify the presence of an ovarian mass. Postmenopausal women should not have palpable ovaries, so a mass of any size should be suspected as possible ovarian cancer. An abdominal or vaginal ultrasound can be used to detect ovarian masses.For women with high risk for ovarian cancer, screening using a combination of the tumor marker, CA-125, and ultrasound is recommended in addition to yearly pelvic examination. CA-125 is positive in 80% of women with epithelial ovarian cancer and is used to monitor the course of the disease. There may be an elevation of CA-125 levels due to non ovarian malignancies or benign conditions such as fibroids or endometriosis.

Ovarian Cancer Risk FactorsWomen between the ages of 50-59 are at a high risk of developing ovarian cancers. There seems to be evidence to support that there are

certain factors, which are associated with a decreased risk of developing ovarian cancer, and seem to be protective.

Ovarian Cancer- Collaborative CareWomen identified as being at high risk based on family and health history may require counseling regarding options such as prophylactic oophorectomy and birth control pills. Although oophorectomy can significantly reduce the risk of ovarian cancer it is important to note that it will not completely eliminate it. If a diagnosis of ovarian cancer is made, staging is critical for guiding treatment decisions.

Stages of Ovarian CancerI—Growth limited to the ovariesII—Growth involves one or both ovaries with pelvic extensionIII—Growth involves one or both ovaries with metastases outside the pelvis or positive retroperitoneal or inguinal nodesIV—Growth involves one or both ovaries with distant metastases

A total abdominal hysterectomy with removal of the fallopian tubes and ovaries and the omentum (bilateral salpingo-oophorectomy and omentectomy) is the standard procedure for early disease. The addition of chemotherapy or the instillation of interperitoneal radioisotopes is usually suggested for stage I disease.

Stage II disease may receive external abdominal and pelvic radiation, or systemic combined chemotherapy in the patient who is clinically free of symptoms. After completion of systemic chemotherapy in the patient who is clinically free of symptoms, a “second-look” surgical procedure is often performed to determine whether there is any evidence of disease. If no disease is found, the patient is monitored for recurrent disease.

Chemotherapy such as cyclophosphamide (Cytoxan), doxorubicin (Adriamycin), cisplatin (Platinol-AQ), carboplatin (Paraplatin), or paclitaxel (Taxol) is used for the treatment of stage III and stage IV of the disease. Hexamethylmelamine (Hexalen), ifosfamide (Ifex), bone marrow transplantation, and peripheral blood stem cell support may also be used. Paclitaxel, cisplatin, and carboplatin are most often used because of their excellent clinical benefits and manageable toxicity. Leukopenia, neurotoxicity, and fever may occur.

In the advanced stages of the disease chemotherapy is the most common form of treatment. Radiation and chemotherapy may be used to shrink the size of the tumor, relieving pressure and pain. Surgical debulking is often done in conjunction with chemotherapy for advanced disease.

Nursing measures include those related to the patient's treatment plan, be it surgery, chemotherapy, radiation, or palliation. Emotional support, comfort measures, and information, plus attentiveness and caring, are meaningful aids to the patient and her family.

Pathophysiology of Prostate Cancer

Prostate cancer is a malignant tumor of the prostate gland, it is the most frequently diagnosed cancer in Canadian males, and is the third most common cause of death due to cancer in men. The Canadian Cancer Society (2005)estimates that 20,500 men will be diagnosed with prostate cancer in 2005 and that 4,300 will die of the disease. Prostate cancer rates are twice as high in African Canadian men as in Caucasian men, and African Canadian men are more likely to die of prostate cancer than men in any other racial or ethnic group.

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Prostate cancer : Is an androgen-dependent adenocarcinoma. The majority of tumors occur in the outer aspect of the

prostate gland. Prostate cancer is usually slow growing. It can spread by three routes:

o direct extensiono through the lymph systemo through the bloodstream.

Prostatic adenocarcinomas, which account for 98% of all primary prostatic cancers, are commonly multicentric and located in the peripheral zones of the prostate. The high frequency of invasion of the prostatic capsule by adenocarcinoma relates to its subcapsular location. Invasion of the urinary bladder is less common and occurs later in the clinical course. Metastasis to the lung reflects lymphatic spread through the thoracic duct and dissemination from the prostatic venous plexus to the inferior vena cava. Bony metastases, particularly to the vertebral column, ribs, and pelvis, produce pain that often presents as a first sign of the disease.

Causes: There is no single cause of prostate cancer; some factors appear to increase the risk of developing it. Nonmodifiable risk factors for prostate cancer include:

Increasing age: the incidence of prostate cancer increases rapidly after the age of 50 years, and more than 70% of cases occur in men over 65 years of age.

Family history of prostate cancer, especially first degree relatives.

African ancestry; rate is twice that of white men, more likely to have prostate cancer at a younger age, have more aggressive tumors at diagnosis, and higher mortality rate.

Obesity, physical inactivity, eating a diet high in fat, working with a metal called cadmium, are being studied as possible risk factors. It is possible to develop prostate cancer without having any of these risk factors.

Prostate Cancer- Clinical Manifestations/DiagnosticsSign and SymptomsProstate cancer may not cause any signs or symptoms, especially in the early stages. The presence of symptoms often suggests locally advanced or metastatic disease. Depending on the size and location of prostatic cancer at the time of diagnosis, there may be changes associated with the voiding pattern similar to those found in BPH. These include urgency, frequency, nocturia, hesitancy, dysuria, hematuria, or blood in the ejaculate. On physical examination, the prostate is nodular and fixed. Bone metastasis often is characterized

by low back pain. Pathologic fractures can occur at the site of metastasis. Symptoms related to metastases include backache, hip pain, perineal and rectal discomfort, anemia, weight loss, weakness, nausea, and oliguria (decreased urine output). Unfortunately, these symptoms may be the first indications of prostate cancer. Early recognition and treatment is required to control growth, prevent metastasis, and preserve quality of life.Diagnostic TestingImproved diagnostic techniques have greatly enhanced the detection of prostate cancer. When prostate cancer is detected early, the likelihood of cure is high. Every man older than 40 years of age should have a DRE (digital rectal examination) as part of his regular health checkup. Routine repeated rectal palpation of the gland (preferably by the same examiner) is important because early cancer may be detected as a nodule within the substance of the gland or as an extensive hardening in the posterior lobe. The more advanced lesion is “stony hard” and fixed.Blood Testing

PSA(prostate-specific antigen), a neutral serine protease, is produced by the normal and neoplastic ductal epithelium of the prostate and secreted into the glandular lumen (Brawer, Cheli, Neaman et al., 2000; Kalish & McKinlay, 1999).

A simple blood test can be used to measure PSA levels. The concentration of PSA in the blood is proportional to the total prostatic mass.

Although the PSA level indicates the presence of prostate tissue, it does not necessarily indicate malignancy.

Imaging Studies TRUS-usually the only imaging study needed to diagnose

prostate cancer. Transrectal ultrasound (TRUS) studies are indicated for men who have elevated PSA levels and abnormal DRE findings. TRUS studies help in detecting nonpalpable prostate cancers and assist with staging localized prostate cancer. Needle biopsies of the prostate are commonly guided by TRUS.

Other imaging may be used if metastases is suspected:o X-rayo CT scan and MRIo Bone scan

Prostate Cancer- Surgical Management and ComplicationsProstate surgery may be indicated for the patient with BPH or prostate cancer. The objectives before prostate surgery are to assess the patient's general health status and to establish optimal renal function. Prostate surgery should be performed before acute urinary retention develops and damages the upper urinary tract and collecting system or, in the case of prostate cancer, before cancer progresses. A radical prostatectomy is the surgical procedure considered to be the most effective treatment for long term survival. This type of surgery is usually performed on those men whose cancer is confined to the prostate, usually stage one or two, and who are in relatively good health. A radical prostatectomy is performed either using the two most common approaches; retropubic or perineal resection.

ComplicationsComplications depend on the type of prostatectomy performed and almost always include:

sexual dysfunction- All prostatectomies carry a risk of impotence because of potential damage to the pudendal nerves. The incidence of erectile dysfunction may depend on age, and preoperative sexual functioning.

Incontinence- nearly all men experience a problem with urinary control post-operatively for one or two months. Incontinence occurs because the bladder must be reattached to the urethra after the prostate is removed. With time the most men regain control as the bladder adjusts.

Other common complications may include:o Hemorrhage,


o Clot formation,o Catheter obstruction,o Urinary retentiono Infectiono Wound dehiscenceo Deep vein thrombosiso Pulmonary emboli

Prostate Cancer Terminology DREDRE (Digital Rectal Examination) is part of a

regular health checkup in which the prostate gland is palpated by the health examiner to detect changes in size, or whether the prostate is becoming hard.

Dysuria A clinical manifestation which may indicate prostate cancer. Dysuria refers to painful urination.

Hematuria A clinical manifestation which may indicate prostate cancer. Hematuria is blood in the urine.

Nocturia A clinical manifestation which may indicate prostate cancer. Nocturia is the awakening in the night during sleep in order to urinate.

Oliguria Refers to a decrease in urine output (or absence of urine output). This is commonly associated with metastases of prostate cancer.

PSA PSA (Prostate Specific Antigen) is a neutral serine protease which can be measured with a simple blood test. Concentration of PSA is proportional to prostatic mass and indicates presence of prostatic tissue, not malignancy.

TRUS (Transrectal Ultrasound) is used when a patient has an increased PSA and abnormal DRE findings. This TRUS assists with detecting non-palpable prostate cancers, staging prostate cancers, and guiding needle biopsies.

Complications of a ProstatectomyA nurse must be aware of potential complications when a patient is undergoing the removal of the prostate. The nurse must be able to communicate with the patient about normal, expected complications. Although there are many potential complications, there are two prostatectomy complications which are almost always expected.

Describe the two most common complications of a prostatectomy, why they occur, and any other things about these complications which a nurse would want to discuss with the patient.

Sexual Dysfunction: risk of impotence occurs from damage done to the pudental nerves during surgery. Erectile dysfunction depends on age and preoperative sexual function. A nurse must be sensitive, and understanding of the anxiety and worry this may cause some men. Self image and confidence may be issues a nurse will need to address as a result of this complication.

Incontinence: most prostatectomy patients will have problems with urinary control for about 1-2 months after surgery. This is caused by the bladder needing to be reattached to the urethra after the prostate is removed. A nurse must inform the patient that with time, most men will regain control of their bladder function. Again, a nurse must be sensitive to self image issues that may be associated with incontinence or having a catheter.

Prostate Cancer- Collaborative CareEarly-stage prostate cancer is a curable disease in the majority of men. Treatment is based on the stage of the disease and the patient's age and symptoms. Partin and associates (1997) combined PSA level with the clinical stage and pathologic grade of the tumor to create a nomogram to predict the pathologic stage of localized prostate cancer. Prostatic adenocarcinoma commonly is classified using the Gleason grading system. Well-differentiated tumors are assigned a grade of 1, and poorly differentiated tumors a grade of 5.The collaborative care of the patient with prostate cancer depends on the stage of the cancer and the overall health of the patient. At all stages, there is more than one possible treatment option.

Table 49-3 • Comparing Surgical Approaches for Treatment of Prostate DisordersThe surgical approach of choice depends on (1) the size of the gland, (2) the severity of the obstruction, (3) the age of the patient, (4) the condition of patient, and (5) the presence of associated diseases.Surgical Approach Advantages Disadvantages Nursing ImplicationsTransurethral Resection(TUR or TURP) (removal of prostatic tissue by instrument introduced through urethra)

Avoids abdominal incisionSafer for surgical-risk patientShorter hospitalization and recovery periodsLower morbidity rateCauses less pain

Requires highly skilled surgeonRecurrent obstruction, urethral trauma, and stricture may develop.Delayed bleeding may occur.

Monitor for hemorrhage.Observe for symptoms of urethral stricture (dysuria, straining, weak urinary stream).

Open Surgical RemovalSuprapubic approach Technically simple

Offers wide area of explorationPermits exploration for cancerous lymph nodes

Requires surgical approach through the bladderControl of hemorrhage difficult.Urine may leak around the

Monitor for indications of hemorrhage and shock.Give meticulous aseptic care to the area around suprapubic tube.


Stage 1: Watchful waiting with annual PSA and DRE -Expectant

therapy (watching and waiting) may be used if the tumor is not producing symptoms, is expected to grow slowly, and is small and contained in one area of the prostate. This approach is particularly suited for men who are elderly or have other health problems.

Radical Prostatectomy-Most men with an anticipated survival greater than 10 years are considered for surgical or radiation therapy. Radical prostatectomy involves complete removal of the seminal vesicles, prostate, and ampullae of the vas deferens.

Radiation Therapy-Radiation therapy can be delivered by a variety of techniques, including external-beam radiation therapy and transperineal implantation of radioisotopes.

Stage 2: Radical Prostatectomy Radiation Therapy

Stage 3: Radical Prostatectomy Radiation Therapy Hormone Therapy-Hormonal therapy is one method used

to control rather than cure prostate cancer (Carroll et al., 2001). Hormonal therapy for advanced prostate cancer suppresses androgenic stimuli to the prostate by decreasing the circulating plasma testosterone levels or interrupting the conversion to or binding of dihydrotestosterone. As a result, the prostatic epithelium atrophies (decreases). This effect is accomplished either by orchiectomy (removal of the testes) or by the administration of medications.

Orchiectomy - Orchiectomy often is effective in reducing symptoms and extending survival.

Stage 4: Hormone therapy Orchiectomy Chemotherapy - Chemotherapy has shown limited

effectiveness in the treatment of prostate cancer.Radiation therapy to metastatic bone areas

Module 09: Upper and Lower Gastrointestinal DisordersGastroesophageal Reflux Disease (GERD)

Gastroesophageal Reflux: a back-flow of gastric or duodenal contents into the esophagus, and is normal to a certain extent in adults and children. However, excessive reflux may be caused by an incompetent lower esophageal sphincter, pyloric stenosis, or motility disorder. Increasing age seems to have an increase in signs of reflux disease.

Clinical manifestations of GERD: Pyrosis: burning sensation in esophagus Dyspepsia: indigestion Regurgitation Dysphagia Odynophagia: difficulty swallowing/ pain with swallowing Hypersalivation Esophagitis Belching Epigastric or retrosternal chest pain Radiating chest pain to shoulder, throat, or back

It is important for a nurse to recognize that often the presenting symptoms mimic those of a patient having a heart attack. Careful

health history is crucial for an accurate diagnosis. GERDs may cause respiratory s&s like wheezing chronic cough, and hoarseness. There is evidence that GERDs is linked to bronchial asthma, Barret Esophagus, and esophageal cancer.

GERDIt is the nurse’s role to perform an accurate assessment of a patient, recognize clinical manifestations of gastroesophageal reflux disease, understand why they are occurring, and document them appropriately. Careful health history and assessment are crucial to differentiate GERD from other diseases or illnesses.

Definition slide:Pyrosis Burning sensation of the esophagusDyspepsia IndigestionDysphasia Difficulty talkingOdynophasia Pain or difficulty swallowingHypersalivation Excessive production of salivaEsophagitis Inflammation of the esophagus

Nausea and Vomiting

Nausea and vomiting: major symptoms related to disorders of the GI tract. Vomiting is usually preceded by nausea. This can be triggered by odors, activity or food intake. The nurse must assess what factors precipitate nausea and vomiting, and help the patient alleviate these factors.

Nausea: results from stimulation of the medullary vomiting centre usually preceded by anorexia. Nausea often occurs with ANS manifestations such as salivation and vasoconstriction with pallor, sweating, and tachycardia.

Vomitting: involves 2 parts of the medullary centre: the vomiting center and the chemoreceptor trigger zone. For a detailed explanation of the physiology of vomiting refer to Porth.

Emesis: (vomitus), varies in color and content. It may contain undigested food particles, bile, or blood (hematemesis). When vomiting occurs after a hemorrhage in the GI tract, the emesis will look bright red (fresh blood). If the blood has been retained for some time within the stomach, it looks like ground coffee beans when vomited. This occurs because of the action of the digestive enzymes within the stomach.

Nursing management: focuses on prevention and alleviation of vomiting. Proper nursing management of nausea and vomiting is to control the symptoms, increase the patient’s comfort level, and ensure proper fluid and electrolyte balance. The nurse must carefully monitor the patient’s fluid and electrolytes if vomiting occurs, to mitigate the high risk for deficiency of fluid volume (hypovolemic shock in extreme cases). There are a variety of medications available to control nausea and vomiting in the patient, which the nurse will administer with a Doctor's order. Due the anticholinergic effects of antiemetics to treat nausea it is important that the nurse assesses bowel sounds to ensure a blockage and/or immobility of the bowel does not exist.

Hematemesis = Vomitus with bloodA nurse must be knowledgeable about concerns with nausea and vomiting. Hematemesis is a cause for concern, and should prompt a nurse to investigate further, as well as properly report and document this finding.

Ulcerative Colitis: Complications, Medical & Nursing Management

Complications:

Table 49-3 • Comparing Surgical Approaches for Treatment of Prostate DisordersThe surgical approach of choice depends on (1) the size of the gland, (2) the severity of the obstruction, (3) the age of the patient, (4) the condition of patient, and (5) the presence of associated diseases.Surgical Approach Advantages Disadvantages Nursing ImplicationsTransurethral Resection(TUR or TURP) (removal of prostatic tissue by instrument introduced through urethra)

Avoids abdominal incisionSafer for surgical-risk patientShorter hospitalization and recovery periodsLower morbidity rateCauses less pain

Requires highly skilled surgeonRecurrent obstruction, urethral trauma, and stricture may develop.Delayed bleeding may occur.

Monitor for hemorrhage.Observe for symptoms of urethral stricture (dysuria, straining, weak urinary stream).

Open Surgical RemovalSuprapubic approach Technically simple

Offers wide area of explorationPermits exploration for cancerous lymph nodes

Requires surgical approach through the bladderControl of hemorrhage difficult.Urine may leak around the

Monitor for indications of hemorrhage and shock.Give meticulous aseptic care to the area around suprapubic tube.


Toxic megacolon: the inflammatory process extends into the muscalaris which inhibits the ability to contract, and results in fever, abdominal pain and distention, fatigue and vomiting. If the patient does not respond to medical management within 2 days, complete colectomy is indicated.

Perforation Bleeding Vascular engorgement Highly vascular granulation tissue Increase in risk of osteoporotic fractures due to decrease in

bone mineral density (corticosteroid therapy may enhance this)

Medical Management:The goal of medicine is to reduce inflammation, suppress inappropriate immune responses, provide rest for the bowel so that it has time to heal, improve QOL, and minimize complications. Nutritional therapy may include a high protein, high calorie diet with supplement. IV therapy may be used to correct fluid and electrolyte imbalances. Sedatives, antidiarrheal, and antiperistalic medications may be used to give time for the bowel to rest and heal. Corticosteroids are used to treat severe cases of this disease, although there are adverse affects with long term use. Medical management may also include the use of immunomodulators in order to alter the immune response. In extreme cases, surgery may also be indicated.

Nursing Management:The nurses’ role is to involve him/herself in the symptomatic care, administration of medications, and post operative care etc. when medical or surgical interventions are indicated. The nurse also must educate recently diagnosed patients in the hospital, and in the community about diet and medicines. Hospitalized patients with severe long standing diseases require careful monitoring, parenteral nutrition, fluid replacement, and surgical care from the nurse. The nurses role is to provide physical and emotional care which may involve teaching about the disease, complications, surgical indications and medications.Assessment/ Diagnostic Findings:The patient should be assessed for hypotension, tachycardia, tachypnea, fever, and pallor. Hydration and nutritional assessment is extremely important as well. Assessment of bowel sounds, distention, and tenderness assists with determining the severity of the disease.Laboratory tests can determine if stool is positive for blood, and can see if there is an elevated WBC count, low albumin levels, and electrolyte imbalances. Abdominal x-rays can assist with determining the cause of presenting symptoms. Sigmoidoscopy, colonoscopy, and barium enemas are used to distinguish ulcerative colitis from other diseases of the colon. CT scans, MRIs, and ultrasounds can help identify abscesses. Leukocyte scanning is used when endoscopy is prohibited to determine the extent of the inflammation. Careful stool examination can rule out other microbial agents which cause similar symptoms.

Clinical Manifestations:usually include exacerbations and remissions. Symptoms include diarrhea, LLQ abdominal pain, and rectal bleeding (may be mild or severe). Patients may also have weight loss, anorexia, vomiting, fever, cramping or dehydration.It is not uncommon for a patient with ulcerative colitis to feel an urgent need to defecate, and have 10- 20 liquid stools each day. Hypocalcemia and anemia are common. Other symptoms outside of the intestine include skin lesions, eye lesions, joint abnormalities, and liver disease. The disease is classified as mild, severe or fulminant.

Pathophysiology:ulcerative colitis is characterized by multiple ulcerations,

inflammation, and shedding of the colonic epithelium. The mucosa becomes edematous and inflamed. The lesions occur one after another, and abscesses form.The disease usually begins in the rectum and eventually spreads to involve the whole colon, in which time the bowel narrows, shortens and thickens because of fat deposits and hypertrophy.

Ulcerative Colitis: a recurrent ulcerative, inflammatory disease which affects the mucosal and submucosal layers of the colon and rectum. This disease is found most commonly in people of Caucasian and Jewish descent, and its peak incidence is between the ages of 30- 50 years. It is a very serious disease because of the systemic complications and increased risk for developing colon cancer.

Assessment/ Diagnostic Findings:The patient should be assessed for hypotension, tachycardia, tachypnea, fever, and pallor. Hydration and nutritional assessment is extremely important as well. Assessment of bowel sounds, distention, and tenderness assists with determining the severity of the disease.Laboratory tests can determine if stool is positive for blood, and can see if there is an elevated WBC count, low albumin levels, and electrolyte imbalances. Abdominal x-rays can assist with determining the cause of presenting symptoms. Sigmoidoscopy, colonoscopy, and barium enemas are used to distinguish ulcerative colitis from other diseases of the colon. CT scans, MRIs, and ultrasounds can help identify abscesses. Leukocyte scanning is used when endoscopy is prohibited to determine the extent of the inflammation. Careful stool examination can rule out other microbial agents which cause similar symptoms.

Clinical Manifestations:usually include exacerbations and remissions. Symptoms include diarrhea, LLQ abdominal pain, and rectal bleeding (may be mild or severe). Patients may also have weight loss, anorexia, vomiting, fever, cramping or dehydration.It is not uncommon for a patient with ulcerative colitis to feel an urgent need to defecate, and have 10- 20 liquid stools each day. Hypocalcemia and anemia are common. Other symptoms outside of the intestine include skin lesions, eye lesions, joint abnormalities, and liver disease. The disease is classified as mild, severe or fulminant.

Pathophysiology:ulcerative colitis is characterized by multiple ulcerations, inflammation, and shedding of the colonic epithelium. The mucosa becomes edematous and inflamed. The lesions occur one after another, and abscesses form.The disease usually begins in the rectum and eventually spreads to involve the whole colon, in which time the bowel narrows, shortens and thickens because of fat deposits and hypertrophy.

Regional Enteritis (Crohn’s Disease)

Regional Enteritis (Crohn’s Disease):Is most common in adolescents and young adults, but can occur at any time. This disease is more common in women, with its incidence rising over the past 30 years. This disease is seen twice as much in smokers than nonsmokers. It can occur anywhere along the GI tract but the most common areas are the distal ileum and the colon.

PathophysiologyIs sub-acute and chronic inflammation which affects all layers of the bowel wall. It is characterized by exacerbations and remissions. The disease begins with edema, then thickening of the mucosal wall. Ulcers begin to appear and are separate by normal tissue. Fistulas, fissures, and abscesses form as the inflammation extends to the peritoneum. Granulomas can also occur in approximately half of patients with Crohn’s disease. The bowel wall then thickens, becomes


fibrotic, and the intestines narrow as disease progresses. In some cases the diseased bowel will begin to adhere to other loops surrounding them.

Clinical ManifestationsProminent LRQ pain Diarrhea unrelieved by defecation Cramping caused by scar tissue constricting transport of materials through the intestine Cramping after meals Weight loss, anemia, malnutrition Ulcers Fever and leukocytosis Extra-GI symptoms include joint involvement, skin lesions, ocular disorders, and oral ulcers.

Assessment and Diagnostic FindingsA proctosigmoidoscopic exam is initially performed to see whether the recto-sigmoid area is inflamed. Stool sample is also examined. The most conclusive method of diagnosis is a barium study of the GI tract. Endoscopy and intestinal biopsy can be used to confirm diagnosis. A complete blood count is taken to assess hematocrit and hemoglobin levels which are usually decreased and WBC count which may be elevated.

Complications Include intestinal obstruction, perianal disease, fluid and electrolyte disturbances, and malnutrition. Fistula formation is another complication which involves an abnormal communication between two body structures. These can be internal (between two structures) or external (between an internal structure and the outside of the body). Patients with Crohn’s Disease are also at an increased risk for colon cancer.

Inflammatory Bowel DiseaseInflammatory Bowel Disease includes both regional enteritis (Crohn’s Disease) and Ulcerative Colitis. Although these two diseases have many of the same clinical manifestations, it is important for a nurse to be able to distinguish one from the other.

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