Patho Test #2 Study Sheet

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Module 05: Upper and Lower Respiratory Tract Disorders
Rhinitis
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
e"cessi#e nasal drainage!, congestion, itchiness or
sneezing.
Viral Rhinitis (Common Cold!$
an afebrile, infectious, acute inflammation of the mucous
membranes of the nasal ca#ity.
highly contagious because the #irus is shed for about t%o
days before the symptoms appear and also during the first
part of the symptomatic phase& 'mmunity and reco#ery is
#ery indi#idualized and depends on personal host resistance
and the #irus, %hich caused the cold.
There are fi#e #iruses (no%n to be lin(ed to #iral rhinitis
)ach #irus has multiple strains$
o Rhino#irus,
o Parainfluenza #irus
o *orona#irus
o Respiratory syncytical #irus RS+!
o 'nfluenza #irus
o Adeno#irus
Clinical Manifestations of Viral Rhinitis$ Symptoms last 1,2
%ee(s!
runny nose
sneezing
sore throat
malaise
lo% grade fe#er
chills, headache
muscle aches.
cough usually appears as the illness progresses.
Medical Manaement:
The treatment for the common cold is symptomatic therapy.
This includes increasing fluid inta(e, encouraging rest,
increasing inta(e of #itamin *, and use of e"pectorant as
needed. -arm salt %ater gargles can sooth a sore throat.
.SA'/s are used to relie#e aches, pains, and fe#ers in
adults. Antihistamines can be used to relie#e sneezing,
rhinorrhea, and nasal congestions. Some research suggests
that zinc lozenges can reduce the duration of the cold if
ta(en %ithin the first 20 hours. Antibiotic use is not
recommended because it does not affect the #irus or reduce
the incidence of bacterial complications.
.urses can be instrumental in teaching patients pts! about
self care and treating the symptoms of their cold. Teaching
about ho% to brea( the chain of infection is crucial because
these #iruses are transmitted by direct contact, and
inhalation of particles. Proper hand %ashing is the best %ay
to pre#ent the transmission of #iruses that cause the
common cold.
1titis 2edia 12!
!cute "titis Media
An acute infection of the middle ear caused by bacterial
infection related to upper respiratory infections,
inflammation of surrounding areas, or allergic reactions.
3acteria enter from contaminated secretions in the
nasopharyn" and the middle ear from a tympanic
membrane perforation. Purulent e"udate is usually present
and can result in conducti#e hearing loss.
Symptoms #ary %ith se#erity of the infection and include
pain, drainage from the ear, fe#er and hearing loss. The
tympanic membrane is erythematous and bulging upon
otoscopic e"amination.
This condition is treated %ith oral antibiotics or antibiotic
otic preparation if drainage occurs!. The outcome depends
on efficacy of the therapy, #irulence of the bacteria, and the
patient4s physical status. The se#erity of the infection may
call for an incision of the tympanic membrane
myringotomy or typmanotomy! to relie#e pressure and
drain fluid from the middle ear.
#erous "titis Media$
implies fluid, %ithout e#idence of infection and is
commonly found in children. *auses include )ustachian
tube obstruction, radiation therapy, carcinoma, or
barotraumas.
Typical symptoms include hearing loss, and congestion, or
popping or crac(ling noises as the )ustachian tube attempts
to open. The tympanic membrane is dull upon e"amination.
Treatment may not be necessary unless infection occurs. 'f
hearing loss is caused by effusion in the middle ear, a
myringotomy may be performed. *orticosteroids
sometimes are used to decrease edema associated %ith
barotraumas.
Chronic "titis Media$
The result of repeated acute otitis media causing
irre#ersible tissue pathology and damage.
*linical manifestations include degrees of hearing loss, and
sometimes a foul smelling otorhrea. 1toscopic e#aluation
may sho% tympanic perforation, or a cholesteatoma in,
gro%th of s(in of the e"ternal layer of the eardrum into the
middle ear!. This creates high negati#e pressure in the
middle ear and the s(in creates sacs %hich collect
degenerated s(in and sebaceous materials. Surgery is
usually recommended.
Treatment includes suctioning of the ear, and use of
antibiotic drops or po%ders 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
remo#al of the cholesteatoma may increase access to
diseased structures, and create a dry, healthy ear.
Acute 3ronchitis
!cute $ronchitis$
inflammation of the bronchi in the lo%er respiratory tract
due to infection. The most common cause is #iral influenza
and rhino#irus!. 5o%e#er, different strains of bacteria may
cause acute bronchitis in both smo(ers and non,smo(ers.
Patho Test #2 Study Sheet
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*ommon symptoms$
o persistent cough %hich follo%s an acute upper
respiratory infection, such as rhinitis or
pharyngitis. *ough usually comes %ith the
production of clear, mucoid sputum. Some
patients ho%e#er may produce purulent sputum.
o 6e#er
o 5eadache
o 2alaise
o S13
o 2ay sho% a slightly ele#ated RR, 5R, and
temperature.
*hest ",rays are used to differentiate acute bronchitis from
pneumonia.
Treatment$ generally includes fluids, rest, and anti,
inflammatory medications. *ough suppressants and
bronchodilators may be used to treat coughing or %heezing
during the night. Antibiotics are usually only prescribed if a
patient has a prolonged infection, or is a chronic smo(er
%ith *1P/.
*hronic 1bstructi#e Pulmonary /isease *1P/!
defined as a disease state in %hich airflo% is limited, and
%hich is not fully re#ersible. *1P/ is commonly lin(ed to
emphysema, chronic bronchitis. *1P/ is the fifth leading
cause of death in the 7S for all ages and genders.
%athophysioloy$
the (ey concept to understand %ith *1P/ is that the
airflo% limitations are both progressi#e, and associated
%ith the inflammatory response.
1#er time the continuous in8ury,repair cycle causes scar
tissue formation in the air%ays.
Chronic $ronchitis$
the presence of cough and sputum production for three
months o#er t%o consecuti#e years.
*onstant irritation smo(e, or other en#ironmental agents!
results in hyper secretion of mucous, and inflammation, and
o#erall dysfunction of the air%ays.
&mphysema:
An impaired gas e"change resulting from destruction of the
%alls of o#er distended al#eoli. The %alls of the al#eoli are
destroyed o#er time from recurrent infections
Ris' factors$
)"posure to tobacco smo(e accounts for 9:,;:< of *1P/
cases.
Passi#e smo(ing
1ccupational e"posures
Air pollution
=enetic deficiency of alpha1,antitripsin an enzyme
inhibitor %hich counteracts the destruction of lung tissue
Clinical Manifestations$
The three main characterizations of *1P/$
o *ough
o Sputum production
o /yspnea on e"ertion
These often %orsen o#er time, and affect a patient4s A/>s.
-eight loss is common %ith dyspnea, as eating and the
%or( of breathing often drains the *1P/ 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 C"%D$
>ife threatening and include respiratory insufficiency or
failure.
Pneumonia
Atelectasis
Pneumothora"
*or pulmonale.
Ris' reduction$
Smo(ing *essation is the single most effecti#e
inter#ention to pre#ent or slo% the progression of *1P/.
3ronchodilators may be used to relie#e bronchospasms
and reduce airflo% obstruction.
*orticosteroids inhaled or systemic! may also be used.
*1P/ patients are strongly ad#ised to get the flu shot
e#ery year as %ell.
1"ygen therapy can be used o#er a long course, during
e"ercise, or to pre#ent acute dyspnea. 'n some cases,
surgery may also be recommended bullectomy, lung
#olume reduction surgery, or lung transplantation!.
Pulmonary )dema
abnormal accumulation of fluid in the lung tissueA al#eolar
space %hich is se#ere and life threatening.
This condition usually occurs from increased micro#ascular
pressure from abnormal cardiac function.
The bac(up of blood in the pulmonary #asculature is
caused by inadeBuate left #entricular function.
6luid then begins to lea( into the interstitial space and
al#eoli.
5yper#olemia or sudden increased intra#ascular pressure in
the lung can also cause pulmonary edema.
An e"ample of this is a patient %ho has had one lung
remo#ed, %here all the cardiac output then goes to one
lung.
Clinical Manifestations$
increased respiratory distress in the patient, %hich includes
dyspnea, central cyanosis, an"iety and agitation.
As fluid lea(s into the al#eolar space and mi"es %ith air, a
froth or foam is formed.
A nurse must loo( for these types of frothy and often blood
tinged secretions %hen suctioning, or if a patient is
coughing up sputum.
'f the patient is in acute respiratory distress, they may
become confused or stuporous.
!ssessment:
Patho Test #2 Study Sheet
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*rac(les in the lungs are due to mo#ement of air through
the al#eolar fluid.
*hest ",rays %ill sho% increased interstitial mar(ings.
The patient may be tachycardic %ith their pulse o"imetry
falling, and A3= #alues indicating hypo"emia.
Medical Manaement:
=oal is to correct the underlying condition %hich is usually
impro#ing left #entricular function.
+asodilators, contractility and other cardiac function
medications are often used.
'n some cases if the patient does not respond to these, an
intra,aortic balloon pump may be indicated.
6luid restriction and diuretics are used to reduce fluid
o#erload.
1"ygen is administered to correct hypo"emia.
2orphine can be administered to reduce an"iety and
control pain.
'ntubation and mechanical #entilation may be necessary in
e"treme cases.
(ursin Manaement:
.urses are responsible for the administering of o"ygen and
other medications, as %ell as monitoring the patient4s
response.
A nurse may need to assist %ith intubation and mechanical
#entilation if necessary.
The nurse must monitor the patient carefully for any
changes and report them immediately.
+entilated patients %ill be monitored in an '*7 setting.
Pneumothora"
1ccurs %hen the pleural space %hich is usually negati#e or
subatomic! is e"posed to positi#e atmospheric pressure.
.egati#e pressure is needed for proper lung function.
-hen air enters the pleural space, the lung, or a portion of
it collapses.
#imple %neumothora)$
A spontaneous collapse usually due to a rupture of a bleb or
bronchopleural fistula, %hich allo%s air from the air%ays to
enter the pleural ca#ity.
This type of pneumothora" may also be associated %ith
interstitial lung disease or se#ere emphysema.
Traumatic %neumothora)$
1ccurs %hen air escapes from a laceration in the lung itself
through a %ound in the chest %all such as rib fractures,
abdominal trauma gunshot, stab %ounds!, in#asi#e
thoracic procedures, or barotrauma from mechanical
#entilation.
1ften accompanied by hemothora" collection of blood in
the pleural space from torn #essels, laceration of greater
#essels or laceration to the lungs!.
Clinical Manifestations$
Pain is usually sudden.
-ith simple or uncomplicated collapses, pts may only ha#e
slight chest discomfort and tachypnea.
-hen the pneumothora" is large or the lung collapses
completely, the patient is in acute respiratory distress,
displaying high an"iety, dyspnea, increased use of
accessory muscles, and may de#elop se#ere central
cyanosis from hypo"emia.
Se#ere chest pain
Tachypnea
/ecreased mo#ement on affected side
Tympanic sound on percussion of chest %all
/ecreased or absent breath sounds
Tactile fremitus may occur.
Medical Manaement:
The goal is to remo#e the blood or air from the pleural
space.
*hest tubes and suctioning may be used to drain fluid or
air.
Auto transfusion ta(ing the patient4s blood that is draining,
filtering it, then transfusing it bac( to their o%n
#asculature! may be necessary.
Antibiotics are used to a#oid infection.
Tension %neumothora)$
1ccurs %hen air enters the lung but cannot lea#e the chest.
As pressure increases, the heart, the great #essels, trachea
etc. are pushed to opposite side of the chest, %hich then
compress the unaffected lung.
'f this type of pneumothora" is suspected, high
concentration of o"ygen is gi#en.
A large bore needle can be used on the affected side to
relie#e the pressure and #ent the positi#e pressure to the
e"ternal en#ironment.
A chest tube is then used to re,establish the negati#e
pressure.
'f prolonged air lea( continues, surgery may be necessary
to close the lea(.
%ulmonary &m*olism (%&+
obstruction of the pulmonary artery by a thrombus %hich
occurs some%here in the #enous system right side of the
heart!.
*ommonly associated %ith trauma, surgery, pregnancy,
heart failure, age D: and older, hypercoagulable states, and
prolonged immobility.
2ost thrombi originate in the deep #eins of the legs. Atrial
6ibrillation can cause blood to stagnate and clot. These
clots are prone to tra#el in the pulmonary circulation.
%athophysioloy:
A thrombus then completely or partially obstructs the
pulmonary artery, in turn there is little or no blood flo%
Patho Test #2 Study Sheet
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Substances are released from the clot and surrounding area
%hich cause blood #essels and bronchioles to constrict.
This results in increased pulmonary arterial pressure, and
an increase in right #entricular %or( to maintain pulmonary
blood flo%.
-or( reBuirements can lead to right #entricular failure,
%hich decreases cardiac output, systemic pressure, and
leads to shoc(.
Clinical Manifestations$
Tachypnea is the most freBuent sign.
*hest pain is common and sudden, and sometimes mimics
angina or an 2'.
An"iety
Tachycardia
Apprehension
*ough
/iaphoresis
5emoptysis
Syncope.
!ssessment, Dianostics:
/eath from P) can occur %ithin an hour of symptoms, so
early detection and treatment is crucial.
The nurse loo(s for signs of /+T %hich is commonly
associated %ith P).
1ther diagnostic tools may include a chest ",ray or
#entilation,perfusion scan. A pulmonary angiography is
considered the gold standard for the diagnosis of P), but is
#ery in#asi#e.
%re-ention:
Acti#e leg e"ercises
)arly ambulation
7se of compression stoc(ings
7se of heparin
Pneumatic leg compression de#ices
Medical Manaement$
general measures to impro#e respiratory and #enous status
12 therapy, ele#ating the leg!
anticoagulant therapy 5eparin!
Thrombolytic Therapy clot busters!
Surgical therapies embolectomy!.
(ursin manaement:
2inimizing the ris(s for P),
Pre#enting thrombus formation
Assessing for P)
2onitoring thrombolytic therapy
2anaging pain and 12 therapy appropriately
Relie#ing an"iety
2onitoring for complications
Pro#iding post operati#e nursing care
Teaching patients self care techniBues.
Module .: Cardio-ascular Disorders
'ntroduction and 5ealth 5istory Assessment
The nurse must understand the ma8or function of the cardio#ascular
system that affects all body systems. The circulatory system is
responsible for the transport of o"ygen and nutrients for metabolic
processes to the tissues, transport of %astes for elimination, and
circulate electrolytes and hormones. The pulmonary circulation
mo#es blood through the lungs and creates a lin( %ith gas e"change
function of the respiratory system %hile the systemic circulation
mo#es blood throughout all other tissues. *entral circulation refers to
blood in the heart and pulmonary circulation and that %hich is outside
the circulation is called central circulation. 3lood mo#es throughout
circulation along a pressure gradient, mo#ing from high,pressure
arterial system to lo% pressure #enous system.
6or a re#ie% of cardio#ascular function and assessment read E1F ch.
2G in addition to reBuired readings and E2F ch. 1G. Hno%ledge of the
nursing implications related to diagnostic testing is essential in caring
for persons %ith cardio#ascular dysfunction. The nurse must ha#e
e"pert assessment and care planning s(ills for patients %ith sIs of
cardio#ascular dysfunction. This module %ill focus on the follo%ing
disorders$ 5ypertension, Arrhythmias, 2' complications, and 56.
/ealth /istory !ssessment
The nurse should include in the health history an e#aluation of the
follo%ing$
Patient4s general appearance
)ffecti#eness of the heart as a pump
6illing #olumes, cardiac output
*ompensatory mechanisms
5o% the patient is affected by any conditions.
'ndications that the heart is not contracting sufficiently or functioning
effecti#ely as a pump include$
Reduced pulse pressure
*ardiac enlargement
2urmurs and gallop rhythms
/iagnostic tests include$
cardiac enzyme analysis particularly in the e#ent of an
2'
lipid profiles
Serum electrolytes
37.
Serum glucose
*oagulation studies
5ematologic studies.
*hest ",ray, fluoroscopy, )H= )*=!, continuous
electrocardiographic monitoring, and
)chocardiography may be indicated.
Arrhythmias and *onduction Problems, Types and 2anagement
!rrhythmiasADysrhythmias 0 disorders of formationA conduction
or both! of the electrical impulse %ithin the heart that disturb heart
rate andAor rhythm.
Sites of 1rigin 2echanisms of
6ormation or
*onduction
Sinus SA! .odes
Atria
Atria A+!
.ormal idio! rhythm
3radycardia
Tachycardia
Patho Test #2 Study Sheet
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.odeAJunction
+entricles
K.amed according to
site and mechanism
Arrhythmias
6lutter
6ibrillation
Premature
*omple"es
3loc(s
Understandin (ormal &lectrical Conduction
The electrical impulse begins in the SA node and tra#els to
the A+ node, and stimulated muscle cells contract in the
atria.
As the A+ node slo%s the impulse, the #entricles fill %ith
blood.
)lectrical impulses then tra#el Buic(ly to the Pur(in8e
6ibers in the #entricles.
This electrical stimulation causes the #entricles to contract
systole!. As the cells repolarize, the #entricles rela"
diastole!.
o Electrical stimulation L /epolarization
mechanical contraction is called systole!
o Electrical Relaxation L Repolarization
mechanical rela"ation is called diastole!
1a-es2 Comple)es2 and 3nter-als
KSho%n and interpreted on an )*=A)H= M sho%s each phase of
cardiac cycle %hich is reflected on a piece of paper.
P Wave, represents electrical impulse starting at SA node
and tra#elling through atria atrial depolarization!
QRS Complex, part of the )*= that represents conduction
of the electrical impulse through the #entricles #entricular
depolarization!
T Wave, part of the )*= that represents #entricular
repolarization
U Wave, part of the )*= that represents Pur(in8e fibers
usually seen in pts %ith lo% serum potassium and may be
mista(en for an e"tra P %a#e!
PR Interval, part of the )*= that represents the conduction
of the electrical impulse from the SA node, through the S+
node
ST Segment, part of the )*= that represents the end of
#entricular depolarization end of the NRS comple"!
through #entricular repolarization end of the T %a#e!
QT Interval, part of the )*= that represents #entricular
depolarization to repolarization
TP Interval, measured from end of the T %a#e until
beginning of ne"t P %a#e isoelectric period!
PP Interval, measured from beginning of one P %a#e to the
ne"t P %a#e Oused to determine atrial rhythm and rate
(ormal #inus Rhythm
Ventricular and trial Rate$ P:,1:: in an adult
Ventricular and trial Rhythm$ Regular
QRS shape and duration$ usually normal but may be
regularly abnormal
P !ave" normal and consistent shape$ al%ays in front of
the NRS
PR interval" consistent inter#al :.12,:.2 seconds!
P"QRS interval ratio$ 1$1
!d4uncti-e Modalities and Manaement
/epends %hether arrhythmia is chronicA acute, cause, and
%hat potential hemodynamic effects
Treated %ith meds listed on table 2G,1! or e"ternal
electrical therapy
2onitor pts response to meds,ma(e sure pt has (no%ledge
to manage medication regimen
%acema'er Therapy
*an be used in patients as a temporary or permanent %ay of
managing conduction problems of the heart.
't pro#ides a regulated electrical stimulus to the heart
muscle to regulate the underlying problem.
This type of management is usually used for patients %ith
slo%er, than, normal impulse formation or conduction
problems that cause symptoms.
Patho Test #2 Study Sheet
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"ther Therapies:
*ardio#ersion
/efibrillation
'mplantable *ardio#erter /efibrillator
)lectrophysiologic Studies
*ardiac *onduction Surgery
5ypertension 5T.!, /efinitions, Ris( 6actors, Pathophysiology and
*linical 2anifestations
*omple", chronic condition that is referred to the ?silent
(iller@ since the patient is often asymptomatic.
/etection and treatment delays result in target organs
becoming damaged and other complications
#e$ined as %lood pressure &'()*+) mm,g
,S- ./))01 in 234 pg 3/ de$ines it" a medical condition in
!hich %lood pressure is consistently a%ove the normal
range5
The pathophysiology of hypertension is comple".
o 2ost hypertensi#e indi#iduals ha#e ?essential@
hypertension, since they ha#e no clear
identifiable cause for their hypertension.
Research tells us that there are
interrelated factors that contribute to
ele#ated blood pressure$ salt, obesity,
insulin resistance, renin,angiotension
system and the sympathetic ner#ous
system.
Complications: ECF pg. 20$
'ncidence of stro(e increases appro". 9,fold
0:< of cases of acute 2' or stro(e are due to hypertension
/irect relationship to #ascular mortality
Accelerates atherosclerosis and blood #essel in8ury
increasing the ris( of #ascular disease and subseBuent organ
damage heart, brain, (idney, eye, or limbs!
/ue to poor adherence to anti,hypertensi#e treatment,
appro". GD< of patients do not achie#e optimal 3P control
Dianosis of /ypertension:
.urses reBuire (no%ledge of the process for establishing a
diagnosis of hypertension so that the nurse can e"pedite and
support the client through the diagnosis phase.
*5)P 2::D! in ECF pg CC states that diagnosis of
hypertension can no% be made in 1,2, or C #isits based on
an algorithm %hich no% e"pedites the assessment and
diagnosis of hypertension to enable more timely treatment.
Summary of recommendations are$
o 6or clients %ith high 3P urgenciesAemergencies a
diagnosis of treatment can be made on the first
#isit.
o 'f client has target organ damage, chronic (idney
disease, diabetes, or 3P L to or Q than 19:A11: a
diagnosis can be made on the second #isit made
to assess blood pressure.
o 6or clients %ith 3PL or Q 1P:,1G;A1::,1:; and
not already diagnosed based on criteria outlined
abo#e!, a diagnosis can be made at the third #isit.
*5)P 2::D! in ECF pg CC recommends all C #alidated 3P
monitoring technologies, officeAclinic,based measurement,
selfAhome and ambulatory 3P monitoring alone or in
combination! to ma(e diagnosis of hypertension. The most
recent e#idence suggests that %hen properly assessed,
selfAhome and A3P2 are as or more effecti#e in facilitating
diagnosis than officeAclinic,based measurement.
5ealth history further includes physical e"am focusing on
e"amination of retina, urinalysis increased 37., *R,
albuminuria, blood chemistry, )H= and )cho results,
history of T'As E1.
Treatment 5ypertension Treatment .ursing best Practice
Types of !rrhythmias
Description !V Rate !V Rhythm
#inus $radycardia$ SA node creates slo%er than normal rate
metabolic needs, #agal stimulation, meds, '*P, 2'!
K>ess than P: in adults

.ormal
#inus Tachycardia: SA node creates rate faster than normal blood
loss, shoc(, hypo#olemiaAhyper#olemia, pain, an"iety, e"ercise!
K=reater than 1:: in
adults
.ormal
#inus !rrhythmias: SA node creates irregular rhythm& usually
increases %ith inspiration, decreases %ith e"piration heartA #al#ular
diseases, respiratory related!
.ormal 'rregular
!trial 5lutter: impulses in atrium of 2D:,0::, but A+ node cannot
conduct all impulses therapeutic bloc( at A+ node$ if #entricular rate
%as 2D:,0::, possibly fatal!
Kcauses chest pain, S13, lo% 3P
KA$ 2D:,0::
K+$ GD,1D:
KAtrial rhythm is regular&
#entricular rhythm is
usually regular but can be
irregular due to change in
A+ conduction
!trial 5i*rillation: rapid, disorganized, uncoordinated t%itching of
atrial muscle& acute or chronic
KA$ C::,P::
K+$ 12:, 2::
untreated!
K5ighly irregular
Ventricular Tachycardia: C or more Premature +entricular
*omple"es P+*! impulse that starts in #entricles and conducted
before ne"t sinus impulse! %hich e"ceed 1:: 3P2& associated %ith
coronary artery disease& pt usually unresponsi#e and pulseless
KA, depends on
underlying sinus
rhythm
K+, 1::,2::
K7sually normal
Patho Test #2 Study Sheet
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=uidelinesECF pg.2D,29.
3lood pressure control is one of se#eral important
components in an anti,atherosclerotic strategy.
1ther factors important in a global *+ ris( management
plan include$
o >ifestyle modifications diet, %t loss, e"ercise,
smo(ing cessation! is the cornerstone of global
management of many atherosclerotic ris( factors
and may be enough to manage 3P control
o *onsideration of both statins and ASA as part of
*+ protection strategy for those %ith
hypertension
o Angiotensin *on#erting )nzyme A*)!
inhibitors for clients %ith established
atherosclerotic disease
o A*) inhibitors or Angiotensin '' Receptor
3loc(ers AR3! for those %ith diabetes and
(idney disease
o Stable, normotensi#e persons should chec( their
3P for a 1 %ee( period e#ery C months. 3P
should be chec(ed more freBuently if they ha#e
diabetes, or ha#e difficulty follo%ing a treatment
plan.
o SelfAhome 3P #alues Q or L 1CDA9D mm5g
should be considered ele#ated and associated
%ith increased o#erall mortality ris( similar to
clinic readings Q 10:A;: mm5g. 'n an
asymptomatic person a 3P of Q2::A1C: mm5= is
a medical emergency.
o The target 3P for a person %ith diabetes or renal
disease and a 3P Q or L 1C:A9: is to ha#e 3P R
than 1C:A9:. 6or the person %ith proteinuria
Q1gmAday the target is R12DAGD.
o See ECF pg 0: to appreciate ho% lifestyle
therapies impact on 3P in hypertensi#e adults
o /ietary Approaches to stop hypertension /AS5!
includes fruits, #egetables, and lo%,fat dairy
products and %ell as reduced sodium inta(e
pro#es to significantly lo%er 3P in persons %ith
stage 1 grade 1! hypertension, high normal 3P,
and isolated systolic hypertension.
o The *5)P 2::D! recommends that sodium
inta(e for hypertensi#e persons be limited to PD,
1:: mmolAday, %hich is eBui#alent of 1D::,20::
milligrams or 2AC,1tsp of table salt.
o Heeping healthy 32' and %aist circumference
R1:2 cm for males, and 99 cm for females %ill
reduce possibility of hypertension
There is rapid decline in *+ ris( up to D:< after 1 year for
those %ho stop smo(ing. The nurse must be (no%ledgeable
about the relationship bet%een smo(ing and ris( of *+
disease and be able to implement 3rief Tobacco
'nter#entions after determining patient readiness. See ECF pg
0D,DP for more on the effects of smo(ing, e"ercise, alcohol,
and stress and hypertension.
.urses must be able to educate clients regarding
pharmacological management of hypertension in
collaboration %ith physicians and pharmacists. 1ne
complication the nurse must ad#ise on is the pre#ention of
rebound hypertension %ith sudden cessation of
antihypertensi#es. Another complication is the side effects
of antihypertensi#e medication.
.urses are in the best position to pro#ide education about
antihypertensi#e medications and monitor their therapeutic
effecti#eness. 5ence nurses must be (no%ledgeable about
classes of anti,hypertensi#e medication
2yocardial 'nfarction, Pathophysiology, *linical 2anifestations I
Assessment
%athophysioloy:
Process in %hich areas of myocardial cells are permanently destroyed
%hich is caused by reduced blood flo%, atherosclerosisA occlusion
embolusAthrombus!. 1ther causes may be #asospasm, decreased 12
supply or increased demand for 12 rapid heart rateAcocaine
ingestion!. -hen cells are depri#ed of 12, ischemia or cellular
in8uryAdeath of cells infarction! occurs. 6or further e"planation of
A2' please be familiar %ith Porth *h.1;.
Clinical Manifestations:
.urses should loo( for signs of chest pain possibly radiation to nec(,
8a%, left arm, especially any that continues %ith rest. .ote that
%omen e"perience atypical SIS and elderly more shortness of breath
S13!. S13, an"iety, restlessness, coolApale s(in, increased 5R and
RR, indigestion, nausea and #omitting are other clinical
manifestations %hich a nurse should be a%are of. Symptoms often
mirror those of unstable angina.
3mmediate 3nter-entions:
Resting position6 legs elevated and supine or semi7-o!ler
8xygen /9 via nasal prongs
:itroglycerin su%lingual 0 minutes apart x3 doses
'/ lead EC; stat
Trans$er to critical care
Throm%olytic therapy usually administered /) minutes
later i$ unrelieved %y nitro
Dianostic 5indins
/iagnosis includes symptoms, 12 lead )*= and lab results.
Patient 5istory$ presenting symptoms, pre#ious illness,
family history
)*=$ monitors location, e#olution and resolution of 2'
*lassic )*= changes$ T,%a#e in#ersion, ST,segment
ele#ation, abnormal N %a#e.
>aboratory Tests$
o *reatine(inase and its 'soenzymes$ *H,23 is
cardiac specific isoenzyme found in cardiac cells
indicating damage to these cells.
o 2yoglobin$ heme,protein that helps transport 12,
le#els increase %ith onset of 2'.
o Troponin$ protein in myocardium responsible for
contractile process, le#els pea( %ith *H,23.
Myocardial %ostinfarction Reco-ery %eriod
=oal$ pre#ent complications
C zones of myocardial tissue damage, including inner zone
of necrosis %ith surrounding zone of cell in8ury, and outer
zone of ischemia.
0,G days post 2', rupture of the #entricle, inter#entricular
septum, or the #al#e structures may occur. Replacement of
necrotic myocardial tissue usually happens by the Gth %ee(.
6ibrous scar tissue de#elops, %hich lac(s the contractile,
elastic, and conducti#e properties of normal myocardial
Patho Test #2 Study Sheet
9
cells.
An aneurism may de#elop due to scar tissue in #entricle,
%hich can create thrombus formation andA or increase
%or(load of left side of heart causing left heart failure.
Stages of reco#ery related to size of infarct and changes
and complications are determined by e"tent and location of
the in8ury.
*omplications include sudden death, heart failure and
cardiogenic shoc(, pericarditis, and /ressler syndrome,
thromboemboli, rupture of the heart, #entricular aneurisms,
deep #ein thrombosis.
"ther Treatments
Emergency Percutaneous Coronary Intervention .PCI1
includes Percutaneous Transluminal Coronary ngioplasty
.PTC17 Treats underlying sclerotic lesion and may be used
to open occluded coronary artery,promote perfusion to area
depri#ed of 12
<rachytherapy
Coronary rtery <ypass ;ra$ting .C<;17 for those %ith
significant *5/ and %ho are not candidates for P*'
%harmacoloic Therapy
Thrombolytics: usually '+, dissol#eAlyse thrombus
dissol#e all clots$ not to be used if pt has protecti#e clot,
after ma8or surgery or hemorrhagic stro(e!, best results if
administered %ithin P:,;: minutes of symptom onset,
typically streto(inase is administered.
Analgesics: usually morphine '+!, reduces painAan"iety,
reduces preload less %or(load on heart!, rela"es
bronchioles increase 12!
Angiotensin-Converting Enzyme Inhibitors (ACE-I): net
resultL decreased 3P, diuresis, decreased 12 demand on
heart, decreases mortality rate& ensure pt is not hypotensi#e,
hypo#olemic, hyponatremic or hyper(alemic& 3P, 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 %or(load, alter resting myocardial membrane
potentials and decrease arrhythmia freBuencies, may aid in
redistributing coronary artery blood flo% and impro#ing
myocardial blood flo%.
Anti-arrhythmia medications: may be gi#en to pre#ent or
treat life,threatening arrhythmias that often occur %ith
A2'.
2yocardial 'nfarction, The .ursing Process
The (ursin %rocess:
Assessment$
o )stablish baseline
o *areful history
o Symptoms time, duration, precipitatingArelie#ing
factors, comparison to pre#ious symptoms!
o Physical assessment detect
changeAcomplications!
o '+ sites.
iagnosis:
o :ursing #iagnosis" based on clinical
manifestations, history, diagnostics )S$
ineffecti#e tissue perfusion related to reduced
coronary blood flo% from coronary thrombus,
an"iety related to fear of death etc.!
o Potential Complications$ pulmonary edema, heart
failure, cardiogenic shoc(, arrhythmias, cardiac
arrest, myocardial rupture, deep #ein thrombosis.
o Planning*;oals$ relief of painA ischemic SIS,
pre#ent further damage, decrease %or(load of
heart, reduce an"iety
!ursing Interventions:
o Immediate administration o$ oxygen and
nitroglycerin
o Relieving Pain*Ischemia" balance heart4s 12
supplyAdemand, meds beta
bloc(er, morphine, nitro, 12 therapy etc.!, assess
+S, promote physical rest bac(rest ele#ated!
o Improving Respiratory -unction" careful
respiratory assessment, encourage pt to breathe
deepAchange positions pre#ent fluid from
pooling!
o Promote Tissue Per$usion" bedAchair rest, monitor
temperatureAperipheral pulses, teach dorsifle"ion
e"ercises and monitor 5oman4s sign, admin. 12,
o Reduce nxiety" create trust, pro#ide info, Buiet
en#ironment, using humor, support beliefs
praying etc.!, music, address fears
o =onitor*=anage Potential Complications$ close
monitoringA early '/,report changes promptly,
elastic stoc(ings, R12 e"ercise, heparin
o Promoting ,ome*Community7<ased Care$ '/
priorities, educate, encourage in#ol#ement in
rehab program
Evaluation:
o Relief of angina
o .o respiratory difficulties
o AdeBuate tissue perfusion
o /ecreased an"iety
o Adherence to self,care program
o Absence of complications
Chronic /eart 5ailure (C/5+
*56 is the inability of the heart to fill diastole! andAor
contract systole! to pump sufficient blood to meet the
needs of the tissues for o"ygen and nutrients.
't is a clinical syndrome including fluid o#erload or
inadeBuate tissue perfusion& ho%e#er, many !ith ,eart
-ailure .,-1 do not mani$est !ith pulmonary or systemic
congestion.
Clinical Manifestations
*56 produces SIS of failure of both #entricles.
SIs tend to be differentiated based on the effect on the
#entricles.
't is the nurseTs role to monitor and manage potential
complications.
Left6sided /eart 5ailure$
Patho Test #2 Study Sheet
;
'ncreased > #entricular end,diastolic blood #olume %hich
increase the > #entricular end,diastolic pressure, %hich
decreases blood flo% from > atrium to > #entricle, during
diastole, resulting in pulmonary #enous congestion
bac(%ard failure.
Pulmonary congestion$ dyspnea, cough, pulmonary
crac(les, lo%er 12 sat le#els, possible SC heard /yspnea,
/1), orthopnea, P./
3i,basilar crac(les that do not clear %ith coughing, then all
lobes affected
*ough,initially dry and unproducti#e mista(en for other
disorder, e#entually se#ere pulmonary edema.
Renal,oliguria, then release of renin then aldosterone, then
.aU and fluid retention intra#ascular #olume. .octuria due
to Vrest and therefore better perfusion.
Altered digestion
*erebral,e.g., dizziness, confusion, an"iety& 6atigue an
'nsomnia
Stimulation of S.S causes further #asoconstriction,cool
clammy s(in, tachycardia, %ea( pulses
Riht6#ided /eart 5ailure
*ongestion of #iscera and peripheral tissues since right
#entricle can not accommodate #enous return of blood
V J+P that is QC cm abo#e sternal angle
)dema of lo%er e"tremities, beginning in an(les, then
up%ards including sacrum if on bed rest, genitalia and
abdomen, hands and arms may become edematous, also
periorbital edema
Ascites
-ea(ness, anore"ia, nausea
6luid retention %eight gain. Pitting edema %ith 0.DU> fluid
%eight gain
5epatomegaly and R7N tenderness, possible secondary
li#er dysfunction, increased li#er may e"ert pressure on
other organs
6atigue due to W cardiac output, circulation, and inadeBuate
remo#al of catabolic %aste products from tissues.
Dianosis
SIs are common %ith other conditions li(e renal failure, li#er failure,
oncologic conditions, and *1P/ therefore, the patient ris(s being
treated as if they ha#e 56. Assessment of #entricular function is
essential to diagnosis of 56.
Dianostics
)chocardiogram,identify cause, location, type, se#erity of
56
Radionuclide #entriculography
+entriculogram %ith cardiac catheterization
*hest,ray and )*=
>abs$ lytes, 37., TS5, *3*, urinalysis
Patient ris( should be determined follo%ing an 2'
3nter-entions and Treatment
=oals$
)liminate or reduce any etiologic contributory factors,
especially those that may be re#ersible, such as A.
6ibrillation or e"cessi#e )T15 ingestion and&
Reduce the %or(load on the heart by reducing afterload and
preload
o .aU X 2,CgAday! and fluid restriction
o 2onitor ris( of hypo(alemia,chec( labs and
increase HU in diet
o 2onitor %eight gain and 'U1 amounts daily
o 2onitor oliguria or anuria
o 2onitor areas of edema
o 2onitor postural hypotension
o 2onitor dehydration,s(in turgor, mucous
membranes, 3P etc
o Regular e"ercise
o W)T15, smo(ing
o 12 therapy,monitor 12 stats, orthopnea, P./,
/1), lung and heart sounds, mental status
o PT*A may be necessary if *A/ in#ol#ed, also
mechanical assist de#ices and transplantation
o Pacing de#ice if electrical conduction defects,left
bundle branch bloc( >333! common
%athophysioloy
Systolic 56 decrease the amount of blood e8ected from the
#entricle, %hich stimulates the sympathetic ner#ous system
sns! to release epinephrine and norepinephrine.
*ontinued 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 (idneys.
Renin promotes formation of angiotensin ' %hich is
con#erted to angiotensin '' %ith production of A*).
Angiotensin '', a #asoconstrictor promote .aU and fluid
retention, and thirst.
Aldosterone e"acerbates myocardial fibrosis.
Angiotensin, aldosterone, and other neurohormones lead to
an increase in preload and afterload, stressing the
#entricular %alls and %or(load of the heart.
As the heartTs %or(load contractility of the myofibrils
decreases.
/ecreased contractility results in increased end,diastolic
blood #olume in the #entricle, stretching the myofibres and
increasing the size of the #entricle that further stresses the
#entricular %all.
To compensate the heart muscle thic(ens #entricular
hypertrophy!& ho%e#er, capillary blood supply cannot
accommodate this gro%th, resulting in myocardial ischemia
further complicated by sympathetic,induced coronary
artery #asoconstriction, V #entricular %all stress, and
decreased mitochondrial energy production.
This scenario has been termed Y#icious cycle of 56Y
because the heart cannot pump sufficiently, yet is
stimulated to %or( harder, and heart failure ensues. The
dominant $eature in ,- is inade>uate tissue per$usion5
%harmacoloical Therapy
Se#eral meds for systolic 56
Patho Test #2 Study Sheet
1:
2eds for diastolic failure depend on underlying condition
such as hypertension or #al#ular dysfunction ,may include
*AUU channel bloc(ers
A*) inhibitor for mild 56
'f unable to continue A*) inhibitor due to renal impairment
V*R and VHU!, then angiotensin '' receptor bloc(er AR3!
or hydralazine and isosorbide dinitrate.
/iuretic, lasi", spironolactone
/igitalis added to A*) inhibitor if symptoms continue
3eta,bloc(ers added to initial meds to impro#e mortality
and morbidity
Possibly Anticaogulation
.SA'/s should be a#oided as Vsystemic #ascular
resistance and renal perfusion
2onitor complications of prolonged diuretic use
5eart 6ailure , A *ase Study
The Case #tudy
A G9,year,old male is admitted to the hospital %ith the chief
complaint of shortness of breath. 5e states the shortness of breath has
been increasing o#er the past 2 months and is aggra#ated by e"ertion.
5e has found that he often a%a(ens at night %ith a sensation of
smothering that is partially relie#ed %hen he gets up and opens the
%indo%. 5e has not noted an(le s%elling or edema.
Past medical history is only positi#e for myocardial infarction 9 years
ago. 5e currently does not ha#e complaints of chest pain.
3lood pressure is 10:A;9. -hen the nurse listens to his heart, she
hears a normal S1 and S2 %ith a rate of 99. -hen listening to the
lungs, the nurse notes bibasilar crac(les. There is no peripheral
edema.
The admission diagnosis for the patient %as left,sided heart failure.
7uestion 8 6 Descri*e the pathophysioloy of left6sided heart
failure9
The left side of the heart is responsible for pumping blood from the
left #entricle to the systemic circulation. 3lood flo%s from the
pulmonary system to the left atrium into the left #entricle. >eft
#entricular failure occurs %hen the %or(load of the left #entricle
increases and the muscle hypertrophies. 1#er time, the increased
%or(load %ill increase the myocardial o"ygen need of the left
#entricle. +entricular hypertrophy %ill cause a decreasing ability of
left #entricular stretch to compensate for increasing end diastolic
#olume. The 6ran(,Starling mechanism in a normal heart is
responsible for an increased stretch of the #entricular muscle,
increasing contractility, %hen there is an increase in left #entricular
end diastolic #olume %ill increase stretch and increase cardiac output.
'n the patient %ith hypertension, the afterload %ill increase secondary
to increased peripheral #ascular resistance. 'ncreased afterload %ill
increase the %or(load of the left #entricle. Progressi#e increased
%or(load %ill cause the left #entricle to fail, decreasing cardiac
output and increasing left #entricular end diastolic pressure. The
increased end diastolic pressure %ill increase the %or(load of the left
atrium. 'ncreased %or(load %ill cause failure of the left atrium and
increased pressure %ithin the pulmonary system, %hich causes the
pulmonary crac(les that are all commonly seen %ith increased
pulmonary pressure.
7uestion : 6 1hich of the clinical manifestations i-en in this
case would *e found in a patient with left6sided heart failure;
The increased pressure %ithin the pulmonary system is responsible
for the pulmonary symptoms seen in left #entricular failure. 'ncreased
pulmonary pressures lead to pulmonary congestion and decreased
ability to o"ygenate. 'nitially, as in this case, the indi#idual %ill ha#e
complaints of increased shortness of breath %ith acti#ity as e"ercise
%ill increase o"ygen needs. 6urther progression %ill lead to
paro"ysmal nocturnal dyspnea, a sensation of increased shortness of
breath at night 1 to 2 hours after bedtime, %hich can be relie#ed %ith
sitting or standing. 1n e"am, the nurse %ill be able to hear pulmonary
crac(les that are a reflection of the fluid that has mo#ed into the
al#eoli.
7uestion < 6 /ow does left6sided heart failure impact preload2
afterload2 and contractility;
Preload is a reflection of left #entricular end diastolic #olume and
pressure. /ecreased ability to empty the left #entricle %ill decrease
cardiac output and increase the amount of blood that is present in the
left #entricle at the end of systole, %hich %ill increase preload.
Afterload is increased by both increased peripheral #ascular
resistance and changes in #entricular %all tension. 'ncreased stretch
of the left #entricle %ill be associated %ith increased #entricular %all
tension and increased myocardial o"ygen need. This can actually
increase ischemia of the left #entricle and %orsen failure.
*ontractility actually is a measure of ho% %ell the left #entricle is
able to mechanically perform its function. 'ncreased contractility %ill
impro#e cardiac output. >eft #entricular failure %ill decrease
contractility. Stretch of the #entricular muscle %ill decrease
effecti#eness of actin and myosin interactions.
7uestion = 6 Descri*e other clinical manifestations the nurse
would monitor for in this patient9 1hich clinical manifestations
would *e seen in only left6sided failure; 1hich symptoms would
occur if riht6sided failure was present also;
*linical manifestations of left #entricular failure %ill al%ays include
the pulmonary symptoms seen in this case. The most common
symptoms are dyspnea on e"ertion /1)!, orthopnea, paro"ysmal
nocturnal dyspnea P./!, and pulmonary crac(les.
The clinical manifestations of right,sided failure are related to
increased pressure %ithin the #enous system. Remember that the
superior and inferior #ena ca#a empty into the right atrium, %hich
then empties into the right #entricle. -hen the right #entricle fails,
there is increased pressure %ithin the right atrium that causes
increased pressure in the #enous system. This increased pressure %ill
cause clinical manifestations of peripheral edema, hepatomegaly, and
increased 8ugular #enous distension.
Remember that many patients ha#e bi#entricular failure, and in this
case, the nurse %ould see a combination of the abo#e symptoms.
7uestion 5 61hat medications would you administer to a patient
with C/5;
/iuretics$ diuretics are gi#en to patient %ith congesti#e heart failure
to decrease #olume. 'n both left, and right,sided heart failure, there is
associated fluid retention. /ecreased cardiac output %ill stimulate the
(idneys to decrease perfusion and retain fluid.
A*) inhibitors$ an A*) inhibitor %ill decrease the release of
aldosterone, %hich %ill decreased blood #olume and preload. The
decreased formation of angiotensin %ill decrease peripheral #ascular
resistance and afterload.
Patho Test #2 Study Sheet
11
3eta,bloc(ers$ 3eta,bloc(ers %ill decrease the %or(load of the heart
and myocardial o"ygen needs by decreasing cardiac output and
contractility.
%athophysioloy of "-arian Cancer
'n the adult female, the o#aries are flat, almond,shaped structures that
measure 0 Z 2.D Z 1.D cm. They are located on either side of the
uterus belo% the ends of the t%o fallopian tubes. The o#aries produce
estrogens, progesterone, and androgens. 'n *anada, gynecologic
tumors cancers of the endometrium, o#aries, #ul#a, #agina, placenta,
and adne"a! account for 11< of malignant tumors in %omen and
91< of genital cancers Public 5ealth Agency of *anada,
2::C15 1#arian cancer causes more deaths than any other cancer of
the female reproducti#e system. About GD< of cases are detected at a
late stage /uffy, 2::1!. The o#ary is a common site of primary as
%ell as metastatic lesions from other cancers. 2ost cases affect
%omen ages D: to D;.
*ancer of the o#ary is comple" because of the di#ersity of tissue
types that originate in the o#ary. As a result of this di#ersity, there are
se#eral types of o#arian cancers$ 2alignant neoplasms of the o#ary
can be di#ided into three cateories$
)pithelial tumors,
=erm cell tumors,
=onadal stromal tumors.
About ;:< of o#arian cancers deri#e from malignant transformation
of the epithelium of the o#ary, %hich is contiguous %ith the
peritoneal mesothelium.
Ris' 5actors$
A strong family history of cancer, particularly breast and
o#arian cancer is the most important ris( factor.
.ulliparity is also associated %ith increased ris(, %hereas
oral contracepti#e use, pregnancy, and lactation are
associated %ith decreased ris(. These obser#ations suggest
that stimulation of the o#arian epithelium %hich occurs
%ith nulliparity and uninterrupted o#ulation may
predispose to o#arian cancer.
A strong family history of breast and o#arian cancer,
sometimes at an early age, may be related to the presence
of an inherited mutation in one of t%o genes, (no%n as
3R*A1 and 3R*A2. 3R*A,1 is a genetic mutation that
results in an increased ris( for breast and o#arian cancer.
3R*A,2 is another genetic mutation that may result in
increased ris( for both female and male breast cancers and
for o#arian cancer
1lder age is a ma8or ris( factor because the incidence of
this disease pea(s in the eighth decade of life.
5igh dietary fat inta(e, mumps before menarche, use of talc
in the perineal area.
2ultiparity, oral contracepti#e use, breastfeeding, and
ano#ulatory disorders may be protecti#e.
Sur#i#al rates depend on the stage of the cancer at
diagnosis.
2uch more needs to be learned about the ris(s associated
%ith some mutations, the reliability of testing, and the
efficacy of follo%,up.
*linical 2anifestations of 1#arian *ancer
#ymptoms are nonspecific and include$
=eneral abdominal discomfort
6latulence
'ndigestion
Pressure
3loating
*ramps
Sense of pel#ic hea#iness
>oss of appetite
6eeling of fullness
*hanges in bo%el habits
!s the malinancy rows2 a -ariety of manifestations such as:
'ncreased abdominal girth
3o%el and bladder dysfunction
Persistent pel#ic or abdominal pain
2enstrual irregularities
>eg pain
Ascites
Symptoms are o$ten vague6 and many !omen ignore the symptoms5
1#arian cancer is often silent, but enlargement of the abdomen from
an accumulation of fluid is the most common sign. Any %oman %ith
gastrointestinal symptoms and %ithout a (no%n diagnosis must be
e#aluated %ith o#arian cancer in mind. 6latulence, fullness after a
light meal, and increasing abdominal girth are significant symptoms.
An o#arian malignancy should be considered %hen abnormal #aginal
bleeding occurs. +ague, undiagnosed, persistent gastrointestinal
symptoms should alert the nurse to the possibility of an early o#arian
malignancy. A palpable o#ary in a %oman %ho has gone through
menopause is in#estigated because o#aries normally become smaller
and less palpable after menopause.
/iagnostic Studies $
.o screening e"ists for o#arian cancer. 3ecause early o#arian cancer
is usually asymptomatic, yearly bimanual pel#ic e"aminations should
be performed to identify the presence of an o#arian mass.
Postmenopausal %omen should not ha#e palpable o#aries, so a mass
of any size should be suspected as possible o#arian cancer. An
abdominal or #aginal ultrasound can be used to detect o#arian
masses.
6or %omen %ith high ris( for o#arian cancer, screening using a
combination of the tumor mar(er, *A,12D, and ultrasound is
recommended in addition to yearly pel#ic e"amination. *A,12D is
Patho Test #2 Study Sheet
12
positi#e in 9:< of %omen %ith epithelial o#arian cancer and is used
to monitor the course of the disease. There may be an ele#ation of
*A,12D le#els due to non o#arian malignancies or benign conditions
such as fibroids or endometriosis.
1#arian *ancer Ris( 6actors
-omen bet%een the ages of D:,D; are at a high ris( of de#eloping
o#arian cancers. There seems to be e#idence to support that there are
certain factors, %hich are associated %ith a decreased ris( of
de#eloping o#arian cancer, and seem to be protecti#e.
1#arian *ancer, *ollaborati#e *are
-omen identified as being at high ris( based on family and health
history may reBuire counseling regarding options such as
prophylactic oophorectomy and birth control pills. Although
oophorectomy can significantly reduce the ris( of o#arian cancer it is
important to note that it %ill not completely eliminate it. 'f a
diagnosis of o#arian cancer is made, staging is critical for guiding
treatment decisions.
#taes of "-arian Cancer
I?;ro!th limited to the ovaries
II?;ro!th involves one or %oth ovaries !ith pelvic extension
III?;ro!th involves one or %oth ovaries !ith metastases outside the
pelvis or positive retroperitoneal or inguinal nodes
IV?;ro!th involves one or %oth ovaries !ith distant metastases
A total abdominal hysterectomy %ith remo#al of the fallopian tubes
and o#aries 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 ' disease.
Stage '' disease may recei#e e"ternal abdominal and pel#ic radiation,
or systemic combined chemotherapy in the patient %ho is clinically
free of symptoms. After completion of systemic chemotherapy in the
patient %ho is clinically free of symptoms, a ?second,loo(@ surgical
procedure is often performed to determine %hether there is any
e#idence of disease. 'f no disease is found, the patient is monitored
for recurrent disease.
*hemotherapy such as cyclophosphamide *yto"an!, do"orubicin
Adriamycin!, cisplatin Platinol,AN!, carboplatin Paraplatin!, or
paclita"el Ta"ol! is used for the treatment of stage ''' and stage '+ of
the disease. 5e"amethylmelamine 5e"alen!, ifosfamide 'fe"!, bone
marro% transplantation, and peripheral blood stem cell support may
also be used. Paclita"el, cisplatin, and carboplatin are most often used
because of their e"cellent clinical benefits and manageable to"icity.
>eu(openia, neuroto"icity, and fe#er may occur.
'n the ad#anced stages of the disease chemotherapy is the most
common form of treatment. Radiation and chemotherapy may be
used to shrin( the size of the tumor, relie#ing pressure and pain.
Surgical debul(ing is often done in con8unction %ith chemotherapy
for ad#anced disease.
.ursing measures include those related to the patientTs treatment plan,
be it surgery, chemotherapy, radiation, or palliation. )motional
support, comfort measures, and information, plus attenti#eness and
caring, are meaningful aids to the patient and her family.
%athophysioloy of %rostate Cancer
%rostate cancer is a malignant tumor of the prostate gland, it is the
most freBuently diagnosed cancer in *anadian males, and is the third
most common cause of death due to cancer in men. The *anadian
*ancer Society 2::D!estimates that 2:,D:: men %ill be diagnosed
%ith prostate cancer in 2::D and that 0,C:: %ill die of the disease.
Prostate cancer rates are t%ice as high in African *anadian men as in
*aucasian men, and African *anadian men are more li(ely to die of
prostate cancer than men in any other racial or ethnic group.
Prostate cancer $
's an androgen,dependent adenocarcinoma.
The ma8ority of tumors occur in the outer aspect of the
prostate gland.
Prostate cancer is usually slo% gro%ing.
't can spread by three routes$
o direct e"tension
o through the lymph system
o through the bloodstream.
%rostatic adenocarcinomas, %hich account for ;9< of all primary
prostatic cancers, are commonly multicentric and located in the
peripheral zones of the prostate. The high freBuency of in#asion of
the prostatic capsule by adenocarcinoma relates to its subcapsular
location. 'n#asion of the urinary bladder is less common and occurs
later in the clinical course. 2etastasis to the lung reflects lymphatic
spread through the thoracic duct and dissemination from the prostatic
#enous ple"us to the inferior #ena ca#a. 3ony metastases, particularly
to the #ertebral column, ribs, and pel#is, 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 ris( of de#eloping it9
(onmodifia*le ris' factors for prostate cancer include:
'ncreasing age$ the incidence of prostate cancer increases
rapidly after the age of D: years, and more than G:< of
cases occur in men o#er PD years of age.
6amily history of prostate cancer, especially first degree
relati#es.
African ancestry& rate is t%ice that of %hite men, more
li(ely to ha#e prostate cancer at a younger age, ha#e more
aggressi#e tumors at diagnosis, and higher mortality rate.
1besity, physical inacti#ity, eating a diet high in fat,
%or(ing %ith a metal called cadmium, are being studied as
possible ris( factors. 't is possible to de#elop prostate
cancer %ithout ha#ing any of these ris( factors.
Prostate *ancer, *linical 2anifestationsA/iagnostics
Patho Test #2 Study Sheet
1C
#in and #ymptoms
Prostate cancer may not cause any signs or symptoms, especially in
the early stages. The presence of symptoms often suggests locally
ad#anced or metastatic disease. /epending on the size and location of
prostatic cancer at the time of diagnosis, there may be changes
associated %ith the #oiding pattern similar to those found in 3P5.
These include urgency, freBuency, nocturia, hesitancy, dysuria,
hematuria, or blood in the e8aculate. 1n physical e"amination, the
prostate is nodular and fi"ed. 3one metastasis often is characterized
by lo% bac( pain. Pathologic fractures can occur at the site of
metastasis. Symptoms related to metastases include bac(ache, hip
pain, perineal and rectal discomfort, anemia, %eight loss, %ea(ness,
nausea, and oliguria decreased urine output!. 7nfortunately, these
symptoms may be the first indications of prostate cancer. )arly
recognition and treatment is reBuired to control gro%th, pre#ent
metastasis, and preser#e Buality of life.
Dianostic Testin
'mpro#ed diagnostic techniBues ha#e greatly enhanced the detection
of prostate cancer. -hen prostate cancer is detected early, the
li(elihood of cure is high. )#ery man older than 0: years of age
should ha#e a DR& digital rectal e"amination! as part of his regular
health chec(up. Routine repeated rectal palpation of the gland
preferably by the same e"aminer! is important because early cancer
may be detected as a nodule %ithin the substance of the gland or as
an e"tensi#e hardening in the posterior lobe. The more ad#anced
lesion is ?stony hard@ and fi"ed.
$lood Testin
%#!prostate,specific antigen!, a neutral serine protease, is
produced by the normal and neoplastic ductal epithelium of
the prostate and secreted into the glandular lumen 3ra%er,
*heli, .eaman et al., 2:::& Halish I 2cHinlay, 1;;;!.
A simple blood test can be used to measure PSA le#els. The
concentration of PSA in the blood is proportional to the
total prostatic mass.
Although the PSA le#el indicates the presence of prostate
tissue, it does not necessarily indicate malignancy.
3main #tudies
TR7S6usually the only imaging study needed to diagnose
prostate cancer. Transrectal ultrasound TR7S! studies are
indicated for men %ho ha#e ele#ated PSA le#els and
abnormal /R) findings. TR7S studies help in detecting
nonpalpable prostate cancers and assist %ith staging
localized prostate cancer. .eedle biopsies of the prostate
are commonly guided by TR7S.
1ther imaging may be used if metastases is suspected$
o S,ray
o *T scan and 2R'
o 3one scan
Prostate *ancer, Surgical 2anagement and *omplications
Prostate surgery may be indicated for the patient %ith 3P5 or
prostate cancer. The ob8ecti#es before prostate surgery are to assess
the patientTs general health status and to establish optimal renal
function. Prostate surgery should be performed before acute urinary
retention de#elops 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 effecti#e treatment for long term sur#i#al. This type of surgery
is usually performed on those men %hose cancer is confined to the
prostate, usually stage one or t%o, and %ho are in relati#ely good
health. A radical prostatectomy is performed either using the t%o
most common approaches& retropubic or perineal resection.
Complications
*omplications depend on the type of prostatectomy performed and
almost al%ays include$
se)ual dysfunction, All prostatectomies carry a ris( of
impotence because of potential damage to the pudendal
ner#es. The incidence of erectile dysfunction may depend
on age, and preoperati#e se"ual functioning.
3ncontinence, nearly all men e"perience a problem %ith
urinary control post,operati#ely for one or t%o months.
'ncontinence occurs because the bladder must be reattached
to the urethra after the prostate is remo#ed. -ith time the
most men regain control as the bladder ad8usts.
"ther common complications may include$
o 5emorrhage,
o *lot formation,
o *atheter obstruction,
o 7rinary retention
o 'nfection
o -ound dehiscence
o /eep #ein thrombosis
o Pulmonary emboli
Prostate *ancer Terminology
DR&M/R) /igital Rectal )"amination! is part of a
regular health chec(up in %hich the prostate gland is
palpated by the health e"aminer to detect changes in size,
or %hether the prostate is becoming hard.
Dysuria0 A clinical manifestation %hich may indicate
prostate cancer. /ysuria refers to painful urination.
/ematuriaM A clinical manifestation %hich may indicate
prostate cancer. 5ematuria is blood in the urine.
(octuria 0A clinical manifestation %hich may indicate
prostate cancer. .octuria is the a%a(ening in the night
during sleep in order to urinate.
"liuria M Refers to a decrease in urine output or absence
of urine output!. This is commonly associated %ith
metastases of prostate cancer.
%#! MPSA Prostate Specific Antigen! is a neutral serine
protease %hich can be measured %ith a simple blood test.
*oncentration of PSA is proportional to prostatic mass and
indicates presence of prostatic tissue, not malignancy.
TRU# MTransrectal 7ltrasound! is used %hen a patient
has an increased PSA and abnormal /R) findings. This
TR7S assists %ith detecting non,palpable prostate cancers,
staging prostate cancers, and guiding needle biopsies.
Complications of a %rostatectomy
A nurse must be a%are of potential complications %hen a patient is
undergoing the remo#al of the prostate. The nurse must be able to
communicate %ith the patient about normal, e"pected complications.
Although there are many potential complications, there are t%o
prostatectomy complications %hich are almost al%ays e"pected.
Patho Test #2 Study Sheet
10
#escri%e the t!o most common complications o$ a prostatectomy6
!hy they occur6 and any other things a%out these complications
!hich a nurse !ould !ant to discuss !ith the patient5
#e)ual Dysfunction: ris( of impotence occurs from damage done to
the pudental ner#es during surgery. )rectile dysfunction depends on
age and preoperati#e se"ual function. A nurse must be sensiti#e, and
understanding of the an"iety and %orry this may cause some men.
Self image and confidence may be issues a nurse %ill need to address
as a result of this complication.
3ncontinence: most prostatectomy patients %ill ha#e problems %ith
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
remo#ed. A nurse must inform the patient that %ith time, most men
%ill regain control of their bladder function. Again, a nurse must be
sensiti#e to self image issues that may be associated %ith
Table "#-$ [ Comparin #urical !pproaches for Treatment of %rostate Disorders
The surgical approach of choice depends on 1! the size of the gland, 2! the se#erity of the obstruction, C! the age of the patient,
0! the condition of patient, and D! the presence of associated diseases.
#urical !pproach !d-antaes Disad-antaes (ursin 3mplications
Transurethral Resection
.TUR or TURP1 remo#al of
prostatic tissue by instrument
introduced through urethra!
A#oids abdominal incision
Safer for surgical,ris( patient
Shorter hospitalization and
reco#ery periods
>o%er morbidity rate
*auses less pain
ReBuires highly s(illed
surgeon
Recurrent obstruction,
urethral trauma, and stricture
may de#elop.
/elayed bleeding may occur.
2onitor for hemorrhage.
1bser#e for symptoms of
urethral stricture dysuria,
straining, %ea( urinary
stream!.
8pen Surgical Removal
Suprapubic approach Technically simple
1ffers %ide area of
e"ploration
Permits e"ploration for
cancerous lymph nodes
Allo%s more complete
remo#al of obstructing gland
Permits treatment of
associated bladder lesions
ReBuires surgical approach
through the bladder
*ontrol of hemorrhage
difficult.
7rine may lea( around the
suprapubic tube.
Reco#ery may be prolonged
and uncomfortable.
2onitor for indications of
hemorrhage and shoc(.
=i#e meticulous aseptic care
to the area around suprapubic
tube.
Perineal approach 1ffers direct anatomic
approach
Permits gra#ity drainage
Particularly effecti#e for
radical cancer therapy
Allo%s hemostasis under
direct #ision
>o% mortality rate
>o%er incidence of shoc(
'deal for #ery old, frail, and
poor,surgical,ris( patient
%ith large prostate
5igher postoperati#e
incidence of impotence and
urinary incontinence
Possible damage to rectum
and e"ternal sphincter
Restricted operati#e field
=reater potential for infection
A#oid using rectal tubes or
thermometers and enemas
after perineal surgery.
7se drainage pads to absorb
e"cess urinary drainage.
Pro#ide foam rubber ring for
patient comfort in sitting.
Anticipate urinary lea(age
around the %ound for se#eral
days after the catheter is
remo#ed.
Retropubic approach A#oids incision into the
bladder
Permits surgeon to see and
control bleeders
Shorter reco#ery period
>ess bladder sphincter
damage
*annot treat associated
bladder disease
'ncreased incidence of
hemorrhage from prostatic
#enous ple"us& pubic osteitis
2onitor for hemorrhage.
Anticipate posturinary
lea(age for se#eral days after
remo#ing the catheter
Transurethral 'ncision T7'P! Results comparable to T7RP
>o%er incidence of erectile
dysfunction
ReBuires highly s(illed
surgeon
Recurrent obstruction and
2onitor for hemorrhage.
Patho Test #2 Study Sheet
1D
incontinence or ha#ing a catheter.
Prostate *ancer, *ollaborati#e *are
)arly,stage prostate cancer is a curable disease in the ma8ority of
men. Treatment is based on the stage of the disease and the patientTs
age and symptoms. Partin and associates 1;;G! combined PSA le#el
%ith 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
=leason grading system. -ell,differentiated tumors are assigned a
grade of 1, and poorly differentiated tumors a grade of D.
The collaborati#e care of the patient %ith prostate cancer depends on
the stage of the cancer and the o#erall health of the patient. At all
stages, there is more than one possible treatment option.
#tae 8:
1atchful waitin with annual %#! and DR& ,)"pectant
therapy %atching and %aiting! may be used if the tumor is
not producing symptoms, is e"pected to gro% slo%ly, and is
small and contained in one area of the prostate. This
approach is particularly suited for men %ho are elderly or
ha#e other health problems.
Radical %rostatectomy,2ost men %ith an anticipated
sur#i#al greater than 1: years are considered for surgical or
radiation therapy. Radical prostatectomy in#ol#es complete
remo#al of the seminal #esicles, prostate, and ampullae of
the #as deferens.
Radiation Therapy,Radiation therapy can be deli#ered by
a #ariety of techniBues, including e"ternal,beam radiation
therapy and transperineal implantation of radioisotopes.
#tae ::
Radical Prostatectomy
Radiation Therapy
#tae <:
Radical Prostatectomy
Radiation Therapy
/ormone Therapy65ormonal therapy is one method used
to control rather than cure prostate cancer *arroll et al.,
2::1!. 5ormonal therapy for ad#anced prostate cancer
suppresses androgenic stimuli to the prostate by decreasing
the circulating plasma testosterone le#els or interrupting the
con#ersion to or binding of dihydrotestosterone. As a result,
the prostatic epithelium atrophies decreases!. This effect is
accomplished either by orchiectomy remo#al of the testes!
or by the administration of medications.
"rchiectomy , 1rchiectomy often is effecti#e in reducing
symptoms and e"tending sur#i#al.
#tae =:
5ormone therapy
1rchiectomy
Chemotherapy 6 *hemotherapy has sho%n limited
effecti#eness in the treatment of prostate cancer.
Radiation therapy to metastatic bone areas
2odule :;$ 7pper and >o%er =astrointestinal /isorders
=astroesophageal Reflu" /isease =)R/!
>astroesophaeal Reflu): a bac(,flo% of gastric or duodenal
contents into the esophagus, and is normal to a certain e"tent in adults
and children. 5o%e#er, e"cessi#e reflu" may be caused by an
incompetent lo%er esophageal sphincter, pyloric stenosis, or motility
disorder. 'ncreasing age seems to ha#e an increase in signs of reflu"
disease.
Clinical manifestations of >&RD:
Pyrosis$ burning sensation in esophagus
/yspepsia$ indigestion
Regurgitation
/ysphagia
1dynophagia$ difficulty s%allo%ingA pain %ith s%allo%ing
5ypersali#ation
)sophagitis
3elching
)pigastric or retrosternal chest pain
Radiating chest pain to shoulder, throat, or bac(
't is important for a nurse to recognize that often the presenting
symptoms mimic those of a patient ha#ing a heart attac(. *areful
health history is crucial for an accurate diagnosis. =)R/s may cause
respiratory sIs li(e %heezing chronic cough, and hoarseness. There
is e#idence that =)R/s is lin(ed to bronchial asthma, 3arret
)sophagus, and esophageal cancer.
>&RD
't is the nurse4s role to perform an accurate assessment of a patient,
recognize clinical manifestations of gastroesophageal reflu" disease,
understand %hy they are occurring, and document them
appropriately. *areful health history and assessment are crucial to
differentiate =)R/ from other diseases or illnesses.
/efinition slide$
Pyrosis 3urning sensation of the esophagus
/yspepsia 'ndigestion
/ysphasia /ifficulty tal(ing
1dynophasia Pain or difficulty s%allo%ing
5ypersali#ation )"cessi#e production of sali#a
)sophagitis 'nflammation of the esophagus
Patho Test #2 Study Sheet
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.ausea and +omiting
(ausea and -omitin: ma8or symptoms related to disorders of the
=' tract. +omiting is usually preceded by nausea. This can be
triggered by odors, acti#ity or food inta(e. The nurse must assess
%hat factors precipitate nausea and #omiting, and help the patient
alle#iate these factors.
(ausea: results from stimulation of the medullary #omiting
centre usually preceded by anore"ia. .ausea often occurs
%ith A.S manifestations such as sali#ation and
#asoconstriction %ith pallor, s%eating, and tachycardia.
Vomittin: in#ol#es 2 parts of the medullary centre$ the
#omiting center and the chemoreceptor trigger zone. 6or a
detailed e"planation of the physiology of #omiting refer to
Porth.
&mesis: #omitus!, #aries in color and content. 't may
contain undigested food particles, bile, or blood
hematemesis!. -hen #omiting occurs after a hemorrhage
in the =' tract, the emesis %ill loo( bright red fresh blood!.
'f the blood has been retained for some time %ithin the
stomach, it loo(s li(e ground coffee beans %hen #omited.
This occurs because of the action of the digesti#e enzymes
%ithin the stomach.
(ursin manaement: focuses on pre#ention and alle#iation of
#omiting. Proper nursing management of nausea and #omiting is to
control the symptoms, increase the patient4s comfort le#el, and ensure
proper fluid and electrolyte balance. The nurse must carefully
monitor the patient4s fluid and electrolytes if #omiting occurs, to
mitigate the high ris( for deficiency of fluid #olume hypo#olemic
shoc( in e"treme cases!. There are a #ariety of medications a#ailable
to control nausea and #omiting in the patient, %hich the nurse %ill
administer %ith a /octorTs order. /ue the anticholinergic effects of
antiemetics to treat nausea it is important that the nurse assesses
bo%el sounds to ensure a bloc(age andAor immobility of the bo%el
does not e"ist.
/ematemesis ? +omitus %ith blood
A nurse must be (no%ledgeable about concerns %ith nausea and
#omiting. 5ematemesis is a cause for concern, and should prompt a
nurse to in#estigate further, as %ell as properly report and document
this finding.
7lcerati#e *olitis$ *omplications, 2edical I .ursing 2anagement
Complications:
Toxic megacolon$ the inflammatory process e"tends into
the muscalaris %hich inhibits the ability to contract, and
results in fe#er, abdominal pain and distention, fatigue and
#omiting. 'f the patient does not respond to medical
management %ithin 2 days, complete colectomy is
indicated.
Perforation
3leeding
+ascular engorgement
5ighly #ascular granulation tissue
'ncrease in ris( of osteoporotic fractures due to decrease in
bone mineral density corticosteroid therapy may enhance
this!
Medical Manaement:
The goal of medicine is to reduce inflammation, suppress
inappropriate immune responses, pro#ide rest for the bo%el so that it
has time to heal, impro#e N1>, and minimize complications.
.utritional therapy may include a high protein, high calorie diet %ith
supplement. '+ therapy may be used to correct fluid and electrolyte
imbalances. Sedati#es, antidiarrheal, and antiperistalic medications
may be used to gi#e time for the bo%el to rest and heal.
*orticosteroids are used to treat se#ere cases of this disease, although
there are ad#erse affects %ith long term use. 2edical management
may also include the use of immunomodulators in order to alter the
immune response. 'n e"treme cases, surgery may also be indicated.
(ursin Manaement:
The nurses4 role is to in#ol#e himAherself in the symptomatic care,
administration of medications, and post operati#e care etc. %hen
medical or surgical inter#entions are indicated. The nurse also must
educate recently diagnosed patients in the hospital, and in the
community about diet and medicines. 5ospitalized patients %ith
se#ere long standing diseases reBuire careful monitoring, parenteral
nutrition, fluid replacement, and surgical care from the nurse. The
nurses role is to pro#ide physical and emotional care %hich may
in#ol#e teaching about the disease, complications, surgical
indications and medications.
!ssessment, Dianostic 5indins:
The patient should be assessed for hypotension, tachycardia,
tachypnea, fe#er, and pallor. 5ydration and nutritional assessment is
e"tremely important as %ell. Assessment of bo%el sounds, distention,
and tenderness assists %ith determining the se#erity of the disease.
>aboratory tests can determine if stool is positi#e for blood, and can
see if there is an ele#ated -3* count, lo% albumin le#els, and
electrolyte imbalances. Abdominal ",rays can assist %ith determining
the cause of presenting symptoms. Sigmoidoscopy, colonoscopy, and
barium enemas are used to distinguish ulcerati#e colitis from other
diseases of the colon. *T scans, 2R's, and ultrasounds can help
identify abscesses. >eu(ocyte scanning is used %hen endoscopy is
prohibited to determine the e"tent of the inflammation. *areful stool
e"amination can rule out other microbial agents %hich cause similar
symptoms.
Clinical Manifestations:
usually include e"acerbations and remissions. Symptoms include
diarrhea, >>N abdominal pain, and rectal bleeding may be mild or
se#ere!. Patients may also ha#e %eight loss, anore"ia, #omiting,
fe#er, cramping or dehydration.
't is not uncommon for a patient %ith ulcerati#e colitis to feel an
urgent need to defecate, and ha#e 1:, 2: liBuid stools each day.
5ypocalcemia and anemia are common. 1ther symptoms outside of
the intestine include s(in lesions, eye lesions, 8oint abnormalities, and
li#er disease. The disease is classified as mild, se#ere or fulminant.
%athophysioloy:
ulcerati#e 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 e#entually spreads to
in#ol#e the %hole colon, in %hich time the bo%el narro%s, shortens
and thic(ens because of fat deposits and hypertrophy.
Ulcerati-e Colitis: a recurrent ulcerati#e, inflammatory disease
%hich affects the mucosal and submucosal layers of the colon and
rectum. This disease is found most commonly in people of *aucasian
and Je%ish descent, and its pea( incidence is bet%een the ages of C:,
D: years. 't is a #ery serious disease because of the systemic
complications and increased ris( for de#eloping colon cancer.
!ssessment, Dianostic 5indins:
The patient should be assessed for hypotension, tachycardia,
tachypnea, fe#er, and pallor. 5ydration and nutritional assessment is
e"tremely important as %ell. Assessment of bo%el sounds, distention,
Patho Test #2 Study Sheet
1G
and tenderness assists %ith determining the se#erity of the disease.
>aboratory tests can determine if stool is positi#e for blood, and can
see if there is an ele#ated -3* count, lo% albumin le#els, and
electrolyte imbalances. Abdominal ",rays can assist %ith determining
the cause of presenting symptoms. Sigmoidoscopy, colonoscopy, and
barium enemas are used to distinguish ulcerati#e colitis from other
diseases of the colon. *T scans, 2R's, and ultrasounds can help
identify abscesses. >eu(ocyte scanning is used %hen endoscopy is
prohibited to determine the e"tent of the inflammation. *areful stool
e"amination can rule out other microbial agents %hich cause similar
symptoms.
Clinical Manifestations:
usually include e"acerbations and remissions. Symptoms include
diarrhea, >>N abdominal pain, and rectal bleeding may be mild or
se#ere!. Patients may also ha#e %eight loss, anore"ia, #omiting,
fe#er, cramping or dehydration.
't is not uncommon for a patient %ith ulcerati#e colitis to feel an
urgent need to defecate, and ha#e 1:, 2: liBuid stools each day.
5ypocalcemia and anemia are common. 1ther symptoms outside of
the intestine include s(in lesions, eye lesions, 8oint abnormalities, and
li#er disease. The disease is classified as mild, se#ere or fulminant.
%athophysioloy:
ulcerati#e 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 e#entually spreads to
in#ol#e the %hole colon, in %hich time the bo%el narro%s, shortens
and thic(ens because of fat deposits and hypertrophy.
Regional )nteritis *rohn4s /isease!
Reional &nteritis (Crohn@s Disease+:
's most common in adolescents and young adults, but can occur at
any time. This disease is more common in %omen, %ith its incidence
rising o#er the past C: years. This disease is seen t%ice as much in
smo(ers than nonsmo(ers. 't can occur any%here along the =' tract
but the most common areas are the distal ileum and the colon.
%athophysioloy
's sub,acute and chronic inflammation %hich affects all layers of the
bo%el %all. 't is characterized by e"acerbations and remissions. The
disease begins %ith edema, then thic(ening of the mucosal %all.
7lcers begin to appear and are separate by normal tissue. 6istulas,
fissures, and abscesses form as the inflammation e"tends to the
peritoneum. =ranulomas can also occur in appro"imately half of
patients %ith *rohn4s disease. The bo%el %all then thic(ens, becomes
fibrotic, and the intestines narro% as disease progresses. 'n some
cases the diseased bo%el %ill begin to adhere to other loops
surrounding them.
Clinical Manifestations
Prominent >RN pain /iarrhea unrelie#ed by defecation *ramping
caused by scar tissue constricting transport of materials through the
intestine *ramping after meals -eight loss, anemia, malnutrition
7lcers 6e#er and leu(ocytosis )"tra,=' symptoms include 8oint
in#ol#ement, s(in lesions, ocular disorders, and oral ulcers.
!ssessment and Dianostic 5indins
A proctosigmoidoscopic e"am is initially performed to see %hether
the recto,sigmoid area is inflamed. Stool sample is also e"amined.
The most conclusi#e method of diagnosis is a barium study of the ='
tract. )ndoscopy and intestinal biopsy can be used to confirm
diagnosis. A complete blood count is ta(en to assess hematocrit and
hemoglobin le#els %hich are usually decreased and -3* count
%hich may be ele#ated.
Complications
'nclude intestinal obstruction, perianal disease, fluid and electrolyte
disturbances, and malnutrition. 6istula formation is another
complication %hich in#ol#es an abnormal communication bet%een
t%o body structures. These can be internal bet%een t%o structures!
or e"ternal bet%een an internal structure and the outside of the
body!. Patients %ith *rohn4s /isease are also at an increased ris( for
colon cancer.
3nflammatory $owel Disease
'nflammatory 3o%el /isease includes both regional enteritis
*rohn4s /isease! and 7lcerati#e *olitis. Although these t%o diseases
ha#e many of the same clinical manifestations, it is important for a
nurse to be able to distinguish one from the other.