 pruritus of the nose, roof of the mouth, throat, eyes, and

UPPER RESPIRATORY TRACT DISORDER

ears
(ENECIO)  Headache (particularly if rhinosinusitis is also present)
 Upper respiratory tract disorders / Upper airway infections
(URIs) are those that involve the nose, paranasal sinuses, Medical Management
pharynx, larynx, trachea, or bronchi.
 Antihistamines = given for sneezing, pruritus, and
 common cold is the most frequently occurring example of a
rhinorrhea
URI
 corticosteroid nasal sprays
 occur when microorganisms such as viruses and bacteria
are inhaled  Brompheniramine/pseudoephedrine (Dimetapp) =
o Viruses = most common cause of URIs, affect the combination antihistamine/decongestant medications
upper respiratory passages and lead to  Cromolyn (NasalCrom) = mast cell stabilizer that inhibits
subsequent mucous membrane inflammation the release of histamine and other chemicals
 URIs affect the nasal cavity; ethmoidal air cells; and frontal,  Oral decongestant agents = for nasal obstruction
maxillary, and sphenoid sinuses; as well as the pharynx,  saline nasal spray = act as a mild decongestant and can
larynx, and trachea liquefy mucus to prevent crusting
 Average = adults develop 2 to 4 URIs per year  Two inhalations of intranasal ipratropium (Atrovent)
given in each nostril two to three times per day for
UPPER AIRWAY INFECTIONS: symptomatic relief of rhinorrhea
 intranasal corticosteroids = for severe congestion
RHINITIS
 ophthalmic agents (cromolyn ophthalmic solution 4%) = to
 is a group of disorders characterized by inflammation and relieve irritation, itching, and redness of the eyes
irritation of the mucous membranes of the nose.  Appropriate allergy treatments:
 often coexists with other respiratory disorders, such as o leukotriene modifiers (e.g., montelukast [Singulair],
asthma zafirlukast [Accolate], zileuton [Zyflo])
 may be acute or chronic, and allergic or nonallergic. o immunoglobulin E modifiers (omalizumab [Xolair])
o Allergic rhinitis is further classified as:
 Seasonal = occurs during pollen Nursing Management
seasons
 Perennial = occurs throughout the year  instructs the patient with allergic rhinitis to avoid or reduce
exposure to allergens and irritants
 To prevent possible drug interactions, the patient is
Pathophysiology
cautioned to read drug labels before taking any OTC
 caused by a variety of factors: medication
o changes in temperature or humidity  instructs the patient about the importance of controlling the
o odors environment at home and at work.
o infection  Saline nasal sprays or aerosols may be helpful in soothing
o age mucous membranes, softening crusted secretions, and
o systemic disease removing irritants
o use of over-the-counter (OTC) and prescribed nasal  instructs the patient in correct administration of nasal
decongestants medications.
o presence of a foreign body o To achieve maximal relief, the patient is instructed to
 Allergic Rhinitis = exposure to allergens such as: blow the nose before applying any medication into the
o foods (e.g., peanuts, walnuts, Brazil nuts, wheat, nasal cavity. In addition, the patient is taught to keep
shellfish, soy, cow’s milk, and eggs), the head upright; spray quickly and firmly into each
o medications (e.g., penicillin, sulfa medications, and nostril away from the nasal septum; and wait at least 1
aspirin) minute before administering the second spray. The
o particles in the indoor and outdoor environment container should be cleaned after each use and should
 Nonallergic Rhinitis = common cold never be shared with other people to avoid cross-
 Drug-induced rhinitis = occur with: contamination.
o Antihypertensives agent  In the case of infectious rhinitis = the nurse reviews
 angiotensin-converting enzyme (ACE) inhibitors hand hygiene technique with the patient as a measure to
 beta-blockers prevent transmission of organisms.
o “statins,”  In older adults and other high-risk populations = the
 atorvastatin (Lipitor) nurse reviews the importance of receiving an influenza
 simvastatin (Zocor) vaccination each year to achieve immunity before the
o antidepressants beginning of the flu season.
o antipsychotics
 risperidone (Risperdal);
VIRAL RHINITIS (COMMON COLD)
o aspirin
o antianxiety medications  most frequent viral infection in the general population
 common cold = used when referring to a URI that is self-
Common Indoor Allergens Common Outdoor limited and caused by a virus
Allergens  cold
Dust mite feces Trees o refers to an infectious, acute inflammation of the
Dog dander Weeds mucous membranes of the nasal cavity characterized
Cat dander Grasses by nasal congestion, rhinorrhea, sneezing, sore throat,
Cockroach droppings Molds and general malaise
Molds
o refers to an acute URI, whereas terms such as rhinitis,
pharyngitis, and laryngitis distinguish the sites of the
Clinical Manifestations symptoms
 rhinorrhea (excessive nasal drainage, runny nose) o used when the causative virus is influenza (the flu)
 nasal congestion o highly contagious because virus is shed for about 2
days before the symptoms appear and during the
 nasal discharge (purulent with bacterial rhinitis)
first part of the symptomatic phase.
 sneezing
 The most common cold-causing viruses survive better
when humidity is low, in the colder months of the year
 Rhinoviruses = most likely causative organisms  can be caused by a bacterial or viral infection
 cold temperatures and exposure to cold rainy weather do
not increase the incidence or severity of the common cold I. ACUTE RHINOSINUSITIS
 is classified as:
Clinical Manifestations
o acute bacterial rhinosinusitis (ABRS)
 low-grade fever o acute viral rhinosinusitis (AVRS)
 nasal congestion  Recurrent acute rhinosinusitis =
 rhinorrhea characterized by four or more acute
 nasal discharge episodes of ABRS per year
 halitosis
 sneezing Pathophysiology
 tearing watery eyes  usually follows a viral URI or cold, such as an unresolved
 “scratchy” or sore throat viral or bacterial infection, or an exacerbation of allergic
 general malaise rhinitis. Normally, the sinus openings into the nasal
 chills passages are clear and infections resolve promptly.
 headache However, if their drainage is obstructed by a deviated
 muscle aches septum or by hypertrophied turbinates, spurs, or nasal
 As the illness progresses = cough usually appears polyps or tumors, sinus infection may persist as a
 In some people, the virus exacerbates herpes simplex, smoldering (persistent) secondary infection or progress to
commonly called a cold sore an acute suppurative process (causing purulent discharge).
 symptoms of viral rhinitis may last from 1 to 2 weeks
Clinical Manifestations
Medical Management
 purulent nasal drainage (anterior, posterior, or both)
 adequate fluid intake  nasal obstruction
 rest  facial pain, pressure, or a sense of fullness (referred to
 prevention of chilling collectively as facial pain– pressure–fullness)
 use of expectorants as needed  cloudy or colored nasal discharge congestion
o Guaifenesin (Mucinex) = to promote removal of  blockage
secretions  stuffiness
 Warm salt-water gargles = soothe the sore throat,  localized or diffuse headache
 NSAIDs = relieve aches and pains  high fever (i.e., 39°C [102°F] or higher)
 Antihistamines = to relieve sneezing, rhinorrhea, and  the occurrence of symptoms for 10 days or more after
nasal congestion the initial onset of upper respiratory symptoms
 Petroleum jelly = soothe irritated, chapped, and raw skin indicates ABRS
around the nares  symptoms of AVRS are similar to those of ABRS, except
 Antimicrobial agents (antibiotics) should not be used = the patient does not present with a high fever, nor with the
do not affect the virus or reduce the incidence of bacterial same intensity of symptoms, nor with symptoms that persist
complications for as long a period of time.
 Topical nasal decongestants and oxymetazoline nasal o Symptoms occur for fewer than 10 days after the
[Afrin]) should be used with caution. onset of upper respiratory symptoms and do not
 alternative medicines worsen
 inhalation of steam or heated, humidified air = mainstay
of home remedies to treat the common cold; however, the Assessment & Diagnostic Findings
value of this therapy has not been demonstrated.
 tenderness to palpation over the infected sinus area
 transillumination of the affected area = decrease in the
Nursing Management transmission of light with rhinosinusitis
 Implementation of appropriate hand hygiene measures =  Diagnostic imaging is not recommended and generally
most effective measure to prevent transmission of not needed for the diagnosis of acute rhinosinusitis if the
organisms patient meets clinical diagnostic criteria
 educates the patient about how to break the chain of  To confirm the diagnosis of maxillary and frontal
infection with appropriate hand hygiene and the use of rhinosinusitis and identify the pathogen, sinus aspirates
tissues to avoid the spread of the virus with coughing and may be obtained
sneezing, and to cough or sneeze into the upper arm if o Flexible endoscopic culture techniques and
tissues are not readily available swabbing of the sinuses used for this purpose
 instructs the patient about methods to treat symptoms of
the common cold and provides both verbal and written Complications
information to assist in the prevention and management of
URIs.  Osteomyelitis
 mucocele (cyst of the paranasal sinuses).
 Intracranial complications = rare, include:
RHINOSINUSITIS o cavernous sinus thrombosis
 formerly called sinusitis o meningitis
 inflammation of the paranasal sinuses and nasal cavity o brain abscess
 recommends the use of the term rhinosinusitis because o ischemic brain infarction
sinusitis is almost always accompanied by inflammation of o severe orbital cellulitis
the nasal mucosa
 Uncomplicated rhinosinusitis = occurs without extension Medical Management
of inflammation outside of the paranasal sinuses and nasal
 bacterial cases = 5- to 7-day course of antibiotics is
cavity
prescribed
 classified by duration of symptoms:
o oral antibiotics are only prescribed when there is
o acute (less than 4 weeks)
sufficient empiric evidence that the patient has
o subacute (4 to 12 weeks)
ABRS
o chronic (more than 12 weeks)
 o should be given as soon as the diagnosis of ABRS Pathophysiology
is established
o Amoxicillin–clavulanic acid (Augmentin) =  Cause of CRS:
antibiotic of choice o Mechanical obstruction in the ostia of the frontal,
 patients who are allergic to penicillin: maxillary, and anterior ethmoid sinuses (known
o doxycycline (Vibramycin) collectively as the ostiomeatal complex)
o respiratory quinolones o cystic fibrosis
 levofloxacin (Levaquin) o ciliary dyskinesia
 moxifloxacin (Avelox) o neoplastic disorders
 Intranasal saline lavage = adjunct therapy to antibiotics; o gastroesophageal reflux disease
relieve symptoms, reduce inflammation, and help clear the o tobacco use
passages of stagnant mucus. o environmental pollution
 Neither decongestants nor antihistamines are
recommended adjunctive medications for treating Clinical Manifestations
ABRS  impaired mucociliary clearance and ventilation
 AVRS = nasal saline lavage and decongestants  cough
(guaifenesin/pseudoephedrine [Entex PSE])  chronic hoarseness
o Topical decongestants should not be used for
 chronic headaches in the periorbital area
longer than 3 or 4 days.
 periorbital edema
o Oral decongestants must be used cautiously in
 facial pain
patients with hypertension.
 Snoring, sore throat, and, adenoidal hypertrophy may also
o OTC antihistamines are used if an allergic
occur
component is suspected.
 Symptoms most pronounced on awakening in the morning
 Intranasal corticosteroids = only recommended for use in
patients with a previous history of allergic rhinitis  Fatigue
 nasal congestion
 decrease in smell and taste
Nursing Management
 sense of fullness in the ears
 instructs the patient about symptoms of complications that
require immediate follow-up. Assessment & Diagnostic Findings
 Referral to the primary provider is indicated if periorbital
edema and severe pain on palpation occur  crooked-appearing external nose = septal deviation
 instructs the patient about methods to promote drainage of internally
the sinuses, including humidification of the air in the home  Pain on examination of the teeth, with tapping with a
and the use of warm compresses to relieve pressure tongue blade = tooth infection
 patient is advised to avoid swimming, diving, and air travel  Assessment of the posterior oropharynx = purulent or
during the acute infection mucoid discharge, which is indicative of an infection caused
 Patients using tobacco are instructed to immediately stop by CRS
smoking or using any form of tobacco
 if an intranasal corticosteroid is prescribed, it is important to Complications
instruct the patient about the correct use of prescribed  severe orbital cellulitis
nasal sprays through demonstration, explanation, and
 subperiosteal abscess
return demonstration to evaluate the patient’s
 cavernous sinus thrombosis
understanding of the correct method of administration.
 meningitis
 educates the patient about the side effects of prescribed
 encephalitis
and OTC nasal sprays and about rebound congestion
(rhinitis medicamentosa)  ischemic infarction
 tells patients with recurrent rhinosinusitis to begin  intracranial infection either by direct spread through bone or
via venous channels, resulting in:
decongestants, at the first sign of rhinosinusitis.
o epidural abscess
 stresses the importance of following the recommended
o subdural empyema
antibiotic regimen because a consistent blood level of the
o meningitis
medication is critical to treat the infection
o brain abscess
 educates the patient about the early signs of a sinus
 Frontal rhinosinusitis can lead to osteomyelitis of the
infection and recommends preventive measures such as
frontal bones
following healthy practices and avoiding contact with
 Ethmoid rhinosinusitis may result in orbital cellulitis
people with URIs
 explains to the patient that fever, severe headache, and
nuchal rigidity (stiffness of the neck or inability to bend the Medical Management
neck) are signs of potential complications.  encouraging adequate hydration
 Patients with chronic symptoms of rhinosinusitis who do not  use of OTC nasal saline sprays
have marked improvement in 4 weeks with continuous  analgesics such as acetaminophen or NSAIDs
medical treatment may be candidates for functional  decongestants (oxymetazoline and pseudoephedrine)
endoscopic sinus surgery (FESS)
 sleep with the head of the bed elevated
 avoid exposure to cigarette smoke and fumes.
II. CHRONIC RHINOSINUSITIS  cautioned to avoid caffeine and alcohol
 diagnosed when the patient has experienced 12 weeks or  Prescribed antibiotics may include (2-4 weeks, indicated for
longer of two or more of the following symptoms: up to 12 months):
o mucopurulent drainage o amoxicillin-clavulanic acid
o nasal obstruction o erythromycin–sulfisoxazole (Eryzole)
o facial pain–pressure–fullness o second- or third-generation cephalosporins
o hyposmia (decreased sense of smell)  cefuroxime
 RECURRENT ACUTE RHINOSINUSITIS = diagnosed  cefixime
when four or more episodes of ABRS occur per year with o newer fluoroquinolones
no signs or symptoms of rhinosinusitis between the  moxifloxacin (Avelox)
episodes.  Corticosteroid nasal sprays
o fluticasone (Flonase)
 o beclomethasone (Beconase AQ) o scarlatina-form rash with urticaria known as
 addition of a mast cell stabilizer such as cromolyn scarlet fever
 leukotriene inhibitors such as montelukast and zafirlukast  patients who have streptococcal pharyngitis:
o painful sore throat 1 to 5 days after being
Surgical Management exposed to the streptococcus bacteria
o Malaise
 FESS = to correct structural deformities that obstruct the o fever (with or without chills)
ostia (openings) of the sinuses o headache
o minimally invasive surgical procedure that is o myalgia
associated with reduced postoperative discomfort o painful cervical adenopathy
and improvement in the patient’s quality of life o nausea
o specific procedures performed include: o tonsils = swollen and erythematous (may or may
 excising and cauterizing nasal polyps not have an exudate)
 correcting a deviated septum o roof of the mouth = erythematous; demonstrate
 incising and draining the sinuses petechiae
 aerating the sinuses o Bad breath
 removing tumors
Assessment & Diagnostic Findings
Nursing Management
 Rapid antigen detection testing (RADT)
 instructed to blow the nose gently and to use tissue to  Negative results confirmed by a throat culture
remove the nasal drainage
 Increasing fluid intake
Pharmacologic Therapy
 applying local heat (hot wet packs)
 elevating the head of the bed  Bacterial = penicillin (treatment of choice)
 instructs the patient about the importance of following the o Penicillin V potassium = orally for 5 days is the
prescribed medication regimen regimen of choice
 instructs the patient about signs and symptoms that require o Penicillin injections = recommended only if there is
follow-up and provides these instructions verbally and in a concern that the patient will not adhere to
writing therapy
 encourages the patient to follow up with their primary  For patients who are allergic to penicillin or have organisms
provider if symptoms persist that are resistant to erythromycin = cephalosporins and
macrolides (clarithromycin and azithromycin)
o Once-daily azithromycin may be given for only 3
PHARYNGITIS days due to its long half-life
o A 5- or 10-day course of cephalosporin may be
I. ACUTE PHARYNGITIS prescribed
 Severe sore throats = analgesic medications, as prescribed
 sudden painful inflammation of the pharynx, the back o severe cases = gargles with benzocaine
portion of the throat that includes the posterior third of the
tongue, soft palate, and tonsils
Nutritional Therapy
 commonly referred to as a sore throat
 liquid or soft diet = during the acute stage of the disease
Pathophysiology  Cool beverages, warm liquids, and flavored frozen desserts
such as ice pops are often soothing.
 Causes:
 severe situations:
o Viral Infections (most cases)
o intravenous (IV) fluids
 Adenovirus
o encouraged to drink as much fluid as possible (at
 influenza virus
least 2 to 3 L/day)
 Epstein–Barr virus
 herpes simplex virus
o Bacterial infection Nursing Management
 Streptococcal pharyngitis = beta-hemolytic streptococcus  instructs the patient about signs and symptoms that warrant
(GABHS), which is commonly referred to as group A prompt contact with the primary provider.
streptococcus (GAS)  instructs the patient to stay in bed during the febrile stage
 Strep throat = GAS of illness and to rest frequently once up and about. Used
tissues should be disposed of properly to prevent the
Complications spread of infection
 should examine the skin once or twice daily for possible
 Rhinosinusitis
rash
 otitis media
 warm saline gargles or throat irrigations
 peritonsillar abscess
 educates the patient about these procedures and about the
 mastoiditis recommended temperature of the solution, which should be
 cervical adenitis high enough to be effective and as warm as the patient can
tolerate, usually 40.6°C to 43.3°C (105°F to 110°F)
Clinical Manifestations  ice collar = relieve severe sore throats
 fiery-red pharyngeal membrane and tonsils  Mouth care = promote the patient’s comfort and prevent the
 lymphoid follicles that are swollen and flecked with white- development of fissures (cracking) of the lips and oral
purple exudate inflammation when bacterial infection is present
 enlarged and tender cervical lymph nodes  instructs the patient to resume activity gradually and to
delay returning to work or school until after 24 hours of
 no cough
antibiotic therapy
 Fever (higher than 38.3°C [101°F])
 instructs the patient and family about the importance of
 Malaise
taking the full course of therapy and informs them about the
 sore throat
symptoms to watch for that may indicate complications
 patients with GAS pharyngitis:
 instructs the patient about preventive measures that include
o vomiting
not sharing eating utensils, glasses, napkins, food, or
o anorexia
 towels; cleaning telephones after use; using a tissue to o mouth breathing
cough or sneeze; disposing of used tissues appropriately; o earache
coughing or sneezing into the upper arm if tissues are not o draining ears
readily available; and avoiding exposure to tobacco and o frequent head colds
secondhand smoke o bronchitis
 instructs the patient with pharyngitis, especially o foul-smelling breath
streptococcal pharyngitis, to replace their toothbrush with a o voice impairment
new one o noisy respiration
o nasal obstruction
II. CHRONIC PHARYNGITIS
Assessment & Diagnostic Findings
 persistent inflammation of the pharynx. It is common in
adults who work in dusty surroundings, use their voice to  acute pharyngitis = RADT
excess, suffer from chronic cough, or habitually use alcohol  tonsillar site is cultured to determine the presence of
and tobacco bacterial infection
 adenoiditis = comprehensive audiometric assessment
Three Types of Chronic Pharyngitis
characterized by general thickening and Medical Management
Hypertrophic congestion of the pharyngeal mucous
membrane  increased fluid intake
probably a late stage of the first type (the  analgesics
Atrophic membrane is thin, whitish, glistening, and at  salt-water gargles
times wrinkled)  rest
Chronic characterized by numerous swollen lymph  Bacterial infections = penicillin (first-line therapy) or
granular follicles on the pharyngeal wall
cephalosporins
 Tonsillectomy (with or without adenoidectomy) = treatment
Clinical Manifestations of choice for chronic tonsillitis; indicated if:
 constant sense of irritation or fullness in the throat o the patient has had repeated episodes of tonsillitis
 mucus that collects in the throat and can be expelled by despite antibiotic therapy;
coughing o hypertrophy of the tonsils and adenoids that could
 difficulty swallowing cause obstruction and obstructive sleep apnea
(OSA)
o repeated attacks of purulent otitis media; and
Medical Management
suspected hearing loss due to serous otitis media
 avoiding exposure to irritants that has occurred in association with enlarged
 correcting any upper respiratory, pulmonary, tonsils and adenoids.
gastrointestinal, or cardiac condition that might be  Indications for adenoidectomy include:
responsible for a chronic cough o chronic nasal airway obstruction
 Nasal congestion = short-term use of nasal sprays or o chronic rhinorrhea
medications containing ephedrine sulfate or phenylephrine o obstruction of the eustachian tube with related ear
 patient with a history of allergy = antihistamine infections
decongestant medications (orally every 4 to 6 hours) o abnormal speech
o pseudoephedrine o developed a peritonsillar abscess that occludes
o brompheniramine/pseudoephedrine, is prescribed the pharynx, making swallowing difficult and
 Aspirin (for patients older than 20 years) endangering the patency of the airway (particularly
 Acetaminophen during sleep).
 Tonsillectomy
Nursing Management
Nursing Management  Postoperative Care:
 recommends avoidance of alcohol, tobacco, secondhand o Continuous nursing observation
smoke, and exposure to cold or to environmental or o comfortable position is prone, with the patient’s
occupational pollutants head turned to the side
o must not remove the oral airway until the patient’s
 wearing a disposable facemask
gag and swallowing reflexes have returned
 encourages the patient to drink plenty of fluids
o applies an ice collar to the neck, and a basin and
 Gargling with warm saline solution = relieve throat
tissues are provided for the expectoration of blood
discomfort
and mucus.
 Lozenges = keep the throat moistened
o Symptoms of postoperative complications:
 Fever
TONSILLITIS AND ADENOIDITIS  throat pain = analgesic meds.
 Acute tonsillitis = confused with pharyngitis  ear pain
 Chronic tonsillitis = less common and may be mistaken  bleeding = If there is no bleeding, water
for other disorders such as allergy, asthma, and and ice chips may be given to the patient
rhinosinusitis. as soon as desired
o instructed to refrain from too much talking and
 Infection of the adenoids frequently accompanies acute
coughing
tonsillitis
o bacterial pathogens = GABHS  Educating patients about self-care:
o viral pathogen = Epstein–Barr virus o patient and family must understand the signs and
symptoms of hemorrhage
 Bleeding may occur up to 8 days after
Clinical Manifestations surgery
 sore throat o instructs the patient about the use of liquid
 fever acetaminophen with or without codeine for pain
 snoring control and explains that the pain will subside
 difficulty swallowing during the first 3 to 5 days
 Enlarged adenoids may cause:
 o informs the patient about the need to take the full
course of any prescribed antibiotic for the first
postoperative week
o Alkaline mouthwashes and warm saline solutions
o explain to the patient that a sore throat, stiff neck,
minor ear pain, and vomiting may occur in the first
24 hours
o patient should eat an adequate diet with soft foods
o patient should avoid spicy, hot, acidic, or rough
foods
o Milk and milk products (ice cream and yogurt) may
be restricted
o instructs the patient about the need to maintain
good hydration
o advised to avoid vigorous tooth brushing or
gargling
o encourages the use of a cool-mist vaporizer or
humidifier in the home postoperatively.
o patient should avoid smoking and heavy lifting or
exertion for 10 days
PERITONSILLAR ABSCESS / QUINSY
 most common major suppurative complication of sore
throat accounting for roughly 30% of soft tissue head and
neck abscesses
 most commonly afflicts adults between the ages of 20 to 40
years, with the incidence roughly the same between men
and women
 may develop after an acute tonsillar infection that
progresses to a local cellulitis and abscess
 can be life threatening with mediastinitis, intracranial
abscess, and empyema resulting from spread of infection
Clinical Manifestations
 acutely ill with a severe sore throat
 fever
 trismus (inability to open the mouth)
 drooling
 Inflammation of the medial pterygoid muscle that lies lateral
to the tonsil results in spasm, severe pain, and difficulty in
opening the mouth fully
 difficulty swallowing saliva
 breath smells rancid
 raspy voice
 odynophagia (a severe sensation of burning, squeezing
pain while swallowing)
 dysphagia (difficulty swallowing)
 otalgia (pain in the ear)
 tender and enlarged cervical lymph nodes
 oropharynx = erythema of the anterior pillar and soft palate
 purulent tonsil on the side of the peritonsillar abscess
o The tonsil is pushed inferomedially
o uvula is shifted contralaterally
Assessment & Diagnostic Findings
 Intraoral ultrasound and transcutaneous cervical ultrasound
are used in the diagnosis of peritonsillar cellulitis and
abscesses
Medical Management
 Antimicrobial agents
 corticosteroid therapy
 Antibiotics = penicillin
 if the abscess does not resolve:
o needle aspiration
o incision and drainage under local or general
anesthesia
o drainage of the abscess with simultaneous
tonsillectomy
 if the patient with a peritonsillar abscess presents with
acute airway obstruction and requires immediate airway
management:
o intubation
o cricothyroidotomy
o tracheotomy
Surgical Management
 Needle aspiration = performed best with the patient in the
sitting position to make it easier to expectorate the pus and
blood that accumulate in the pharynx
 Incision and drainage = more painful than needle
aspiration
 Tonsillectomy = for patients who are poor candidates for
needle aspiration or incision and drainage
Nursing Management
 assists with the procedure and provides support to the
patient before, during, and after the procedure
 assists with the needle aspiration when indicated
 encourages the patient to use prescribed topical anesthetic
agents and assists with throat irrigations or the frequent
use of mouthwashes or gargles, using saline or alkaline
solutions at a temperature of 40.6°C to 43.3°C (105°F to
110°F)
 Gentle gargling after the procedure with a cool normal
saline gargle may relieve discomfort
o patient must be upright and clearly expectorate
forward
o instructs the patient to gargle gently at intervals of
1 or 2 hours for 24 to 36 hours
 Liquids that are cool or at room temperature are usually
well tolerated
 Adequate fluids must be provided
 observes the patient for complications and instructs the
patient about signs and symptoms of complications that
require prompt attention by the patient’s primary provider
 At discharge, provides verbal and written instructions
regarding foods to avoid, when to return to work, and the
need to refrain from or cease smoking. The need for
continuation of good oral hygiene is also reinforced.
LARYNGITIS
 an inflammation of the larynx, often occurs as a result of
voice abuse or exposure to dust, chemicals, smoke, and
other pollutants or as part of a URI
 may be caused by isolated infection involving only the vocal
cords
 associated with gastroesophageal reflux (referred to as
reflux laryngitis)
 most common cause is a virus (viral laryngitis), and
laryngitis is often associated with allergic rhinitis or
pharyngitis
Clinical Manifestations
 Acute Laryngitis:
o hoarseness or aphonia (loss of voice)
o severe cough
o sudden onset made worse by cold dry wind
o throat feels worse in the morning and improves
when the patient is indoors in a warmer climate
o dry cough
o dry, sore throat that worsens in the evening hours
o uvula visibly edematous
o “tickle” in the throat that is made worse by cold air
or cold liquids
 Chronic laryngitis:
o persistent hoarseness
Medical Management
 Acute laryngitis:
o resting the voice
o avoiding irritants (including smoking)
o resting
o inhaling cool steam or an aerosol
 If the laryngitis is part of a more extensive respiratory
infection caused by a bacterial organism or if it is severe =
antibacterial therapy
 chronic laryngitis:
o resting the voice
o eliminating any primary respiratory tract infection
o eliminating smoking
o avoiding secondhand smoke
o Corticosteroids (beclomethasone)
 reflux laryngitis = proton pump inhibitors = omeprazole
(Prilosec) given once daily
Nursing Management
 instructs the patient to rest the voice and to maintain a well
humidified environment
 If laryngeal secretions are present during acute episodes =
expectorant agents with a daily fluid intake of 2 to 3 L to
thin secretions
 instructs the patient about the importance of taking
prescribed medications, including proton pump inhibitors,
and using continuous positive airway therapy at bedtime, if
prescribed for OSA.
 In cases involving infection = informs the patient that the
symptoms of laryngitis often extend a week to 10 days after
completion of antibiotic therapy
 instructs the patient about signs and symptoms that require
contacting the primary provider
o loss of voice with sore throat that makes
swallowing saliva difficult
o hemoptysis
o noisy respirations.
 Continued hoarseness after voice rest or laryngitis that
persists for longer than 5 days must be reported.
OBSTRUCTION AND TRAUMA OF THE UPPER
RESPIRATORY AIRWAY:
OBSTRUCTIVE SLEEP APNEA (OSA)
 disorder characterized by recurrent episodes of upper
airway obstruction and a reduction in ventilation
 defined as cessation of breathing (apnea) during sleep
usually caused by repetitive upper airway obstruction
 Risk factors for OSA include:
o Obesity = major risk factor
o male gender
o postmenopausal status
o advanced age
o alterations in the upper airway
Pathophysiology
 Mechanical factors such as reduced diameter of the upper
airway or dynamic changes in the upper airway during
sleep may result in obstruction. These sleep-related
changes may predispose to upper airway collapse when
small amounts of negative pressure are generated during
inspiration. Repetitive apneic events result in hypoxia
(decreased oxygen saturation) and hypercapnia (increased
concentration of carbon dioxide), which triggers a
sympathetic response.
Clinical Manifestations
 frequent and loud snoring with breathing cessation for 10
seconds or longer, for at least five episodes per hour,
followed by awakening abruptly with a loud snort as the
blood oxygen level drops
 Patients with sleep apnea may have anywhere from five
apneic episodes per hour to several hundred per night
 Classic signs and symptoms of OSA include the “3S’s”:
o Snoring
o Sleepiness
o significant-other report of sleep apnea episodes
 Pathologic hypersomnolence = sleeping during normal
activities such as eating or talking
Assessment & Diagnostic Findings
 diagnosis of sleep apnea is based on clinical features plus
a polysomnographic finding (which is the definitive test
for OSA)
o an overnight study, performed in a specialized
sleep disorders center, which continuously
measures multiple physiologic signals while the
patient sleeps
 Characteristic findings consistent with OSA include:
o apneic episodes occurring in the presence of
respiratory muscle effort
o clinically significant apneic episodes lasting 10
seconds or longer
o apneic episodes most prevalent during the rapid
eye movement (REM) stage of sleep
Medical Management
 First steps:
o Weight loss
o avoidance of alcohol
o positional therapy (using devices that prevent
patients from sleeping on their backs)
o oral appliances such as mandibular advancement
devices (MADs) are the first steps (American
Sleep
 severe cases involving hypoxemia and severe
hypercapnia:
o Continuous positive airway pressure (CPAP) =
prevent airway collapse
o bilevel positive airway pressure (BiPAP) therapy =
makes breathing easier and results in a lower
average airway pressure
o supplemental oxygen via nasal cannula
Surgical Management
 Simple tonsillectomy = for patients with larger tonsils
when deemed clinically necessary, or when other options
have failed or are refused by patients
 Uvulopalatopharyngoplasty = resection of pharyngeal
soft tissue and removal of approximately 15 mm of the free
edge of the soft palate and uvula.
 Nasal septoplasty = for gross anatomic nasal septal
deformities
 Maxillomandibular surgery = to advance the maxilla and
mandible forward in order to enlarge the posterior
pharyngeal region
 Tracheostomy relieves upper airway obstruction but has
numerous adverse effects, including speech difficulties and
increased risk of infections
Pharmacologic Therapy
 Modafinil (Provigil) = to reduce daytime sleepiness
 Protriptyline (Triptil) = given at bedtime may increase the
respiratory drive and improve upper airway muscle tone
 Medroxyprogesterone acetate (Provera) and
acetazolamide (Diamox) = for sleep apnea associated
with chronic alveolar hypoventilation
 low-flow nasal oxygen at night = help relieve hypoxemia
in some patients but has little effect on the frequency or
severity of apnea.
Nursing Management
 explains the disorder in terms that are understandable to
the patient and relates symptoms (daytime sleepiness) to
the underlying disorder
 instructs the patient and family about treatments, including
the correct and safe use of CPAP, BiPAP, MAD, and
oxygen therapy, if prescribed
 educates the patient about the risk of untreated OSA and
the benefits of treatment approaches
EPISTAXIS (NOSEBLEED)
 hemorrhage from the nose, is caused by the rupture of tiny,
distended vessels in the mucous membrane of any area of
the nose
 Most common site = anterior septum, where three major
blood vessels enter the nasal cavity:
o anterior ethmoidal artery on the forward part of the
roof (Kiesselbach plexus),
o sphenopalatine artery in the posterosuperior
region
o internal maxillary branches (the plexus of veins
located at the back of the lateral wall under the
inferior turbinate)
Medical Management
 nasal speculum, penlight, or headlight = to identify the site
of bleeding in the nasal cavity
 Initial treatment = applying direct pressure
o patient sits upright with the head tilted forward to
prevent swallowing and aspiration of blood and is
directed to pinch the soft outer portion of the nose
against the midline septum for 5 or 10 minutes
continuously.
 Application of nasal decongestants (phenylephrine, one or
two sprays) = act as vasoconstrictors
 If these measures are unsuccessful in stopping the
bleeding, the nose must be examined using good
illumination and suction to determine the site of bleeding
o cauterized with silver nitrate
o electrocautery (high-frequency electrical current)
o supplemental patch of Surgicel or Gelfoam may
be used
 cotton tampon = to try to stop the bleeding
 Suction = to remove excess blood and clots from the field
of inspection
 search for the bleeding site should shift from the
anteroinferior quadrant to the anterosuperior, then to the
posterosuperior, and finally to the posteroinferior area
 If the origin of the bleeding cannot be identified, the nose
may be packed with gauze impregnated with petrolatum
jelly or antibiotic ointment; a topical anesthetic spray and
decongestant agent may be used before the gauze packing
is inserted, or a balloon-inflated catheter may be used
 compressed nasal sponge may be used
o Once the sponge becomes saturated with blood or
is moistened with a small amount of saline, it will
expand and produce tamponade to halt the
bleeding. The packing may remain in place for 3 to
4 days if necessary, to control bleeding
 Antibiotics = for risk of iatrogenic rhinosinusitis and sepsis
Nursing Management
 monitors the patient’s vital signs, assists in the control of
bleeding, and provides tissues and an emesis basin to
allow the patient to expectorate any excess blood.
 Assuring the patient in a calm, efficient manner that
bleeding can be controlled can help reduce anxiety.
 continuously assesses the patient’s airway and breathing
as well as vital signs.
 Once the bleeding is controlled = instructs the patient to
avoid vigorous exercise for several days and to avoid hot or
spicy foods and tobacco, because this may cause
vasodilation and increase the risk of rebleeding
 Discharge education includes reviewing ways to prevent
epistaxis: avoiding forceful nose blowing, straining, high
altitudes, and nasal trauma (including nose picking)
 Adequate humidification may prevent drying of the nasal
passages
 explains how to apply direct pressure to the nose with the
thumb and the index finger for 15 minutes in the case of a
recurrent nosebleed
NASAL OBSTRUCTION
 Persistent nasal obstruction also may lead to chronic
infection of the nose and result in frequent episodes of
nasopharyngitis. Frequently, the infection extends to the
nasal sinuses. When rhinosinusitis develops and the
drainage from these cavities is obstructed by deformity or
swelling within the nose, pain is experienced in the region
of the affected sinus.
Medical Management
 removal of the obstruction
 nasal corticosteroids (1-3 months)
 oral leukotriene inhibitors (montelukast)
 short course of oral corticosteroids (6-day course of
prednisone) = obstruction due to polyps
 antibiotics = for underlying infection
 antihistamines = for allergies
 astringent agent = for hypertrophied turbinates
 surgical reduction (functional rhinoplasty) = for turbinate
hypertrophy
Nursing Management
 explains the procedure to the patient.
 Postoperatively, elevates the head of the bed to promote
drainage and to alleviate discomfort from edema
 Frequent oral hygiene is encouraged
 Before discharge, instructed to avoid blowing the nose with
force during the postoperative recovery period
 instructed about the signs and symptoms of bleeding and
infection and when to contact the primary provider
 provided with written postoperative instructions, including
emergency phone numbers
FRACTURES OF THE NOSE
 most common facial fracture and the most common fracture
in the body
 result from a direct assault
 may affect the ascending process of the maxilla and the
septum. The torn mucous membrane results in a nosebleed
 Complications include:
o Hematoma
o Infection
o Abscess
o avascular or septic necrosis
Clinical Manifestations
 pain
 bleeding from the nose externally and internally into the
pharynx
 swelling of the soft tissues adjacent to the nose
 periorbital ecchymosis
 nasal obstruction
 deformity
 nose may have an asymmetric appearance that may not be
obvious until the edema subsides
Assessment & Diagnostic Findings
 An x-ray may reveal displacement of the fractured bones
and may help rule out extension of the fracture into the
skull
Medical Management
 bleeding is controlled with the use of packing
 Cold compresses = to prevent or reduce edema
 ensure a patent airway and to rule out a cervical spine
fracture
 Uncomplicated nasal fractures may be treated initially with
antibiotics, analgesic agents, and a decongestant nasal
spray
 septorhinoplasty = performed when the nasal septum
needs to be repaired
Nursing Management
 applies ice o positron emission tomography (PET) scan
 encourages the patient to keep the head elevated
 instructs the patient to apply ice packs to the nose to Medical Management
decrease swelling
 surgery
 Mouth rinses = to moisten the mucous membranes and to
o Early stage tumors (Stages I-II) = conservation
reduce the odor and taste of dried blood in the oropharynx
surgery
and nasopharynx
o Stages III-IV = total laryngectomies with or without
 analgesic agents such as acetaminophen or NSAIDs
postoperative radiation therapy or radiation
 inspects the mucosa for lacerations or a septal hematoma
therapy with concurrent adjuvant chemotherapy
 instructs the patient to avoid sports activities for 6 weeks
 radiation therapy
o Early stage tumors (Stages I-II) = external beam
LARYNGEAL OBSTRUCTION radiation therapy
 Causes:  adjuvant chemoradiation therapy
o History of allergies  speech therapy
o Foreign body o The three most common techniques of alaryngeal
o Heavy alcohol consumption and heavy tobacco communication:
use  esophageal speech = patient needs the
o Family history of airway problems ability to compress air into the esophagus
o Use of ACE inhibitors and expel it, setting off a vibration of the
o Recent throat pain or recent fever pharyngeal esophageal segment for
o History of surgery or previous tracheostomy esophageal speech.
 artificial larynx (electric larynx) =
batterypowered apparatus projects sound
Clinical Manifestations
into the oral cavity
 lowered oxygen saturation  tracheoesophageal puncture = valve is
 use of accessory muscles to maximize airflow may occur placed in the tracheal stoma to divert air
and is often manifested by retractions in the neck or into the esophagus and out the mouth.
abdomen during inspirations Once the puncture is surgically created
and has healed, a voice prosthesis
Medical Management (BlomSinger) is fitted over the puncture
site
 If all efforts are unsuccessful = immediate tracheotomy
 If the obstruction is caused by edema resulting from an
Surgical Management
allergic reaction = immediate administration of
subcutaneous epinephrine and a corticosteroid  Vocal Cord Stripping
 Ice = to reduce edema o used to treat dysplasia, hyperkeratosis, and
 Continuous pulse oximetry leukoplakia and is often curative for these lesions
o involves removal of the mucosa of the edge of the
vocal cord, using an operating microscope
CANCER OF THE LARYNX
 Cordectomy
 Risk factors: o excision of the vocal cord, is usually performed via
o Carcinogens transoral laser
o Nutritional deficiencies (vitamins) o procedure is used for lesions limited to the middle
o History of alcohol abuse third of the vocal cord
o Genetic predisposition  Laser Surgery
o Age (higher incidence after 65 years of age) o Laser microsurgery = early glottic cancers
o Gender (more common in men) o Microelectrodes = for surgical resection of smaller
o Race (more prevalent in African Americans and laryngeal carcinomas
Caucasians) o CO2 laser = laryngeal tumors (except large
o Weakened immune system vascular tumors)
 Partial Laryngectomy (Laryngofissure–Thyrotomy)
Clinical Manifestations o used for patients in the early stages of cancer in
the glottic area when only one vocal cord is
 Hoarseness of more than 2 weeks’ duration = cancer in the
involved.
glottic area
o portion of the larynx is removed, along with one
o voice may sound harsh, raspy, and lower in pitch
vocal cord and the tumor; all other structures
 persistent cough or sore throat and pain and burning in the
remain. The airway remains intact, and the patient
throat
is expected to have no difficulty swallowing. The
 lump may be felt in the neck
voice quality may change, or the patient may
 Later symptoms include: sound hoarse.
o Dysphagia  Total Laryngectomy
o dyspnea (difficulty breathing) o Complete removal of the larynx
o unilateral nasal obstruction or discharge
o results in permanent loss of the voice and a
o persistent hoarseness change in the airway, requiring a permanent
o persistent ulceration tracheostomy
o foul breath
o Cervical lymph adenopathy, unintentional weight
loss, a general debilitated state, and pain radiating
to the ear may occur with metastasis

Assessment & Diagnostic Findings

CORONARY VASCULAR DISORDERS AND
 Diagnostic procedures that may be used include: HYPERTENSION (GOMEZ)
o fine-needle aspiration (FNA) biopsy
o a barium swallow
o endoscopy CORONARY ARTERY DISEASE (CAD)
o CT or MRI scan
 Refers to any narrowing or obstruction of arterial lumina  Emotion
that interferes with cardiac perfusion.  Environment
 Results to decrease oxygenation leading to angina pectoris,  Eating a heavy meal
MI, heart failure and even death.
 Causes: Nursing Diagnosis
o Fatty deposits (atherosclerosis)
o Clot (thrombus/embolus)  Altered Tissue Perfusion
 Altered Comfort: Pain
Total HDL LDF
Triglyceride
Cholester Cholester Cholester Medical Management
s
ol ol ol
Ideal is 60  Promote rest
or higher Less than  Oxygen therapy
Less than
Men = 40 100 Less than
200 but the  Medications:
Good or higher Below 70 if 149
lower the o Coronary vasodilator
Women = CAD is Ideal = <100
better
50 or present o Nitrates
higher  nitroglycerine (Nitrostat)
Borderline  isosorbide dinitrate (Isordil) (Imdur)
to
200-239 n/a 130-159 150-199 o Calcium channel blockers (CCB)
moderatel
y elevated  Amlodipine (Amlor) (Norvasc)
160 or
200 or higher
 Felodipine (Plendil)
higher  Verapamil (Calan) (Isoptin)
240 or 60 or 500
High 190
higher higher considered  Deltiazim (Dilzem)
considered
very high
very high
Less than KEY POINTS IN GIVING NITROGLYCERINE:
Low n/a n/a n/a
40  Give sublingual (SL)
 Fizzling or burning sensation
Medical Management (CAD)  Loses potency after 3-6 months
 Dark colored container
 Exercise Program – 30 mins, increase regularly
 Dosing: maximum of 3 doses with 5 min. interval
 Pharmacologic Management:
o Anticholesterol agent – to decrease cholesterol
CLINICAL MANIFESTATIONS OF CAD:
level
o Fibrates – lopid (Gemifibrazil) MYOCARDIAL INFARCTION
o Statins – atorvastatin (Lipitor), simvastatin (Zocor)  Is prolonged ischemia more than 30 minutes long
 Surgical Management:
o Percutaneous Transluminal Coronary Angioplasty
Clinical Manifestations
(PTCA)
o Coronary Artery Bypass Graft (CABG)  Chest pain
*saphenous vein  Indigestion
*Internal mammary/thoracic artery  Nausea and vomiting
 Fever
Clinical Manifestations  Lab result changes
o Leukocytosis – increased WBCs
 Angina pectoris (AP)
o Increased ESR
 Myocardial infarction
o Cardiac enzymes:
 Increased CPK-MB
CLINICAL MANIFESTATIONS OF CAD:
 Increased Troponin I and Troponin T
ANGINA PECTORIS o ECG changes:
 chest pain brought about by myocardial ischemia  Pathologic Q wave – widened QRS
o Stable Angina – pain is predictable in frequency  ST elevations
and duration  T inversions
- trigger with activity/ exercise
- relieve with rest and nitrate Nursing Diagnosis
o Unstable Angina – increased pain that’s easily  Altered tissue perfusions
induced
 Altered comfort: pain
- occurs even at rest
o Prinzmetal’s or variant – pain that results from
unpredictable coronary spasm Medical Management (MONAF)
- results from SNS effect  Morphine – narcotic analgesic
- triggers with stress  Oxygen Therapy
o microvascular – angina- like chest pain in a  Rest
patient with normal coronary arteries that results  Nitrates – coronary vasodilator
from impaired vasodilator effect.
 Aspirin (NSAIDS) – dose: 81-82mg (low dose or baby
aspirin) act as platelet aggregator
Characteristics of AP (SAVERS) o *it is contraindicated in patient with PUD
 Substernal o *may use: clopidogrel (Plavix); ticlopine (Ticlid)
 Anterior Chest Wall (ACW)  Fibrinolytic Agent or Thrombolytic Agent – is the cause of
 Vague in nature – radiation of pain (Levine sign) MI is clot; should be started within 30 minutes after MI
o U- ukinase
 Exercise-related
o S- streptokinase
 Relieved by rest and/or NTG
o A – alteplase
 Short duration
 Adverse Effect of FA/TA: massive
bleeding
Factors of AP (4Es)  Antidote: aminocaproic acid (Amicor)
 Exercise  Continuous cardiac monitoring
 Health Teaching about sexual activity  K-sparring Diuretic
 S- spironolactone
 A – amiloride
COMPLICATIONS OF CAD:  T – triamterene
CONGESTIVE HEART FAILURE (CHF) o Beta Blockers:
 Selective Beta1 blocker agent
 leads to accumulation of blood in the heart chambers due
 metoprolol (Betaloc)
to decrease force of cardiac contractility
 Atenolol (Tenormin)
 Nonselective Beta Blocker agent
Definition Signs and Symptoms
 Propranolol (Inderal)
failure of the left chambers  dyspnea  Carvidelol (Carvid)
of the heart to pump out  SOB o Calcium Channel Blocker (CCBs)
I. LEFT HF

blood to the circulatory  difficulty in breathing at  amlodipine (Norvasc)

system causing the blood supine position  Nefidipine (Calcibloc)
to go back to the  nocturnal dyspnea
pulmonary system and  Verapamil
 pulmonary edema  Delthiazem
produce pulmonary (crackles)
symptoms o Alpha1 blocker
failure of the right  hepatomegaly  minipress
II. RIGHT HF

chambers of the heart to  splenomegaly o A2 agonist

pump blood the pulmonary  dependent edema  catapress
system causing backflow  neck vein or jugular o Renin inhibitor
of the heart to the systemic vein distention  Aliskiren (Tektuma)
circulation.  increased CVP o ACE inhibitor
 Captopril (Capoten)
Medical Management  Enalapril (Vasotec)
 Quinapril (Acupril)
 Cardiac Glycosides/Digitalis o Angiotensin-II Receptor Blocker
o Digoxin (Lanoxin)  Irbesartan (Approvel)
 (+) inotrophic effect – increased force of  Losartan (Cozaar)
cardiac contractility  Telmisartan (Micardis)
 (-) chonotrophic effect – decreased HR  Valsartan (Diovan)
 Diuretic Agent
o K-Sparring diuretic – stabilize K level
 S – spironolactone STRUCTURAL, INFECTIOUS, &
 A – amiloride INFLAMMATORY CARDIAC DISORDERS
 T – triamterene (GOMEZ)
 Monitor I&O
 Weigh patient regularly
VALVULAR HEART DISEASE
 Anti-Hypertensive Agent
occurs when the heart valves cannot open fully (stenosis) or
KEY POINTS IN DIGOXIN TREATMENT: close completely (insufficiency or regurgitation). – prevents
 Check HR for 1 full minute efficient blood flow through the heart.
o HR <60 bpm for adult-hol
o HR <70 bpm children-hold TYPES:
o HR <90 bpm in infants-hold 1. Mitral stenosis – tissue thickens and narrows the valve
 Therapeutic level: 0.5-2.0 ng/mL opening, preventing blood from flowing from the left atrium to
o >2.0 ng/mL can lead to Digoxin toxicity the left ventricle.
o Signs and symptoms of Digoxin Toxicity:
 N – nausea 2. Mitral insufficiency, regurgitation – valve is incompetent,
 A – anorexia preventing complete valve closure during systole
 V – vomiting
 D – diarrhea 3. Mitral valve prolapse – valve leaflets protrude into the left
 V – visual changes atrium during systole.

4.Aortic stenosis – valvular tissue thickens and narrows the

HYPERTENSION
valve opening, preventing blood from flowing from the left
 A sustained increased of blood pressure >140/90 mmHg ventricle into the aorta
 Types of Hypertension:
o Primary HTN/Idiopathic/Essential 5. Aortic insufficiency – valve is incompetent, preventing
 unknown cause complete valve closure during diastole.
 most common, 90%
o Secondary HTN 6. Tricuspid Valve Stenosis & Insufficiency
 etiologic factor 7. Pulmonary Valve Stenosis & Insufficiency
 Pheochromocytoma
 DM Clinical Manifestations
 Renal Failure
 Cushing’s Disease
 Syndrome of Inappropriate Anti-diuretic
Hormone

Medical Management

 Lifestyle Modification
o Diet therapy
o exercise program
 Continuous Lifestyle Modification + Medications
o Diuretic Agent:

Valve Repair Procedures
1. Balloon Valvuloplasty
a. a balloon catheter is passed from the femoral vein
through the atrial septum to the mitral valve or through
the femoral artery to the aortic valve.
b. The balloon is inflated to enlarge the orifice
c. institute precautions for arterial puncture if
appropriate
d. Monitor for bleeding from the catheter insertion site
e. Monitor for signs of systemic emboli
f. Monitor for signs of a regurgitant valve by monitoring
cardiac rhythm, heart sounds, and cardiac output.
2. Mitral annuloplasty – tightening and suturing the
malfunctioning valve annulus to eliminate or greatly reduce
regurgitation
3. Commissurotomy, valvotomy
a. the procedure is accomplished with cardiopulmonary
bypass during open heart surgery
b. The valve is visualized, thrombi are removed from
the atria, fused leaflets are incised, and calcium is
debrided from the leaflets, thus widening the orifice.
Valve Replacement Procedures
1. Mechanical prosthetic valves
2. Bioprosthetic valves
CARDIOMYOPATHY
is a subacute or chronic disorder of the heart muscle;
Treatment is palliative, not curative, and the client needs to deal
with numerous lifestyle changes and a shortened life span.
Types, S&S, and Treatment
INFLAMMATORY DIEASES OF THE HEART
Pericarditis – an acute or chronic inflammation of the
pericardium
- Often occurs after a respiratory infection,
neoplasm, bacteria and fungi infection, high-dose
radiation to chest, uremia
- Pericardial sac becomes inflamed
- Result in loss of pericardial elasticity or an
accumulation of fluid within the sac.
- Heart failure or cardiac tamponade may result
Chronic pericarditis – a chronic inflammatory thickening of the
pericardium, constricts the heart, causing compression
Myocarditis – acute or chronic inflammation of the myocardium
as a result of pericarditis, systemic infection, or allergic
response.
- Common cause are viral and bacterial infections,
hypersensitivity reactions(RHF), radiation, chronic
alcoholism
Endocarditis – is an inflammation of the inner lining of the
heart and valves.
- Occurs primarily in clients who are IV drug
abusers, have had valve replacements or repair of
valves with prosthetic materials, or have other
structural cardiac defects.
- Ports of entry for the infecting organism include:
*oral cavity (if the client has had a dental
procedure in the previous 3 to 6 months)
*infections (cutaneous, genitourinary, GI, and
systemic)
*surgery or invasive procedures, including IV line
placement
CHEST AND LOWER RESPIRATORY TRACT
DISORDERS (ENECIO)
ATELECTASIS
 refers to closure or collapse of alveoli and often is
described in relation to x-ray findings and/or clinical signs
and symptoms.
 may be acute or chronic
o micro atelectasis (which is not detectable on
chest x-ray)
o macro atelectasis with loss of segmental, lobar,
or overall lung volume.
Pathophysiology
 ADULTS: result of reduced ventilation (nonobstructive
atelectasis) or any blockage that obstructs passage of air to
and from the alveoli (obstructive atelectasis), thus reducing
alveolar ventilation.
 Obstructive atelectasis; most common type; results from
reabsorption of gas (trapped alveolar air is absorbed into
the bloodstream); no additional air can enter into the alveoli
because of the blockage. As a result, the affected portion of
the lung becomes airless and the alveoli collapse.
 Causes of atelectasis include:
o foreign body
o tumor or growth in an airway
o altered breathing patterns
o retained secretions
o pain
o alterations in small airway function
o prolonged supine positioning
o increased abdominal pressure
o reduced lung volumes due to musculoskeletal or
neurologic disorders
o restrictive defects
o specific surgical procedures.
  lung volume expansion maneuvers (e.g., deep-breathing
exercises, incentive spirometry),
 and coughing, also serve as the first-line measures to
minimize or treat atelectasis by improving ventilation.
 In patients who do not respond to first-line measures or
who cannot perform deep-breathing exercises, other
treatments such as positive end-expiratory pressure (PEEP;
a simple mask and one-way valve system that provides
varying amounts of expiratory resistance, usually 10 to 15
cm H2O),
 continuous positive pressure breathing (CPPB), or
 bronchoscopy may be used.

RESPIRATORY INFECTION:
ACUTE TRACHEOBRONCHITIS
 acute inflammation of the mucous membranes of the
trachea and the bronchial tree, often follows infection of the
Clinical Manifestations upper respiratory tract.
 Patients with viral infections have decreased resistance
 Increasing dyspnea and can readily develop a secondary bacterial infection.
 Cough  Adequate treatment of upper respiratory tract infection is
 Sputum production one of the major factors in the prevention of acute
bronchitis.
ACUTE ATELECTASIS:  A subcategory of tracheobronchitis is ventilator-associated
 tachycardia, tachypnea, pleural pain, and central cyanosis tracheobronchitis, which is a common illness in chronically
(a bluish skin hue that is a late sign of hypoxemia) may be ventilated patients. If managed appropriately, ventilator-
anticipated. associated pneumonia (VAP) may be prevented
 Patients characteristically have difficulty breathing in the
supine position and are anxious.
Pathophysiology

CHRONIC ATELECTASIS:  the inflamed mucosa of the bronchi produces mucopurulent

 Same with acute atelectasis
 predisposes patients to infection distal to the obstruction
 signs and symptoms of a pulmonary infection also may be
present.
Assessment & Diagnostic Findings
 Increased work of breathing and hypoxemia.
 Decreased breath sounds and crackles are heard over the
affected area.
 chest x-ray may suggest a diagnosis of atelectasis before
clinical symptoms appear, the x-ray may reveal patchy
infiltrates or consolidated areas.
 Depending on the degree of hypoxemia, pulse oximetry
(SPO2 ) may demonstrate a low saturation of hemoglobin
with oxygen (less than 90%) or a lower-than-normal partial
pressure of arterial oxygen (PaO2).
Hallmarks of the Severity of the Atelectasis:
 Tachypnea
 Dyspnea
 Mild to moderate hypoxemia
Prevention
 Change patient’s position frequently, especially from supine
to upright position, to promote ventilation and prevent
secretions from accumulating.
 Encourage early mobilization from bed to chair followed by
early ambulation.
 Encourage appropriate deep breathing and coughing to
mobilize secretions and prevent them from accumulating.
 Educate/reinforce appropriate technique for incentive
spirometry.
 Administer prescribed opioids and sedatives judiciously to
prevent respiratory depression.
 Perform postural drainage and chest percussion, if
indicated.
 Institute suctioning to remove tracheobronchial secretions,
if indicated.
Management
 frequent turning,
 early ambulation,
sputum, often in response to infection by Streptococcus
pneumoniae, Haemophilus influenzae, or Mycoplasma
pneumoniae.
 In addition, a fungal infection (e.g., Aspergillus) may also
cause tracheobronchitis.
 inhalation of physical and chemical irritants, gases, or other
air contaminants can also cause acute bronchial irritation.
Clinical Manifestations
 the patient has a dry, irritating cough and expectorates a
scanty amount of mucoid sputum
 may report sternal soreness from coughing and have fever
or chills, night sweats, headache, and general malaise.
 As the infection progresses, the patient may be short of
breath, have noisy inspiration and expiration (inspiratory
stridor and expiratory wheeze), and produce purulent (pus-
filled) sputum
 In severe tracheobronchitis, blood-streaked secretions may
be expectorated as a result of the irritation of the mucosa of
the airways.
Nursing Management
 A primary nursing function is to encourage bronchial
hygiene, such as increased fluid intake and directed
coughing to remove secretions
 The nurse encourages and assists the patient to sit up
frequently to cough effectively and to prevent retention of
mucopurulent sputum
 Fatigue is a consequence of tracheobronchitis; therefore,
the nurse cautions the patient against overexertion, which
can induce a relapse or exacerbation of the infection.
 The patient is advised to rest.
RESPIRATORY INFECTION:
PNEUMONIA
 an inflammation of the lung parenchyma caused by various
microorganisms, including bacteria, mycobacteria, fungi,
and viruses.
 Pneumonitis is a more general term that describes an
inflammatory process in the lung tissue that may
predispose or place the patient at risk for microbial invasion.
Classifications:
 Pneumonia occurring in the community
Community-
or ≤48 hours of hospital admission in
Acquired
patients who do not meet the criteria for
Pneumonia
health care–associated pneumonia
(CAP)
(HCAP).
 Pneumonia occurring in a non-
hospitalized patient with extensive health
care contact with one or more of the
following:
 Hospitalization for ≥2 days in an acute
care facility within 90 days of infection
 Residence in a nursing home or long-
Health Care–
term care facility
Associated
 Antibiotic therapy, chemotherapy, or
Pneumonia
wound care within 30 days of current
(HCAP)
infection
 Hemodialysis treatment at a hospital or
clinic
 Home infusion therapy or home wound
care
 Family member with infection due to
multidrug-resistant bacteria
Hospital-  Pneumonia occurring ≥48 hours after
Acquired hospital admission that did not appear to
Pneumonia be incubating at the time of admission
(HAP)
Ventilator-  A type of HAP that develops ≥48 hours
Associated after endotracheal tube intubation
Pneumonia
(VAP)
I. ASPIRATION PNEUMONIA
 refers to the pulmonary consequences resulting from entry
of endogenous or exogenous substances into the lower
airway.
 The most common form of aspiration pneumonia is bacterial
infection from aspiration of bacteria that normally reside in
the upper airways.
 Aspiration pneumonia may occur in the community or
hospital setting.
 Common pathogens are anaerobes, S. aureus,
Streptococcus species, and gram-negative bacilli
 Substances other than bacteria may be aspirated into the
lung, such as gastric contents, exogenous chemical
contents, or irritating gases
o This type of aspiration or ingestion may impair the
lung defenses, cause inflammatory changes, and
lead to bacterial growth and a resulting pneumonia.
Pathophysiology
 Normally, the upper airway prevents potentially infectious
particles from reaching the sterile lower respiratory tract
 Pneumonia arises from normal flora present in patients
whose resistance has been altered or from aspiration of
flora present in the oropharynx; patients often have an
acute or chronic underlying disease that impairs host
defenses
 Pneumonia may also result from bloodborne organisms
that enter the pulmonary circulation and are trapped in the
pulmonary capillary bed
 Pneumonia affects both ventilation and diffusion
 An inflammatory reaction can occur in the alveoli,
producing an exudate that interferes with the diffusion of
oxygen and carbon dioxide.
 White blood cells, mostly neutrophils, also migrate into the
alveoli and fill the normally air-filled spaces
 Areas of the lung are not adequately ventilated because of
secretions and mucosal edema that cause partial occlusion
of the bronchi or alveoli, with a resultant decrease in
alveolar oxygen tension
 Bronchospasm may also occur in patients with reactive
airway disease. Because of hypoventilation, a ventilation-
perfusion (v/q ) mismatch occurs in the affected area of the
lung
 Venous blood entering the pulmonary circulation passes
through the under ventilated area and travels to the left side
of the heart poorly oxygenated
 The mixing of oxygenated and unoxygenated or poorly
oxygenated blood eventually results in arterial hypoxemia
 If a substantial portion of one or more lobes is involved, the
disease is referred to as lobar pneumonia
 The term bronchopneumonia is used to describe
pneumonia that is distributed in a patchy fashion, having
originated in one or more localized areas within the bronchi
and extending to the adjacent surrounding lung
parenchyma
 Bronchopneumonia is more common than lobar pneumonia
II. BRONCHIAL PNEUMONIA
 Patchy areas of consolidation occur
III. LOBAR PNEUMONIA
 Entire lobe is consolidated
Clinical Manifestations
 sudden onset of chills, rapidly rising fever (38.5° to 40.5°C
[101° to 105°F]), and pleuritic chest pain that is aggravated
by deep breathing and coughing
 The patient is severely ill, with marked tachypnea (25 to 45
breaths/min), accompanied by other signs of respiratory
distress (e.g., shortness of breath, the use of accessory
muscles in respiration)
 A relative bradycardia (a pulse–temperature de cit in which
the pulse is slower than that expected for a given
temperature) may suggest viral infection, mycoplasma
infection, or infection with a Legionella organism
 Some patients exhibit an upper respiratory tract infection
(nasal congestion, sore throat), and the onset of symptoms
of pneumonia is gradual and nonspecific. The predominant
symptoms may be headache, low-grade fever, pleuritic pain,
myalgia, rash, and pharyngitis
 After a few days, mucoid or mucopurulent sputum is
expectorated. In severe pneumonia, the cheeks are flushed
and the lips and nail beds demonstrate central cyanosis (a
late sign of poor oxygenation [hypoxemia])
 The patient may exhibit orthopnea (shortness of breath
when reclining or in the supine position), preferring to be
propped up or sitting in bed leaning forward (orthopneic
position) in an e ort to achieve adequate gas exchange
without coughing or breathing deeply
Assessment & Diagnostic Findings
 The diagnosis of pneumonia is made by history (particularly
of a recent respiratory tract infection), physical examination,
chest x-ray, blood culture (bloodstream invasion
[bacteremia] occurs frequently), and sputum examination
 The sputum sample is obtained by having patients do the
following: (1) rinse the mouth with water to minimize
contamination by normal oral ora, (2) breathe deeply
several times, (3) cough deeply, and (4) expectorate the
raised sputum into a sterile container.
 Complications
 Severe complications of pneumonia include hypotension
and septic shock and respiratory failure (especially with
gram-negative bacterial disease in older adult patients)
 These complications are encountered chiefly in patients
who have received no specific treatment or inadequate or
delayed treatment.
 These complications are also encountered when the
infecting organism is resistant to therapy, when a comorbid
disease complicates the pneumonia, or when the patient is
immunocompromised.
Nursing Interventions
 Improving Airway Patency - Removing secretions is
important because retained secretions interfere with gas
exchange and may slow recovery. The nurse encourages
hydration (2 to 3 L/day), because adequate hydration thins
and loosens pulmonary secretions
 Promoting Rest and Conserving Energy - The nurse
encourages the debilitated patient to rest and avoid
overexertion and possible exacerbation of symptoms. The
patient should assume a comfortable position to promote
rest and breathing (e.g., semi-Fowler’s position) and should
change positions frequently to enhance secretion clearance
and pulmonary ventilation and perfusion.
 Promoting Fluid Intake - The respiratory rate of patients
with pneumonia increases because of the increased
workload imposed by labored breathing and fever. An
increased respiratory rate leads to an increase in insensible
fluid loss during exhalation and can lead to dehydration.
Therefore, unless contraindicated, increased fluid intake (at
least 2 L/day) is encouraged
 Maintaining Nutrition - Many patients with shortness of
breath and fatigue have a decreased appetite and consume
only fluids. Fluids with electrolytes (commercially available
drinks, such as Gatorade) may help provide fluid, calories,
and electrolytes. Small, frequent meals may be advisable
 Promoting Patients’ Knowledge - The patient and family are
instructed about the cause of pneumonia, management of
symptoms, signs and symptoms that should be reported to
the primary provider or nurse, and the need for follow-up
ASPIRATION
 is inhalation of foreign material (e.g., oropharyngeal or
stomach contents) into the lungs
 It is a serious complication that can cause pneumonia and
result in the following clinical picture: tachycardia, dyspnea,
central cyanosis hypertension, hypotension, and potentially
death
Risk Factors:
 Seizure activity
 Brain injury
 Decreased level of consciousness from trauma, drug or
alcohol intoxication, excessive sedation, or general
anesthesia
 Flat body positioning
 Stroke
 Swallowing disorders
 Cardiac arrest
SEVERE ACUTE RESPIRATORY SYNDROME (SARS)
 is a viral respiratory illness caused by a coronavirus, called
SARS-associated coronavirus
 It was first reported in Asia in 2003 and quickly spread to
countries in North America, South America, Europe, and
Asia.
 SARS develops in people who either have close contact
with a person who has been diagnosed with the disease or
a history of travel or residence in an area with known cases.
 The SARS-associated coronavirus is transmitted via
respiratory droplets when an infected person coughs or
sneezes; the droplets may be deposited on the mucous
membranes (mouth, nose, eyes) of a nearby person.
 The virus may also be spread when a person touches a
surface or object contaminated by the droplets and then
touches his or her mucous membranes
Signs and Symptoms
 fever (greater than 38°C [100.4°F]), coughing, and difficulty
breathing.
 Additional symptoms include headache, overall feeling of
discomfort, body aches, and diarrhea.
 Most patients develop pneumonia
 atypical symptoms, elevated serum lactate dehydrogenase
on admission, and acute renal failure
 The incubation period is usually 2 to 7 days
PULMONARY TUBERCULOSIS
 is an infectious disease that primarily affects the lung
parenchyma. It also may be transmitted to other parts of
the body, including the meninges, kidneys, bones, and
lymph nodes
 The primary infectious agent, M. tuberculosis, is an acid-
fast aerobic rod that grows slowly and is sensitive to heat
and ultraviolet light
 TB is a worldwide public health problem that is closely
associated with poverty, malnutrition, overcrowding,
substandard housing, and inadequate health care.
Transmission and Risk Factors:
 TB spreads from person to person by airborne transmission
 An infected person releases droplet nuclei (usually particles
1 to 5 mcm in diameter) through talking, coughing,
sneezing, laughing, or singing
 Close contact with someone who has active TB. Inhalation
of airborne nuclei from an infected person is proportional to
the amount of time spent in the same air space, the
proximity of the person, and the degree of ventilation.
 Immunocompromised status (e.g., those with HIV infection,
cancer, transplanted organs, and prolonged high-dose
corticosteroid therapy)
 Substance abuse (IV/injection drug users and alcoholics)
 Any person without adequate health care (the homeless;
impoverished; minorities, particularly children <15 years
and young adults between ages 15 and 44 years)
 Preexisting medical conditions or special treatment (e.g.,
diabetes, chronic renal failure, malnourishment, selected
malignancies, hemodialysis, transplanted organ,
gastrectomy, jejunoileal bypass)
 Immigration from countries with a high prevalence of TB
(southeastern Asia, Africa, Latin America, Caribbean)
 Institutionalization (e.g., long-term care facilities, psychiatric
institutions, prisons) Living in overcrowded, substandard
housing Being a health care worker performing high-risk
activities: administration of aerosolized pentamidine and
other medications, sputum induction procedures,
bronchoscopy, suctioning, coughing procedures, caring for
the immunosuppressed patient, home care with the high-
risk population, and administering anesthesia and related
procedures (e.g., intubation, suctioning)
Pathophysiology
 begins when a susceptible person inhales mycobacterium
and becomes infected.
 The bacteria are transmitted through the airways to the
alveoli, where they are deposited and begin to multiply.
 The bacilli also are transported via the lymph system and
bloodstream to other parts of the body (kidneys, bones,
cerebral cortex) and other areas of the lungs (upper lobes)
 The body’s immune system responds by initiating an
inflammatory reaction.
 Phagocytes (neutrophils and macrophages) engulf many of
the bacteria, and TB-specific lymphocytes lyse (destroy)
the bacilli and normal tissue
 This tissue reaction results in the accumulation of exudate  Combination medications, such as INH and rifampin
in the alveoli, causing bronchopneumonia. The initial (Rifamate) or INH, pyrazinamide, and rifampin (Rifater) and
infection usually occurs 2 to 10 weeks after exposure. medications given twice a week (e.g., rifapentine [Priftin])
 Granulomas, new tissue masses of live and dead bacilli, are available to help improve patient adherence
are surrounded by macrophages, which form a protective
wall. Nursing Management
 They are then transformed to a fibrous tissue mass, the
central portion of which is called a Ghon tubercle  Promoting Airway Clearance - Copious secretions obstruct
the airways in many patients with TB and interfere with
 The material (bacteria and macrophages) becomes
adequate gas exchange. Increasing the fluid intake
necrotic, forming a cheesy mass.
promotes systemic hydration and serves as an effective
 This mass may become calcified and form a collagenous
expectorant.
scar
 Promoting Adherence to Treatment Regimen - The
 At this point, the bacteria become dormant, and there is no
multiple-medication regimen that the patient must follow
further progression of active disease
can be quite complex. Understanding of the medications,
 After initial exposure and infection, active disease may
schedule, and side effects is important.
develop because of a compromised or inadequate immune
 Promoting Activity and Adequate Nutrition - Patients with
system response. Active disease also may occur with
TB are often debilitated from prolonged chronic illness and
reinfection and activation of dormant bacteria.
impaired nutritional status. The patient’s willingness to eat
 In this case, the Ghon tubercle ulcerates, releasing the
may be altered by fatigue from excessive coughing; sputum
cheesy material into the bronchi
production; chest pain; generalized debilitated state; or cost,
 The bacteria then become airborne, resulting in further
if the patient has few resources.
spread of the disease.
 Preventing Transmission of Tuberculosis Infection - the
 Then, the ulcerated tubercle heals and forms scar tissue.
nurse carefully instructs the patient about important
This causes the infected lung to become more inflamed,
hygiene measures, including mouth care, covering the
resulting in further development of bronchopneumonia and
mouth and nose when coughing and sneezing, proper
tubercle formation.
disposal of tissues, and hand hygiene.

Clinical Manifestations
LUNG ABSCESS
 Low-grade fever, cough, night sweats, fatigue, and weight
 is necrosis of the pulmonary parenchyma caused by
loss.
microbial infection
 cough may be nonproductive, or mucopurulent sputum may
 It is generally caused by aspiration of anaerobic bacteria.
be expectorated
By definition, in a lung abscess, the chest x-ray
 Hemoptysis also may occur. Both the systemic and the demonstrates a cavity of at least 2 cm.
pulmonary symptoms are chronic and may have been
 Patients who are at risk for aspiration of foreign material
present for weeks to months.
and development of a lung abscess include those with
 If the patient is infected with TB, the chest x-ray usually impaired cough re exes who cannot close the glottis and
reveals lesions in the upper lobes those with swallowing difficulties.

Diagnostic Findings
Pathophysiology
 Tuberculin Skin Test –  Most lung abscesses are a complication of bacterial
o The Mantoux method is used to determine pneumonia or are caused by aspiration of oral anaerobes
whether a person has been infected with the TB into the lung.
bacillus and is used widely in screening for latent
 Abscesses also may occur secondary to mechanical or
M. tuberculosis infection.
functional obstruction of the bronchi by a tumor, foreign
o A reaction of 0 to 4 mm is considered not
body, or bronchial stenosis, or from necrotizing
significant.
pneumonias, TB, pulmonary embolism (PE), or chest
o A reaction of 5 mm or greater may be significant in
trauma.
people who are considered to be at risk.
 Most lung abscesses are found in areas of the lung that
 QuantiFERON-TB Gold Test –
may be affected by aspiration. The site of the lung abscess
o The QuantiFERON-TB Gold (QFT-G) test is an
is related to gravity and is determined by position
enzyme-linked immunosorbent assay (ELISA) that
 For patients who are confined to bed, the posterior
detects the release of interferon-gamma by white
segment of an upper lobe and the superior segment of the
blood cells when the blood of a patient with TB is
lower lobe are the most common areas.
incubated with peptides similar to those in M.
 If the pleura is involved, an empyema result. A
tuberculosis.
communication or connection between the bronchus and
o The results of the QFT-G test are available in less
pleura is known as a bronchopleural fistula.
than 24 hours and are not affected by prior
 The organisms frequently associated with lung abscesses
vaccination with BCG.
are S. aureus, Klebsiella, and other gram-negative species
 Sputum Culture
o The presence of AFB on a sputum smear may
indicate disease but does not confirm the Assessment & Diagnostic Findings
diagnosis of TB because some AFB are not M.  Physical examination of the chest may reveal dullness on
tuberculosis. percussion and decreased or absent breath sounds with an
o A culture is done to confirm the diagnosis. intermittent pleural friction rub (grating or creaking sound)
on auscultation.
Medical Management  Crackles may be present. Confirmation of the diagnosis is
made by chest x-ray, sputum culture, and, in some cases,
 Pulmonary TB is treated primarily with anti-TB agents for 6
fiber optic bronchoscopy
to 12 months
 The chest x-ray reveals an infiltrate with an air–fluid level. A
 four first-line medications:
computed tomography (CT) scan of the chest may be
o INH
required to provide more detailed images of different cross-
o rifampin (Rifadin)
sectional areas of the lung.
o pyrazinamide (PZA)
o ethambutol (Myambutol)
Prevention
 Appropriate antibiotic therapy before any dental procedures
in patients who must have teeth extracted while their gums
and teeth are infected
 Adequate dental and oral hygiene, because anaerobic
bacteria play a role in the pathogenesis of lung abscess
 Appropriate antimicrobial therapy for patients with
pneumonia
Nursing Management
 The nurse administers antibiotics and IV treatments as
prescribed and monitors for adverse effects.
 Chest physiotherapy is initiated as prescribed to facilitate
drainage of the abscess.
 The nurse educates the patient to perform deep-breathing
and coughing exercises to help expand the lungs.
 To ensure proper nutritional intake, the nurse encourages a
diet that is high in protein and calories.
PLEURISY
 refers to inflammation of both layers of the pleurae (parietal
and visceral).
 Pleurisy may develop in conjunction with pneumonia or an
upper respiratory tract infection, TB, or collagen disease;
after trauma to the chest, pulmonary infarction, or PE; in
patients with primary or metastatic cancer; and after
thoracotomy.
 The parietal pleura has nerve endings, and the visceral
pleura does not.
 When the inflamed pleural membranes rub together during
respiration (intensified on inspiration), the result is severe,
sharp, knifelike pain
Clinical Manifestations
 The key characteristic of pleuritic pain is its relationship to
respiratory movement
 Taking a deep breath, coughing, or sneezing worsens the
pain
 Pleuritic pain is limited in distribution rather than di use; it
usually occurs only on one side
 The pain may become minimal or absent when the breath
is held. It may be localized or radiate to the shoulder or
abdomen. Later, as pleural fluid develops, the pain
decreases.
Assessment & Diagnostic Findings
 In the early period, when little fluid has accumulated, a
pleural friction rub can be heard with the stethoscope, only
to disappear later as more fluid accumulates and separates
the inflamed pleural surfaces
 Diagnostic tests may include chest x-rays, sputum analysis,
thoracentesis to obtain a specimen of pleural fluid for
examination, and, less commonly, a pleural biopsy.
Nursing Management
 Because the patient has pain on inspiration, the nurse
offers suggestions to enhance comfort, such as turning
frequently onto the affected side to splint the chest wall and
reduce the stretching of the pleurae.
 The nurse also educates the patient to use the hands or a
pillow to splint the rib cage while coughing.
PLEURAL EFFUSION
 a collection of fluid in the pleural space, is rarely a primary
disease process; it is usually secondary to other diseases.
 Normally, the pleural space contains a small amount of fluid
(5 to 15 mL), which acts as a lubricant that allows the
pleural surfaces to move without friction
 Pleural effusion may be a complication of heart failure, TB,
pneumonia, pulmonary infections (particularly viral
infections), nephrotic syndrome, connective tissue disease,
PE and neoplastic tumors.
 The most common malignancy associated with a pleural
effusion is bronchogenic carcinoma.
Pathophysiology
 In certain disorders, fluid may accumulate in the pleural
space to a point at which it becomes clinically evident, this
almost always has pathologic significance.
 The effusion can be a relatively clear fluid, or it can be
bloody or purulent.
 An effusion of clear fluid may be a transudate or an
exudate. A transudate (filtrate of plasma that moves across
intact capillary walls) occurs when factors influencing the
formation and reabsorption of pleural fluid are altered,
usually by imbalances in hydrostatic or oncotic pressures.
 The finding of a transudative effusion generally implies that
the pleural membranes are not diseased.
 A transudative effusion most commonly results from heart
failure
 An exudate (extravasation of fluid into tissues or a cavity)
usually results from inflammation by bacterial products or
tumors involving the pleural surfaces.
Clinical Manifestations
 the clinical manifestations are caused by the underlying
disease
 Pneumonia causes fever, chills, and pleuritic chest pain,
whereas a malignant effusion may result in dyspnea,
difficulty lying flat, and coughing.
 The severity of symptoms is determined by the size of the
effusion, the speed of its formation, and the underlying lung
disease. A large pleural effusion causes dyspnea.
Assessment & Diagnostic Findings
 Assessment of the area of the pleural effusion reveals
decreased or absent breath sounds; decreased fremitus;
and a dull, flat sound on percussion.
 In the case of an extremely large pleural effusion, the
assessment reveals a patient in acute respiratory distress.
Tracheal deviation away from the affected side may also be
apparent.
 Physical examination, chest x-ray, chest CT, and
thoracentesis confirm the presence of fluid. In some
instances, a lateral decubitus x-ray is obtained.
Medical Management
 The objectives of treatment are to discover the underlying
cause of the pleural effusion; to prevent re-accumulation of
fluid; and to relieve discomfort, dyspnea, and respiratory
compromise.
 Specific treatment is directed at the underlying cause (e.g.,
heart failure, pneumonia, cirrhosis).
 If the pleural fluid is an exudate, more extensive diagnostic
procedures are performed to determine the cause.
 Thoracentesis is performed to remove fluid, to obtain a
specimen for analysis, and to relieve dyspnea and
respiratory compromise
Nursing Management
 The nurse’s role in the care of patients with a pleural
effusion includes supporting the medical regimen.
 The nurse prepares and positions the patient for
thoracentesis and offers support throughout the procedure.
 The nurse is responsible for making sure the thoracentesis
fluid amount is recorded and sent for appropriate laboratory
testing.
 If a chest tube drainage and water-seal system is used, the
nurse is responsible for monitoring the system’s function
and recording the amount of drainage at prescribed
intervals.
 If a chest tube is inserted for talc instillation, pain
management is a priority and the nurse helps the patient
assume positions that are the least painful
 However, frequent turning and movement are important to
facilitate adequate spreading of the talc over the pleural
surface.
 The nurse evaluates the patient’s pain level and
administers analgesic agents as prescribed and as needed.
EMPYEMA
 is an accumulation of thick, purulent fluid within the pleural
space,
 often with fibrin development and a loculated (walled-off)
area where infection is located.
Pathophysiology
 Most empyema occurs as complications of bacterial
pneumonia or lung abscess.
 They also result from penetrating chest trauma,
hematogenous infection of the pleural space, nonbacterial
infections, and iatrogenic causes (after thoracic surgery or
thoracentesis).
 At first the pleural fluid is thin, with a low leukocyte count,
but it frequently progresses to a micro purulent stage and,
finally, to a stage where it encloses the lung within a thick
exudative membrane (loculated empyema).
Clinical Manifestations
 The patient is acutely ill and has signs and symptoms
similar to those of an acute respiratory infection or
pneumonia (fever, night sweats, pleural pain, cough,
dyspnea, anorexia, weight loss).
 If the patient is immunocompromised, the symptoms may
be vague. If the patient has received antimicrobial therapy,
the clinical manifestations may be less obvious.
Assessment & Diagnostic Findings
 Chest auscultation demonstrates decreased or absent
breath sounds over the affected area, and there is dullness
on chest percussion as well as decreased fremitus.
 The diagnosis is established by chest CT. Usually, a
diagnostic thoracentesis is performed, often under
ultrasound guidance.
Medical Management
 The objectives of treatment are to drain the pleural cavity
and to achieve complete expansion of the lung.
 The fluid is drained, and appropriate antibiotics (usually
begun by the IV route) in large doses are prescribed based
on the causative organism
 Sterilization of the empyema cavity requires 4 to 6 weeks of
antibiotics. Drainage of the pleural fluid depends on the
stage of the disease and is accomplished by one of the
following methods:
 Needle aspiration (thoracentesis) with a thin percutaneous
catheter, if the volume is small and the fluid is not too
purulent or too thick
 Tube thoracostomy (chest drainage using a large-diameter
intercostal tube attached to water-seal drainage with
fibrinolytic agents instilled through the chest tube in patients
with loculated or complicated pleural effusions
 Open chest drainage via thoracotomy, including potential
rib resection, to remove the thickened pleura, pus, and
debris and to remove the underlying diseased pulmonary
tissue
Nursing Management
 Resolution of empyema is a prolonged process. The nurse
helps the patient cope with the condition and instructs the
patient in lung-expanding breathing exercises to restore
normal respiratory function.
 The nurse also provides care specific to the method of
drainage of the pleural fluid (e.g., needle aspiration, closed
chest drainage, rib resection and drainage)
 When the patient is discharged home with a drainage tube
or system in place, the nurse instructs the patient and
family on care of the drainage system and drain site,
measurement and observation of drainage, signs and
symptoms of infection, and how and when to contact the
primary provider
PULMONARY EDEMA (NONCARDIOGENIC)
 is defined as abnormal accumulation of fluid in the lung
tissue, the alveolar space, or both.
 It is a severe, life-threatening condition.
 Pulmonary edema can be classified as cardiogenic or non-
cardiogenic.
 Non cardiogenic pulmonary edema occurs due to damage
of the pulmonary capillary lining.
 It may be due to direct injury to the lung (e.g., chest trauma,
aspiration, smoke inhalation), hematogenous injury to the
lung (e.g., sepsis, pancreatitis, multiple transfusions,
cardiopulmonary bypass), or injury plus elevated
hydrostatic pressures.
 Management of noncardiogenic pulmonary edema mirrors
that of cardiogenic pulmonary edema, however, hypoxemia
may persist despite high concentrations of supplemental
oxygen, due to the intrapulmonary shunting of blood.
ACUTE RESPIRATORY FAILURE
 Respiratory failure is a sudden and life-threatening
deterioration of the gas exchange function of the lung and
indicates failure of the lungs to provide adequate
oxygenation or ventilation for the blood
 is defined as a decrease in arterial oxygen tension (PaO2)
to less than 50 mm Hg (hypoxemia) and an increase in
arterial carbon dioxide tension (PaCO2) to greater than 50
mm Hg (hypercapnia), with an arterial pH of less than 7.35.
 It is important to distinguish between acute and chronic
respiratory failure. Chronic respiratory failure is defined as
deterioration in the gas exchange function of the lung that
has developed insidiously or has persisted for a long period
after an episode of acute respiratory failure.
 The absence of acute symptoms and the presence of a
chronic respiratory acidosis suggest the chronicity of the
respiratory failure.
 Two causes of chronic respiratory failure are COPD and
neuromuscular diseases. Patients with these disorders
develop a tolerance to the gradually worsening hypoxemia
and hypercapnia.
Pathophysiology
 In acute respiratory failure, the ventilation or perfusion
mechanisms in the lung are impaired.
 Ventilatory failure mechanisms leading to acute respiratory
failure include impaired function of the central nervous
system (i.e., drug overdose, head trauma, infection,
hemorrhage, sleep apnea)
 neuromuscular dysfunction (i.e., myasthenia gravis,
Guillain-Barré syndrome, amyotrophic lateral sclerosis,
spinal cord trauma)
 musculoskeletal dysfunction (i.e., chest trauma,
kyphoscoliosis, malnutrition)
 pulmonary dysfunction (i.e., COPD, asthma, cystic fibrosis)
 Oxygenation failure mechanisms leading to acute
respiratory failure include pneumonia, acute respiratory
distress syndrome, heart failure, COPD, PE, and restrictive
lung diseases (diseases that cause decrease in lung
volumes)
 In the postoperative period, acute respiratory failure may be
caused by the effects of anesthetic, analgesic, and sedative
agents, which may depress respiration or enhance the
effects of opioids and lead to hypoventilation.
 Pain may interfere with deep breathing and coughing.
 Clinical Manifestations
 Early signs are those associated with impaired oxygenation
and may include restlessness, fatigue, headache, dyspnea,
air hunger, tachycardia, and increased blood pressure.
 As the hypoxemia progresses, more obvious signs may be
present, including confusion, lethargy, tachycardia,
tachypnea, central cyanosis, diaphoresis, and finally
respiratory arrest.
 Physical findings are those of acute respiratory distress,
including the use of accessory muscles, decreased breath
sounds if the patient cannot adequately ventilate, and other
findings related specifically to the underlying disease
process and cause of acute respiratory failure.
 In the early phase of acute respiratory failure, vague signs
and symptoms such as restlessness, fatigue, and
headache make it di cult to determine what the patient is
experiencing. However, as oxygenation becomes more
impaired, hypoxemia increases and leads to more obvious
signs.
Nursing Management
 Nursing management of patients with acute respiratory
failure includes assisting with intubation and maintaining
mechanical ventilation.
 The nurse assesses the patient’s respiratory status by
monitoring the level of responsiveness, arterial blood gases,
pulse oximetry, and vital signs.
 In addition, the nurse assesses the entire respiratory
system and implements strategies (e.g., turning schedule,
mouth care, skin care, range of motion of extremities) to
prevent complications.
ACUTE RESPIRATORY DISTRESS SYNDROME
 can be thought of as a spectrum of disease, from its milder
form (acute lung injury) to its most severe form of fulminate,
life-threatening.
 This clinical syndrome is characterized by a severe
inflammatory process causing diffuse alveolar damage that
results in sudden and progressive pulmonary edema,
increasing bilateral infiltrates on chest x-ray, hypoxemia
unresponsive to oxygen supplementation regardless of the
amount of PEEP, and the absence of an elevated left atrial
pressure.
 A wide range of factors are associated with the
development of ARDS including direct injury to the lungs
(e.g., smoke inhalation) or indirect insult to the lungs (e.g.,
shock).
Etiologic Factors Related to Acute Respiratory Distress
Syndrome:
 Aspiration (gastric secretions, drowning, hydrocarbons)
 Drug ingestion and overdose
 Hematologic disorders (disseminated intravascular
coagulopathy, massive transfusions, cardiopulmonary
bypass)
 Prolonged inhalation of high concentrations of oxygen,
smoke, or corrosive substances
 Localized infection (bacterial, fungal, viral pneumonia)
 Metabolic disorders (pancreatitis, uremia)
 Shock (any cause)
 Trauma (pulmonary contusion, multiple fractures, head
injury)
 Major surgery
 Fat or air embolism
 Sepsis
Clinical Manifestations
 ARDS closely resembles severe pulmonary edema
 The acute phase of ARDS is marked by a rapid onset of
severe dyspnea that usually occurs less than 72 hours after
the precipitating event
 Arterial hypoxemia that does not respond to supplemental
oxygen is characteristic. Findings on chest x-ray are similar
to those seen with cardiogenic pulmonary edema and are
visible as bilateral infiltrates that quickly worsen.
 The acute lung injury then progresses to fibrosing alveolitis
with persistent, severe hypoxemia.
 The patient also has increased alveolar dead space
(ventilation to alveoli but poor perfusion) and decreased
pulmonary compliance (“stiff lungs,” which are difficult to
ventilate)
Assessment & Diagnostic Findings
 On physical examination, intercostal retractions and
crackles may be present as the fluid begins to leak into the
alveolar interstitial space.
 Common diagnostic tests performed in patients with
potential ARDS include plasma brain natriuretic peptide
(BNP) levels, echocardiography, and pulmonary artery
catheterization.
 The BNP level is helpful in distinguishing ARDS from
cardiogenic pulmonary edema.
Nursing Management
 Most of the respiratory modalities are oxygen
administration, nebulizer therapy, chest physiotherapy,
endotracheal intubation or tracheostomy, mechanical
ventilation, suctioning, bronchoscopy.
 Frequent assessment of the patient’s status is necessary to
evaluate the effectiveness of treatment.
 In addition to supporting the medical plan of care, the nurse
considers other needs of the patient. Positioning is
important
 The nurse turns the patient frequently to improve ventilation
and perfusion in the lungs and enhance secretion drainage.
 Oxygenation in patients with ARDS is sometimes improved
in the prone position.
PULMONARY HYPERTENSION
 characterized by elevated pulmonary arterial pressure and
secondary right heart ventricular failure
 may be suspected in a patient with dyspnea with exertion
without other clinical manifestations
 Unlike systemic blood pressure, the pulmonary pressures  Right heart catheterization is necessary to confirm the
cannot be measured indirectly. In the absence of these diagnosis of pulmonary hypertension and to accurately
measurements, clinical recognition becomes the only assess the hemodynamic abnormalities
indicator of PH. However, PH is a condition that is often not  pulmonary hypertension is confirmed with a mean
clinically evident until late in its progression. pulmonary artery pressure greater than 25 mm Hg
 If left heart disease is identified via echocardiography and
Clinical Classification of Pulmonary Hypertension correlates with the degree of estimated PH, then exercise
 Sporadic idiopathic PAH testing and both a right and left heart catheterization may
 Heritable idiopathic PAH be done to determine the functional severity of the disease
 Drug and toxin-induced PAH and the abnormalities in pressures (left heart filling,
Group 1: Pulmonary
Arterial Hypertension  PAH due to diseases such as pulmonary vascular resistance, transpulmonary gradient)
(PAH) connective tissues disorders,  Pulmonary function studies may be normal or show a slight
HIV infection, portal decrease in vital capacity and lung compliance, with a mild
hypertension, congenital heart decrease in the diffusing capacity
disease
 The PaO2 also is decreased (hypoxemia)
Group 2: Pulmonary  Systolic dysfunction
 The ECG reveals right ventricular hypertrophy, right axis
Hypertension (PH) due  Diastolic dysfunction
to left heart disease deviation, and tall peaked P waves in inferior leads; tall
 Valvular heart disease
anterior R waves; and ST-segment depression, T-wave
 Chronic obstructive pulmonary
inversion, or both anteriorly.
Group 3: Pulmonary disease
Hypertension (PH) due  Interstitial lung disease  An echocardiogram can assess the progression of the
to lung diseases or  Mixed restrictive and obstructive disease and rule out other conditions with similar signs and
hypoxemia lung disease symptoms.
 Sleep disordered breathing  A ventilation–perfusion scan or pulmonary angiography
Group 4: Chronic  Due to thromboembolic detects defects in pulmonary vasculature.
thromboembolic occlusion of the proximal or
pulmonary distal pulmonary vasculature Clinical Manifestations
hypertension (CTEPH)
Group 5: Pulmonary  Hematologic disorders  occurs at first with exertion and eventually at rest
Hypertension (PH) with  Systemic disorders (e.g.,  Substernal chest pain also is common
unclear multifactorial sarcoidosis)  Other signs and symptoms include weakness, fatigue,
mechanisms  Metabolic disorders syncope, occasional hemoptysis, and signs of right-sided
heart failure (peripheral edema, ascites, distended neck
Risk Factors: veins, liver engorgement, crackles, heart murmur)
 Conditions such as collagen vascular disease, congenital  Anorexia and abdominal pain in the right upper quadrant
heart disease, anorexigens (specific appetite depressants), may also occur
chronic use of stimulants, portal hypertension, and HIV
infection increase the risk of PH in susceptible patients Medical Management

 All patients with pulmonary hypertension should be

Pathophysiology
 Vascular injury occurs with endothelial dysfunction and
vascular smooth muscle dysfunction, which leads to
disease progression (vascular smooth muscle hypertrophy,
adventitial and intimal proliferation [thickening of the wall],
and advanced vascular lesion formation).
 Normally, the pulmonary vascular bed can handle the blood
volume delivered by the right ventricle.
 It has a low resistance to blood flow and compensates for
increased blood volume by dilation of the vessels in the
pulmonary circulation.
 However, if the pulmonary vascular bed is destroyed or
obstructed, as in PH, the ability to handle whatever flow or
volume of blood it receives is impaired, and the increased
blood flow then increases the pulmonary artery pressure.
 As the pulmonary arterial pressure increases, the
pulmonary vascular resistance also increases
 Both pulmonary artery constriction (as in hypoxemia or
hypercapnia) and a reduction of the pulmonary vascular
bed (which occurs with PE) result in increased pulmonary
vascular resistance and pressure.
 This increased workload affects right ventricular function
 The myocardium ultimately cannot meet the increasing
demands imposed on it, leading to right ventricular
hypertrophy (enlargement and dilation) and failure. Passive
hepatic congestion may also develop.
Assessment & Diagnostic Findings
 Initial diagnostic evaluation includes a history, physical
examination, chest x-ray, pulmonary function studies,
electrocardiogram (ECG), and echocardiogram.
 Echocardiography can be used to estimate the pulmonary
artery systolic pressure and to assess right ventricular size,
thickness, and function.
 It can also evaluate the right atrial size, left ventricular
system, and diastolic function as well as valve function
considered for the following therapies: diuretics, oxygen,
anticoagulation, digoxin, and exercise training.
 Diuretics and oxygen should be added as needed.
 Appropriate oxygen therapy reverses the vasoconstriction
and reduces the PH in a relatively short time. Most patients
with PH do not have hypoxemia at rest but require
supplemental oxygen with exercise.
 Anticoagulation should be considered for patients at risk for
intrapulmonary thrombosis.
 Digoxin may improve right ventricular ejection fraction in
some patients and may help to control heart rate; however,
patients must be monitored closely for potential
complications.
Pharmacologic Therapy
 calcium channel blockers, prostanoids, endothelin
antagonists, and phosphodiesterase-5 inhibitors. The
choice of therapeutic agents is based on many facets,
including the classification group status and the patient’s
tolerance of the agents.
 In addition, a vasoreactivity test may be done to identify
which medication is best suited for the patient with PH; this
is done during cardiac catheterization using vasodilating
medications such as nitric oxide.
 A positive vasoreactivity test occurs when there is a
decrease of at least 10 mm Hg in the pulmonary artery
pressure with an overall pressure that is less than 40 mm
Hg in the presence of both an increased or unchanged
cardiac output and a minimally decreased or unchanged
systemic blood pressure.
 Patients with a positive vasoreactivity test may be
prescribed calcium channel blockers.
 However, because calcium channel blockers are indicated
in only a small percentage of patients, other treatment
options, including prostanoids, are often necessary.
 Prostanoids mimic the effect of the prostaglandin
prostacyclin. Prostacyclin relaxes vascular smooth muscle
 by stimulating the production of cyclic 3′,5′-adenosine
monophosphate (AMP) and inhibits the growth of smooth
muscle cells.
 Prostanoids used to treat PH include epoprostenol (Flolan),
treprostinil (Remodulin), and iloprost (Ventavis)
Surgical Management
 Lung transplantation remains an option for a select group of
patients with PH who are refractory to medical therapy.
 Bilateral lung or heart–lung transplantation is the procedure
of choice.
 Atrial septostomy may be considered for selected patients
with severe disease; this procedure results in shunting of
blood from the right side of the heart to the left, decreasing
the strain on the right side of the heart and maintaining left
ventricular output.
Nursing Management
 The major nursing goal is to identify patients at high risk
such as those with COPD, PE, congenital heart disease,
and mitral valve disease so that early treatment can
commence
 The nurse must be alert for signs and symptoms,
administer oxygen therapy appropriately, and instruct the
patient and family about the use of home oxygen therapy.
 In patients treated with prostanoids (e.g., epoprostenol or
treprostinil), education about the need for central venous
access (epoprostenol), subcutaneous infusion (treprostinil),
proper administration and dosing of the medication, pain at
the injection site, and potential severe side effects is
extremely important.
PULMONARY HEART DISEASE (COR PULMONALE)
 is a condition that results from pulmonary hypertension,
which causes the right side of the heart to enlarge because
of the increased work required to pump blood against high
resistance through the pulmonary vascular system.
 This causes right-sided heart failure
PULMONARY EMBOLISM
 refers to the obstruction of the pulmonary artery or one of
its branches by a thrombus (or thrombi) that originates
somewhere in the venous system or in the right side of the
heart
 Deep vein thrombosis (DVT), a related condition, refers to
thrombus formation in the deep veins, usually in the calf or
thigh, but sometimes in the arm, especially in patients with
peripherally inserted central catheters.
 Venous thromboembolism is a term that includes both DVT
and PE
 PE is a common disorder and often is associated with
trauma, surgery (orthopedic, major abdominal, pelvic,
gynecologic), pregnancy, heart failure, age older than 50
years, hypercoagulable states, and prolonged immobility
 The area, although continuing to be ventilated, receives
little or no blood flow. Therefore, gas exchange is impaired
or absent in this area.
 In addition, various substances are released from the clot
and surrounding area that cause regional blood vessels
and bronchioles to constrict. This results in an increase in
pulmonary vascular resistance—a reaction that compounds
the ventilation–perfusion imbalance
Pathophysiology
 Most commonly, PE is due to a blood clot or thrombus.
However, there are other types of emboli: air, fat, amniotic
fluid, and septic (from bacterial invasion of the thrombus)
 When a thrombus completely or partially obstructs a
pulmonary artery or its branches, the alveolar dead space
is increased.
 The area, although continuing to be ventilated, receives
little or no blood flow. Therefore, gas exchange is impaired
or absent in this area.
 In addition, various substances are released from the clot
and surrounding area that cause regional blood vessels
and bronchioles to constrict
 This results in an increase in pulmonary vascular
resistance—a reaction that compounds the ventilation–
perfusion imbalance.
 The hemodynamic consequences are increased pulmonary
vascular resistance due to the regional vasoconstriction
and reduced size of the pulmonary vascular bed.
 This results in an increase in pulmonary arterial pressure
and, in turn, an increase in right ventricular work to
maintain pulmonary blood flow.
 When the work requirements of the right ventricle exceed
its capacity, right ventricular failure occurs, leading to a
decrease in cardiac output followed by a decrease in
systemic blood pressure and the development of shock.
 Atrial fibrillation also causes PE. An enlarged right atrium in
fibrillation causes blood to stagnate and form clots in this
area. These clots are prone to travel into the pulmonary
circulation.
 A massive PE is best defined by the degree of
hemodynamic instability rather than the percentage of
pulmonary vasculature occlusion
 It is described as an occlusion of the outflow tract of the
main pulmonary artery or of the bifurcation of the
pulmonary arteries.
 Multiple small emboli can lodge in the terminal pulmonary
arterioles, producing multiple small infarctions of the lungs.
A pulmonary infarction causes ischemic necrosis of part of
the lung
Clinical Manifestations
 Dyspnea is the most frequent symptom; the duration and
intensity of the dyspnea depend on the extent of
embolization.
 Chest pain is common and is usually sudden and pleuritic
in origin
 It may be substernal and may mimic angina pectoris or a
myocardial infarction. Other symptoms include anxiety,
fever, tachycardia, apprehension, cough, diaphoresis,
hemoptysis, and syncope.
 The most frequent sign is tachypnea (very rapid respiratory
rate).
 The clinical picture may mimic that of bronchopneumonia or
heart failure. In atypical instances, PE causes few signs
and symptoms, whereas in other instances, it mimics
various other cardiopulmonary disorders
Assessment & Diagnostic Findings
 Initially, a clinical assessment will focus on the clinical
probability of risk, clinical history, symptoms, signs, and
testing.
 The initial diagnostic workup may include chest x-ray, ECG,
pulse oximetry, arterial blood gas analysis, and ventilation–
perfusion ( ) scan.
 The chest x-ray is usually normal but may show infiltrates,
atelectasis, elevation of the diaphragm on the affected side,
or a pleural effusion.
 In addition to sinus tachycardia, the most frequent ECG
abnormality is T-wave inversion in leads V1 to V4.
 If an arterial blood gas analysis is performed, it may show
hypoxemia and hypocapnia (from tachypnea); however,
arterial blood gas measurements may be normal even in
the presence of PE.
 Pulmonary angiography is considered the best method to
diagnose PE; however, it may not be feasible, cost-
effective, or easily performed, especially with critically ill
patients.
 The pulmonary angiogram allows for direct visualization
under fluoroscopy of the arterial obstruction and accurate
assessment of the perfusion deficit. A specially trained
team must be available to perform the procedure, in which
a catheter is threaded through the vena cava to the right
 side of the heart to inject dye, similar to a cardiac
catheterization.
 The v/Q scan continues to be used to diagnose PE,
especially in facilities that do not use pulmonary
angiography or do not have access to a spiral CT scanner.
The scan is minimally invasive, involving the IV
administration of a contrast agent. This scan evaluates
different regions of the lung (upper, middle, lower) and
allows comparisons of the percentage of ventilation and
perfusion in each area. This test has a high sensitivity but
can be more cumbersome than a CT scan and is not as
accurate as a pulmonary angiogram.
 A high suspicion of PE may warrant a spiral CT scan of the
lung
 In spiral CT, the examination table advances at a constant
rate through the scanner while the x-ray tube rotates
continuously around the patient, following a spiral path,
thus allowing the gathering of continuous data with no gaps
between images.
Prevention
 For patients at risk for PE, the most effective approach is to
prevent DVT
 Active leg exercises to avoid venous stasis, early
ambulation, and the use of anti-embolism stockings are
general preventive measures
Medical Management
 After emergency measures have been initiated and the
patient is stabilized, the treatment goal is to dissolve (lyse)
the existing emboli and prevent new ones from forming.
 Treatment may include a variety of modalities: general
measures to improve respiratory and vascular status,
anticoagulation therapy, thrombolytic therapy, and surgical
intervention.
Emergency Management
 Nasal oxygen is administered immediately to relieve
hypoxemia, respiratory distress, and central cyanosis;
severe hypoxemia may necessitate emergent endotracheal
intubation and mechanical ventilatory support.
 IV infusion lines are inserted to establish routes for
medications or uids that will be needed.
 For hypotension that does not resolve with IV uids, prompt
initiation of vasopressor therapy is recommended, with
agents that may include dobutamine, dopamine, or
norepinephrine. Norepinephrine is the agent least likely to
cause tachycardia.
 A perfusion scan, hemodynamic measurements, and
evaluation for hypoxemia (pulse oximetry or arterial blood
gas) are performed. Spiral (helical) CT or pulmonary
angiography may be performed
 The ECG is monitored continuously for dysrhythmias and
right ventricular failure, which may occur suddenly.
 Blood is drawn for serum electrolytes, complete blood
count, and coagulation studies.
 If the patient has suffered massive embolism and is
hypotensive, an indwelling urinary catheter is inserted to
monitor urinary output.
 Small doses of IV morphine or sedatives are administered
to relieve patient anxiety, to alleviate chest discomfort, to
improve tolerance of the endotracheal tube, and to ease
adaptation to the mechanical ventilator, if necessary.
General Management
 Oxygen therapy is administered to correct the hypoxemia,
relieve the pulmonary vascular vasoconstriction, and
reduce the PH.
 The use of anti-embolism stockings or intermittent
pneumatic leg compression devices reduces venous stasis.
 These measures compress the superficial veins and
increase the velocity of blood in the deep veins by
redirecting the blood through the deep veins.
 Elevating the leg (above the level of the heart) also
increases venous ow. However, increasing ow may
cause a volume challenge to a hemodynamically unstable
patient.
Pharmacologic Therapy
 Anticoagulation Therapy - initial phase, early
maintenance phase, and long-term secondary prevention
phase.
 Low-molecular-weight heparin and fondaparinux (Arixtra)
are the cornerstones of therapy, but IV unfractionated
heparin may be used during the initial phase
 The early maintenance phase of anticoagulation typically
consists of overlapping regimens of heparins or
fondaparinux for at least 5 days with an oral vitamin K
antagonist (e.g., warfarin [Coumadin]). A 3- to 6-month
regimen of long-term maintenance with warfarin is typical
but depends on the risks of recurrence and bleeding. Other
heparinoids may also be used for PE. These include
dalteparin (Fragmin), tinzaparin (Innohep), lepirudin
(Re udan), and argatroban
 Thrombolytic (Fibrinolytic) Therapy – is used in treating
massive PE, particularly in patients who are severely
compromised (e.g., those who are hypotensive and have
significant hypoxemia despite oxygen supplementation)
o Thrombolytic therapy resolves the thrombi or
emboli quickly and restores more normal
hemodynamic functioning of the pulmonary
circulation, thereby reducing PH and improving
perfusion, oxygenation, and cardiac output.
o Contraindications to thrombolytic therapy include a
cerebrovascular accident (CVA) within the past 2
months, other active intracranial processes, active
bleeding, surgery within 10 days of the thrombotic
event, recent labor and delivery, trauma, or severe
hypertension.
o Before thrombolytic therapy is started,
international normalized ratio (INR), partial
thromboplastin time (PTT), hematocrit, and
platelet counts are obtained.
o An anticoagulant is stopped prior to administration
of a thrombolytic agent.
o During therapy, all but essential invasive
procedures are avoided because of potential
bleeding.
o If necessary, fresh whole blood, packed red cells,
cryoprecipitate, or frozen plasma is administered
to replace blood loss and reverse the bleeding
tendency.
Surgical Management
 A surgical embolectomy is rarely performed but may be
indicated if the patient has a massive PE or hemodynamic
instability or if there are contraindications to thrombolytic
(fibrinolytic) therapy.
o Embolectomy can be performed using catheters or
surgically. Surgical removal must be performed by
a cardiovascular surgical team with the patient on
cardiopulmonary bypass.
o Although surgical embolectomy ensures removal
of the clot, it is not without risk.
 Transvenous catheter embolectomy is a variety of
techniques. For a suction embolectomy, a large-lumen
catheter is inserted and the thrombus is suctioned by
manually applying negative pressure with an aspiration
syringe.
 Rheolytic embolectomy is accomplished by injecting
pressurized saline through the catheter’s distal tip that
macerates the emboli.
 A rotational embolectomy involves a rotating device
within the catheter to fragment the thrombus. The
fragments are continuously aspirated. In addition, catheter-
directed ultrasound combined with low-dose thrombolytic
therapy has been studied and may offer benefit.
 An inferior vena cava (IVC) filter may be inserted at the
time of surgery to protect against a recurrence. IVC lters
are not recommended for the initial treatment of patients
with PE
Nursing Management
 Minimizing the Risk of Pulmonary Embolism - The nurse
must have a high degree of suspicion for PE in all patients,
but particularly in those with conditions predisposing to a
slowing of venous return.
 Preventing Thrombus Formation - The nurse encourages
ambulation and active and passive leg exercises to prevent
venous stasis in patients prescribed bed rest. The nurse
instructs the patient to move the legs in a “pumping”
exercise so that the leg muscles can help increase venous
flow. The nurse also advises the patient not to sit or lie in
bed for prolonged periods, not to cross the legs, and not to
wear constrictive clothing. Legs should not be dangled or
feet placed in a dependent position while the patient sits on
the edge of the bed; instead, feet should rest on the floor or
on a chair.
 Assessing Potential for Pulmonary Embolism - The nurse
conducts a careful assessment of the patient’s health
history, family history, and medication record. On a daily
basis, the patient is asked about pain or discomfort in the
extremities
 Monitoring Thrombolytic (Fibrinolytic) Therapy - The nurse
is responsible for monitoring thrombolytic ( brinolytic) and
anticoagulant therapy. Thrombolytic (fibrinolytic) therapy
(streptokinase, urokinase, tissue plasminogen activator)
causes lysis of deep vein thrombi and PE, which helps
dissolve the clots. During thrombolytic infusion, while the
patient remains on bed rest, vital signs are assessed every
2 hours and invasive procedures are avoided
 Managing Pain - Chest pain, if present, is usually pleuritic
rather than cardiac in origin. A semi- Fowler’s position
provides a more comfortable position for breathing.
 Managing Oxygen Therapy - The patient must understand
the need for continuous oxygen therapy. The nurse
assesses the patient frequently for signs of hypoxemia and
monitors the pulse oximetry values to evaluate the
effectiveness of the oxygen therapy.
 Relieving Anxiety - The nurse encourages the stabilized
patient to talk about any fears or concerns related to this
frightening episode, answers the patient’s and family’s
questions concisely and accurately.
 Monitoring for Complications - When caring for a patient
who has had PE, the nurse must be alert for the potential
complication of cardiogenic shock or right ventricular failure
subsequent to the e ect of PE on the cardiovascular
system.
 Providing Postoperative Nursing Care - If the patient has
undergone surgical embolectomy, the nurse measures the
patient’s pulmonary arterial pressure and urinary output.
The nurse also assesses the insertion site of the arterial
catheter for hematoma formation and infection.
SARCOIDOSIS
 is a type of interstitial lung disease, a multisystem,
granulomatous disease of unknown etiology. Although 90%
of patients demonstrate thoracic involvement, any organ
may be affected.
Pathophysiology
 is thought to be a hypersensitivity response to one or more
exogenous agents (bacteria, fungi, virus, chemicals) in
people with an inherited or acquired predisposition to the
disorder.
 The hypersensitivity response and inflammation results in
the formation of a noncaseating granuloma, which is a
noninfectious organized collection of macrophages that
appear as a nodule. In the lung, granuloma infiltration and
fibrosis may occur, resulting in low lung compliance,
impaired diffusing capacity, and reduced lung volumes.
Clinical Manifestations
 Hallmarks of sarcoidosis are its insidious onset and lack of
prominent clinical signs or symptoms.
 The clinical picture depends on the systems affected. The
lung is most commonly involved; signs and symptoms may
include dyspnea, cough, hemoptysis, and congestion.
 Generalized symptoms include anorexia, fatigue, and
weight loss. Other signs include uveitis; joint pain; fever;
and granulomatous lesions of the skin, liver, spleen, kidney,
and central nervous system.
 The granulomas may disappear or gradually convert to
fibrous tissue.
 With multisystem involvement, patients may also have
fatigue, fever, anorexia, and weight loss.
Assessment & Diagnostic Findings
 Chest x-rays and CT scans are used to assess pulmonary
adenopathy
 These may show hilar adenopathy and disseminated
miliary and nodular lesions in the lungs.
 A mediastinoscopy or transbronchial biopsy (in which a
tissue specimen is obtained through the bronchial wall)
may be used to confirm the diagnosis. In rare cases, an
open lung biopsy is performed.
 Diagnosis is confirmed by a biopsy that shows
noncaseating granulomas.
 Pulmonary function test results are abnormal if there is
restriction of lung function (reduction in total lung capacity).
 Arterial blood gas measurements may be normal or may
show reduced oxygen levels (hypoxemia) and increased
carbon dioxide levels (hypercapnia).
Medical Management
 Many patients undergo remission without specific treatment.
Corticosteroids may be bene cial because of their anti-
inflammatory effects.
 Short-course, moderate-dose therapy with prednisone has
been suggested as initial management of symptoms.
 Corticosteroids have been shown to be useful in patients
with ocular and myocardial involvement, skin involvement,
extensive pulmonary disease that compromises pulmonary
function, hepatic involvement, and hypercalcemia.
OCCUPATIONAL LUNG DISEASE:
PNEUMOCONIOSES
 Pneumoconiosis refers to a nonneoplastic alteration of the
lung resulting from inhalation of mineral or inorganic dust
(e.g., “dusty lung”).
 Pneumoconioses are caused by inhalation and deposition
of mineral dusts in the lungs, resulting in pulmonary fibrosis
and parenchymal changes.
 Many people with early pneumoconiosis are asymptomatic,
but advanced disease often is accompanied by disability
and premature death.
 Smoking may compound the problem and may increase the
risk of lung cancers in people exposed to the mineral
asbestos and other potential carcinogens.
 The effects of inhaling these materials depend on the
composition of the substance, its concentration, its ability to
initiate an immune response, its irritating properties, the
duration of exposure, and the individual’s response or
susceptibility to the irritant.
 Key aspects of any assessment of patients with a potential
occupational respiratory history include job and job
activities, exposure levels, general hygiene, time frame of
exposure, effectiveness of respiratory protection used, and
direct versus indirect exposures.
 The most common pneumoconioses are silicosis,
asbestosis, and coal worker’s pneumoconiosis
CHEST TUMORS
 Tumors of the lung may be benign or malignant. A  The most frequent symptom of lung cancer is cough or
malignant chest tumor can be primary, arising within the change in a chronic cough.
lung, chest wall, or mediastinum or it can be a metastasis  People frequently ignore this symptom and attribute it to
from a primary tumor site elsewhere in the body. smoking or a respiratory infection.
 The cough may start as a dry, persistent cough, without
LUNG CANCER (BRONCHOGENIC CARCINOMA) sputum production. When obstruction of airways occurs,
the cough may become productive due to infection.
 Lung cancer is the leading cancer killer among men and
 Dyspnea is prominent in patients early in their disease.
women in the United States, with almost 161,000 deaths
Causes of dyspnea may include tumor occlusion of the
estimated in 2012. Approximately 226,000 new cases of
airway or lung parenchyma, pleural effusion, pneumonia, or
lung cancer are diagnosed annually; 14% of new cancers
complications of treatment.
for men and women involve the lung or bronchus.
 Chest or shoulder pain may indicate chest wall or pleural
involvement by a tumor.
Pathophysiology  Pain also is a late manifestation and may be related to
 The most common cause of lung cancer is inhaled metastasis to the bone.
carcinogens, most often cigarette smoke (90%); other
carcinogens include radon gas and occupational and Assessment & Diagnostic Findings
environmental agents.
 If pulmonary symptoms occur in heavy smokers, cancer of
 Lung cancers arise from a single transformed epithelial cell
the lung should always be considered.
in the tracheobronchial airways, in which the carcinogen
 A chest x-ray is performed to search for pulmonary density,
binds to and damages the cell’s DNA.
a solitary pulmonary nodule (coin lesion), atelectasis, and
 This damage results in cellular changes, abnormal cell
infection.
growth, and eventually a malignant cell.
 CT scans of the chest are used to identify small nodules
 As the damaged DNA is passed on to daughter cells, the
not easily visualized on the chest x-ray and also to serially
DNA undergoes further changes and becomes unstable.
examine areas for lymphadenopathy.
 With the accumulation of genetic changes, the pulmonary
 Fiberoptic bronchoscopy is commonly used; it provides a
epithelium undergoes malignant transformation from
detailed study of the tracheobronchial tree and allows for
normal epithelium eventually to invasive carcinoma.
brushings, washings, and biopsies of suspicious areas.
 Carcinoma tends to arise at sites of previous scarring (TB,
 a transthoracic fine-needle aspiration may be performed
fibrosis) in the lung.
under CT guidance to aspirate cells from a suspicious area.
 A variety of scans may be used to assess for metastasis of
Classification and Staging:
the cancer. These may include bone scans, abdominal
Small Cell two general cell types include:
scans, positron emission tomography (PET) scans, and
Lung (1) small cell
Cancer (2) combined small cell liver ultrasound. CT scan of the brain, magnetic resonance
(SCLC) imaging (MRI), and other neurologic diagnostic procedures
the cell types include: are used to detect central nervous system metastases.
(1) squamous cell carcinoma (25% to 30%)  Mediastinoscopy or mediastinotomy may be used to obtain
- usually more centrally located and arises biopsy samples from lymph nodes in the mediastinum.
more commonly in the segmental and
subsegmental bronchi. Medical Management
(2) large cell carcinoma (10% to 15%) -
(also called undifferentiated carcinoma) is a  General, treatment may involve surgery, radiation therapy,
Non–Small
fast-growing tumor that tends to arise or chemotherapy—or a combination of these.
Cell Lung
peripherally.  SCLC treatment includes surgery (but only if the cancer is
Cancer
(3) adenocarcinoma (40%) - most prevalent in one lung and there is no metastasis)
(NSCLC)
carcinoma of the lung in both men and  Radiation therapy, laser therapy to open airways blocked
women; it occurs peripherally as peripheral
by tumor growth, and endoscopic stent placement.
masses or nodules and often metastasizes.
(4) bronchoalveolar carcinoma - found in
the terminal bronchi and alveoli and is Surgical Management
usually slower growing compared with other
 Surgical resection is the preferred method of treating
bronchogenic carcinomas.
patients with localized non– small cell tumors, no evidence
of metastatic spread, and adequate cardiopulmonary
Risk Factors:
function.
 Environmental factors
 If the patient’s cardiovascular status, pulmonary function,
 Other factors that have been associated with lung cancer
and functional status are satisfactory, surgery is generally
include male gender, genetic predisposition, dietary deficits,
well tolerated.
and underlying respiratory diseases, such as COPD and
 However, coronary artery disease, pulmonary insufficiency,
TB
and other comorbidities may contraindicate surgical
 Tobacco Smoke
intervention.
 Risk is determined by the pack-year history (number of
 Surgery is primarily used for NSCLCs, because small cell
packs of cigarettes used each day, multiplied by the
cancer of the lung grows rapidly and metastasizes early
number of years smoked), the age of initiation of smoking,
and extensively.
the depth of inhalation, and the tar and nicotine levels in the
cigarettes smoked.
 The younger a person is when he or she starts smoking,
the greater the risk of developing lung cancer.
 Second hand Smoke
Types of Lung Resection:
 Environmental and Occupational Exposure
Lobectomy a single lobe of the lung is removed
 Chronic exposure to industrial carcinogens Bilobectomy two lobes of the lung are removed
Sleeve resection cancerous lobe(s) is removed and a
Clinical Manifestations segment of the main bronchus is
resected
 The signs and symptoms depend on the location and size Pneumonectomy removal of entire lung
of the tumor, the degree of obstruction, and the existence Segmentectomy a segment of the lung is removed*
of metastases to regional or distant sites. Wedge resection removal of a small, pie-shaped area
 of the segment*
Chest wall resection for cancers that have invaded the
with removal of chest wall
cancerous lung tissue
Radiation Therapy
 Radiation therapy may offer cure in a small percentage of
patients. It is useful in controlling neoplasms that cannot be
surgically resected but are responsive to radiation.
 Irradiation also may be used to reduce the size of a tumor,
to make an inoperable tumor operable, or to relieve the
pressure of the tumor on vital structures.
 It can reduce symptoms of spinal cord metastasis and
superior vena caval compression.
 Radiation therapy may help relieve cough, chest pain,
dyspnea, hemoptysis, and bone and liver pain. Relief of
symptoms may last from a few weeks to many months and
is important in improving the quality of the remaining period
of life.
 Radiation therapy usually is toxic to normal tissue within the
radiation field, and this may lead to complications such as
esophagitis, pneumonitis, and radiation lung fibrosis.
 These complications may impair ventilatory and diffusion
capacity and significantly reduce pulmonary reserve.
Chemotherapy
 Chemotherapy is used to alter tumor growth patterns, to
treat distant metastases or small cell cancer of the lung,
and as an adjunct to surgery or radiation therapy.
 Chemotherapy may provide relief, especially of pain, but it
does not usually cure the disease or prolong life to any
great degree.
 Chemotherapy is also accompanied by side effects. It is
valuable in reducing pressure symptoms of lung cancer and
in treating brain, spinal cord, and pericardial metastasis.
Nursing Management
 Managing Symptoms - The nurse educates the patient
and family about the potential side effects of the specific
treatment and strategies to manage them. Strategies for
managing such symptoms as dyspnea, fatigue, nausea and
vomiting, and anorexia help the patient and family cope
with therapeutic measures.
 Relieving Breathing Problems - Airway clearance
techniques are key to maintaining airway patency through
the removal of excess secretions. This may be
accomplished through deep-breathing exercises, chest
physiotherapy, directed cough, suctioning, and in some
instances bronchoscopy.
 Reducing Fatigue - Fatigue is a devastating symptom that
affects quality of life in patients with cancer. It is commonly
experienced by patients with lung cancer and may be
related to the disease itself, the cancer treatment and
complications.
TUMORS OF THE MEDIASTINUM
 Tumors of the mediastinum include neurogenic tumors,
tumors of the thymus, lymphomas, germ cell tumors, cysts,
and mesenchymal tumors.
 These tumors may be malignant or benign. They are
usually described in relation to location: anterior, middle, or
posterior masses or tumors.
Clinical Manifestations
 Nearly all symptoms of mediastinal tumors result from the
pressure of the mass against important intrathoracic organs.
 Symptoms may include cough, wheezing, dyspnea, anterior
chest or neck pain, bulging of the chest wall, heart
palpitations, angina, other circulatory disturbances, central
cyanosis, superior vena cava syndrome (i.e., swelling of the
face, neck, and upper extremities), marked distention of the
veins of the neck and the chest wall (evidence of the
obstruction of large veins of the mediastinum by
extravascular compression or intravascular invasion), and
dysphagia and weight loss from pressure or invasion into
the esophagus
Assessment & Diagnostic Findings
 Chest x-rays are the major method used initially to
diagnose mediastinal tumors and cysts.
 A CT scan is the standard diagnostic test for assessment of
the mediastinum and surrounding structures.
 MRI, as well as PET, may be used in some circumstances
Medical Management
 If the tumor is malignant and has in ltrated the surrounding
tissue and complete surgical removal is not feasible,
radiation therapy, chemotherapy, or both are used
 Many mediastinal tumors are benign and operable. The
location of the tumor (anterior, middle, or posterior
compartment) in the mediastinum dictates the type of
incision.
 The common incision used is a median sternotomy;
however, a thoracotomy may be used, depending on the
location of the tumor.
CHEST TRAUMA
 Major chest trauma may occur alone or in combination with
multiple other injuries. Chest trauma is classified as either
blunt or penetrating.
I. BLUNT CHEST TRAUMA
 results from sudden compression or positive pressure
inflicted to the chest wall.
II. PENETRATING TRAUMA
 occurs when a foreign object penetrates the chest wall.
 Any organ or structure within the chest is potentially
susceptible to traumatic penetration.
 These organs include the chest wall, lung and pleura,
tracheobronchial system, esophagus, diaphragm, and
major thoracic blood vessels, as well as heart and other
mediastinal structures. Common injuries include
pneumothorax and cardiac tamponade.
Pathophysiology
 The most common causes of blunt chest trauma are motor
vehicle crashes (trauma from steering wheel, seat belt),
falls, and bicycle crashes (trauma from handlebars).
 Types of blunt chest trauma include chest wall fractures,
dislocations, and barotraumas (including diaphragmatic
injuries); injuries of the pleura, lungs, and aerodigestive
tracts; and blunt injuries of the heart, great arteries, veins,
and lymphatics.
 Injuries to the chest are often life threatening and result in
one or more of the following pathologic states:
 Hypoxemia from disruption of the airway; injury to the lung
parenchyma, rib cage, and respiratory musculature;
massive hemorrhage; collapsed lung; and pneumothorax
 Hypovolemia from massive fluid loss from the great vessels,
cardiac rupture, or hemothorax
 Cardiac failure from cardiac tamponade, cardiac contusion,
or increased intrathoracic pressure.
Assessment & Diagnostic Findings
 the patient must be assessed immediately to determine the
following: time elapsed since injury occurred; mechanism of
injury; level of responsiveness; specific injuries; estimated
blood loss; recent drug or alcohol use; prehospital
treatment
 Initial assessment of thoracic injuries includes assessment
for airway obstruction, tension pneumothorax, open
pneumothorax, massive hemothorax, flail chest, and
cardiac tamponade.
 Secondary assessment includes assessment for simple
pneumothorax, hemothorax, pulmonary contusion,
traumatic aortic rupture, tracheobronchial disruption,
esophageal perforation, traumatic diaphragmatic injury, and
penetrating wounds to the mediastinum.
 The physical examination includes inspection of the airway,
thorax, neck veins, and breathing difficulty.
 Specifics include assessing the rate and depth of breathing
for abnormalities such as stridor, cyanosis, nasal flaring,
the use of accessory muscles, drooling, and overt trauma
to the face, mouth, or neck.
 The chest is assessed for symmetric movement, symmetry
of breath sounds, open chest wounds, entrance or exit
wounds, impaled objects, tracheal shift, distended neck
veins, subcutaneous emphysema, and paradoxical chest
wall motion
 the chest wall is assessed for bruising, petechiae,
lacerations, and burns.
 The vital signs and skin color are assessed for signs of
shock. The thorax is palpated for tenderness and crepitus,
and the position of the trachea is also assessed.
 The initial diagnostic workup includes a chest x-ray, CT
scan, complete blood count, clotting studies, type and
cross-match, electrolytes, oxygen saturation, arterial blood
gas analysis, and ECG.
Medical Management
 The goals of treatment are to evaluate the patient’s
condition and to initiate aggressive resuscitation.
 An airway is immediately established with oxygen support
and, in some cases, endotracheal intubation and ventilatory
support.
 Reestablishing fluid volume and negative intrapleural
pressure and draining intrapleural fluid and blood are
essential.
Medical Management (Penetrating T.)
 The objective of immediate management is to restore and
maintain cardiopulmonary function.
 After an adequate airway is ensured and ventilation is
established, examination for shock and intrathoracic and
intra-abdominal injuries is necessary.
 The diagnostic workup includes a chest x-ray, chemistry
profile, arterial blood gas analysis, pulse oximetry, and
ECG gastrointestinal tract.
 Hemorrhagic shock is treated simultaneously with colloid
solutions, crystalloids, or blood, as indicated by the
patient’s condition
STERNAL AND RIB FRACTURES
 Sternal fractures are most common in motor vehicle
crashes with a direct blow to the sternum via the steering
wheel.
 Rib fractures are the most common type of chest trauma,
occurring in more than 50% of patients admitted with blunt
chest injury.
 Most rib fractures are benign and are treated conservatively;
ribs 4 through 10 are most frequently involved.
 Fractures of the first three ribs are rare but can result in a
high mortality rate because they are associated with
laceration of the subclavian artery or vein.
 Fractures of the lower ribs are associated with injury to the
spleen and liver, which may be lacerated by fragmented
sections of the rib.
Clinical Manifestations
 Patients with sternal fractures have anterior chest pain,
overlying tenderness, ecchymosis, crepitus, swelling, and
possible chest wall deformity.
 For patients with rib fractures, clinical manifestations are
similar: severe pain, point tenderness, and muscle spasm
over the area of the fracture that are aggravated by
coughing, deep breathing, and movement.
 The area around the fracture may be bruised.
 To reduce the pain, the patient splints the chest by
breathing in a shallow manner and avoids sighs, deep
breaths, coughing, and movement.
 This reluctance to move or breathe deeply results in
diminished ventilation, atelectasis (collapse of unaerated
alveoli), pneumonitis, and hypoxemia.
Assessment & Diagnostic Findings
 A crackling, grating sound in the thorax (subcutaneous
crepitus) may be detected with auscultation.
 The diagnostic workup may include a chest x-ray, rib films
of a specific area, ECG, continuous pulse oximetry, and
arterial blood gas analysis
Medical Management
 Medical management is directed toward relieving pain,
avoiding excessive activity, and treating any associated
injuries.
 Surgical fixation is rarely necessary unless fragments are
grossly displaced and pose a potential for further injury.
 The goals of treatment for rib fractures are to control pain
and to detect and treat the injury.
 Sedation is used to relieve pain and to allow deep
breathing and coughing.
FLAIL CHEST
 Flail chest is frequently a complication of blunt chest
trauma from a steering wheel injury.
 It occurs when three or more adjacent ribs (multiple
contiguous ribs) are fractured at two or more sites, resulting
in free-floating rib segments.
 It may also result as a combination fracture of ribs and
costal cartilages or sternum.
Pathophysiology
 During inspiration, as the chest expands, the detached part
of the rib segment (flail segment) moves in a paradoxical
manner (pendelluft movement) in that it is pulled inward
during inspiration, reducing the amount of air that can be
drawn into the lungs.
 On expiration, because the intrathoracic pressure exceeds
atmospheric pressure, the flail segment bulges outward,
impairing the patient’s ability to exhale.
 The mediastinum then shifts back to the affected side.
 This paradoxical action results in increased dead space, a
reduction in alveolar ventilation, and decreased compliance.
 Retained airway secretions and atelectasis frequently
accompany flail chest.
 The patient has hypoxemia, and if gas exchange is greatly
compromised, respiratory acidosis develops as a result of
carbon dioxide retention.
 Hypotension, inadequate tissue perfusion, and metabolic
acidosis often follow as the paradoxical motion of the
mediastinum decreases cardiac output.
Medical Management
 As with rib fracture, treatment of flail chest is usually
supportive. Management includes providing ventilatory
support, clearing secretions from the lungs, and controlling
pain.
 If only a small segment of the chest is involved, the
objectives are to clear the airway through positioning,
coughing, deep breathing, and suctioning to aid in the
expansion of the lung, and to relieve pain by intercostal
nerve blocks, high thoracic epidural blocks, or cautious use
of IV opioids.
 For mild to moderate flail chest injuries, the underlying
pulmonary contusion is treated by monitoring fluid intake
and appropriate uid replacement while relieving chest pain.
 For severe flail chest injuries, endotracheal intubation and
mechanical ventilation are required to provide internal
 pneumatic stabilization of the flail chest and to correct
abnormalities in gas exchange.
PULMONARY CONTUSION
 is a common thoracic injury and is frequently associated
with flail chest.
 It is defined as damage to the lung tissues resulting in
hemorrhage and localized edema.
 It is associated with chest trauma when there is rapid
compression and decompression to the chest wall.
 Pulmonary contusion represents a spectrum of lung injury
characterized by the development of infiltrates and various
degrees of respiratory dysfunction and sometimes
respiratory failure.
 It is often cited as the most common potentially life-
threatening chest injury; however, mortality is often
attributed to other associated injuries.
Clinical Manifestations
 Pulmonary contusion may be mild, moderate, or severe.
The clinical manifestations vary from decreased breath
sounds, tachypnea, tachycardia, chest pain, hypoxemia,
and blood-tinged secretions to more severe tachypnea,
tachycardia, crackles, frank bleeding, severe hypoxemia
(cyanosis), and respiratory acidosis.
 Patients with moderate pulmonary contusion have a large
amount of mucus, serum, and frank blood in the
tracheobronchial tree; patients often have a constant cough
but cannot clear the secretions.
 Patients with severe pulmonary contusion have signs and
symptoms that mirror ARDS, which may include central
cyanosis; agitation; combativeness; and productive cough
with frothy, bloody secretions.
Assessment & Diagnostic Findings
 The efficiency of gas exchange is determined by pulse
oximetry and arterial blood gas measurements.
 Pulse oximetry is also used to measure oxygen saturation
continuously.
Medical Management
 Treatment priorities include maintaining the airway,
providing adequate oxygenation, and controlling pain.
 In mild pulmonary contusion, adequate hydration via IV
fluids and oral intake is important to mobilize secretions.
 Volume expansion techniques, postural drainage,
physiotherapy including coughing, and endotracheal
suctioning are used to remove the secretions.
 Pain is managed by intercostal nerve blocks or by opioids
via patient-controlled analgesia or other methods.
 In patients with moderate pulmonary contusion,
bronchoscopy may be required to remove secretions.
Intubation and mechanical ventilation with PEEP may also
be necessary to maintain the pressure and keep the lungs
inflated.
 In patients with severe contusion, who may develop
respiratory failure, aggressive treatment with endotracheal
intubation and ventilatory support, diuretics, and fluid
restriction may be necessary.
PNEUMOTHORAX
 occurs when the parietal or visceral pleura is breached and
the pleural space is exposed to positive atmospheric
pressure.
Types:
air enters the pleural space through a breach
of either the parietal or visceral pleura. Most
Simple
commonly, this occurs as air enters the pleural
Pneumothorax
space through the rupture of a bleb or a
bronchopleural fistula.
Spontaneous occur in an apparently healthy person in the
Pneumothorax absence of trauma due to rupture of an air-
filled bleb, or blister, on the surface of the
lung, allowing air from the airways to enter the
pleural cavity.
occurs when air escapes from a laceration in
the lung itself and enters the pleural space or
from a wound in the chest wall. It may result
Traumatic
from blunt trauma (e.g., rib fractures),
Pneumothorax
penetrating chest or abdominal trauma (e.g.,
stab wounds or gunshot wounds), or
diaphragmatic tears.
occurs when air is drawn into the pleural
space from a lacerated lung or through a small
Tension
opening or wound in the chest wall. It may be
Pneumothorax
a complication of other types of
pneumothorax.
Clinical Manifestations
 Pain is usually sudden and may be pleuritic
 The patient may have only minimal respiratory distress with
slight chest discomfort and tachypnea with a small simple
or uncomplicated pneumothorax.
 If the pneumothorax is large and the lung collapses totally,
acute respiratory distress.
 The patient is anxious, has dyspnea and air hunger, has
increased use of the accessory muscles, and may develop
central cyanosis from severe hypoxemia.
 In assessing the chest for any type of pneumothorax, the
nurse assesses tracheal alignment, expansion of the chest,
breath sounds, and percussion of the chest.
Medical Management
 The goal of treatment is to evacuate the air or blood from
the pleural space.
 A small chest tube (28 Fr) is inserted near the second
intercostal space; this space is used because it is the
thinnest part of the chest wall, minimizes the danger of
contacting the thoracic nerve, and leaves a less visible scar.
 If a patient also has a hemothorax, a large diameter chest
tube (32 Fr or greater) is inserted, usually in the fourth or
fifth intercostal space at the midaxillary line.
 The tube is directed posteriorly to drain the fluid and air.
Once the chest tube or tubes are inserted and suction is
applied (usually to 20 mm Hg suction), effective
decompression of the pleural cavity (drainage of blood or
air) occurs.
SUBCUTANEOUS EMPHYSEMA
 No matter what kind of chest trauma a patient has, when
the lung or the air passages are injured, air may enter the
tissue planes and pass for some distance under the skin
(e.g., neck, chest).
 The tissues give a crackling sensation when palpated, and
the subcutaneous air produces an alarming appearance as
the face, neck, body, and scrotum become misshapen by
subcutaneous air.
 Subcutaneous emphysema is of itself usually not a serious
complication.
 The subcutaneous air is spontaneously absorbed if the
underlying air leak is treated or stops spontaneously.
NON-MALIGNANT HEMATOLOGIC
DISORDERS (BERNARDO)
HYPOPROLIFERATIVE ANEMIA:
IRON DEFICIENCY ANEMIA (IDA)
 typically results when the intake of dietary iron is
inadequate for hemoglobin synthesis.
 is the most common type of anemia in all age groups, and it
is the most common anemia in the world.
 It is particularly prevalent in developing countries, where
inadequate iron stores can result from inadequate intake of
 iron (seen with vegetarian diets) or from blood loss (e.g.,
from intestinal hookworm) VIT B12 DEFICIENCY (PERNICIOUS ANEMIA)
 Anemia in Men and Postmenopausal women is bleeding
from ulcers, gastritis, inflammatory bowel disease, or GI  Can occur in several ways:
tumors. o Inadequate dietary intake (very rare)
 premenopausal women are menorrhagia (i.e., excessive o Faulty absorption from the GIT (most common)
menstrual bleeding). o An absence of intrinsic factor normally secreted by the
cells in the stomach which is common in the elderly
 Pregnancy with inadequate iron supplementation.
and has a familial tendency
 Patients with chronic alcoholism often have chronic blood
o Disease involving the ileum and pancreas which
loss from the GI tract, which causes iron loss and eventual
impairs absorption
anemia.
o Gastrectomy can also cause vitamin B12 deficiency
 bleeding or malabsorption (especially after gastric resection)

Vitamin B12 Absorption

Clinical Manifestations

 Fatigue
 Irritability
 Numbness
 And tingling of extremities

Clinical Manifestations (Severe Case)

 smooth, sore tongue

 brittle and ridged nails
 Thin, spoon-shaped nails
 angular cheilosis (Mouth ulcerations)
 Pica (unusual cravings, such for a clay, ice, or laundry
starch)

 History of multiple pregnancies, or gastrointestinal bleeding.

 Hemoglobin proportionately lower than hematocrit and Red
Blood Cell count
 Serum Iron concentration low
 Total Iron-Binding capacity (TIBC) high; serum ferritin low
Assessment & Diagnostic Findings
 Bone marrow aspiration - (few patients with suspected
iron deficiency anemia undergo bone marrow aspiration. In
many patients, the diagnosis can be established with other
tests)
o Decrease in red cell and hemoglobin count
o RBC hypochromia (hallmark of IDA)
o With symptoms of anemia (exertional
dyspnea, fatigue, tachycardia)
 Colonoscopy and/or endoscopy or other radiographic
examination of the gastrointestinal tract to detect
ulcerations, gastritis, polyps, or cancer(particularly for
people 50 years or older).
Medical Management
 Test stool specimen for occult blood
 Administer prescribed iron preparations (oral, intramuscular,
or intravenous).
 Avoid tablets with enteric coating (may be poorly absorbed)
 Continue iron for a year after bleeding has been controlled.
 NOTE: IM iron administration should be done through the
Z-tract technique
 Parenteral iron (Jectofer) administration can cause
occasional febrile and allergic reaction
 Patient with iron supplement (ferrous sulfate) is encouraged
to have frequent oral hygiene to prevent deposition in gums
and teeth
Clinical Manifestations
 After the body’s store of vitamin B12 are used up, patient
begins to show signs of anemia
 Gradually become weak, listless, and pale
 Hematologic effects of deficiency are accompanied by
effects on:
 Smooth red tongue (beefy tongue)
 Mild diarrhea
 Confusion
 Paresthesia in extremities
 Difficulty keeping balance (spinal cord defect)
 Loss of position sense
 Symptoms are progressive, without treatment, patient die
after several years, usually from CHF secondary to anemia
Assessment & Diagnostic Findings
 Schilling’s Test
o Patient is placed on NPO for 12 hours
o Given with a small dose of oral radioactive vitamin B12 in
the drink
o Followed by a large, non-radioactive vitamin B12 IM dose
o A 24-hour urine is collected and measured for radioactivity
o Interpretation:
 When oral vitamin B12 is absorbed, it will be excreted
in the urine resulting into increase radioactive content
of the urine
 The IM non-radioactive vitamin B12 helps to flush the
radioactive vitamin B12 into the urine
 However, if no radioactivity in the urine, it indicates that
the GIT is unable to absorb vitamin B12.

Nursing Management
 Preventive education is important
 Encouragement to eat foods high in iron content
 Taking iron-rich foods with a source of vitamin C enhances
absorption
 Iron supplement is best absorbed on an empty stomach,
taking it with foods is usually advised to minimize gastric
irritation
 Warn patient that iron salt often change the stools to a
darker color.
 Nutritional counseling is provided when needed
Medical Management
 Treated by replacement (Replacement is by IM injection of
vitamin B12)
 Strict vegetarian can prevent or treat deficiency with oral
supplementation or fortified soy milk
 When deficiency is due to defective absorption or absence
of intrinsic factor:
 Neurologic manifestations require more time for recovery
 If there is severe neuropathy, paralysis, or incontinence,
patient may never recover fully
 Lifetime vitamin B12 therapy is required to patient with
pernicious anemia or non-correctable malabsorption. Complications

 infection
Nursing Management
 stroke
 Patient may need support during diagnostic tests  renal failure
 If with incontinence or paralysis, care must be taken to  impotence
prevent pressure ulcer and contracture deformities  heart failure
 Schilling test can be used only if the urine collection are  pulmonary hypertension
complete  Bacterial Infection
 Patient must be taught of the chronicity of the disease and  Organ Dysfunction
the necessity from monthly injection even when they are  Cerebral Vessel Occlusion
asymptomatic  Death
 Gastric atrophy associated with pernicious anemia
increases the risk of gastric carcinoma, medical follow-up is
Assessment & Diagnostic Findings
important.
 Hemoglobin Electrophoresis
HEMOLYTIC ANEMIA:  Prognosis:
SICKLE CELL ANEMIA o Patients with sickle cell anemia are usually diagnosed
in childhood because they become anemic in infancy
 Sickle cell anemia is a severe hemolytic anemia that results and begin to have sickle cell crises at 1 or 2 years of
from inheritance of the sickle hemoglobin (HbS) gene, age.
which causes the hemoglobin molecule to be defective. o Some children die in the first year of life, typically of
 The oxygen level in venous blood can be low enough to infection
cause this change; consequently, the erythrocyte
containing HbS loses its round, pliable, biconcave disk
Medical Management
shape and becomes dehydrated, rigid, and sickle shaped.
 These long, rigid erythrocytes can adhere to the  Hematopoietic Stem Cell Transplant
endothelium of small vessels; when they adhere to each o may cure sickle cell anemia.
other, blood flow to a region or an organ may be reduced.  Pharmacologic Therapy
 If ischemia or infarction results, the patient may have pain, o Hydroxyurea (Hydrea)
swelling, and fever. o Patients with sickle cell anemia may require daily
 The sickling process takes time folic acid replacements to maintain the supply
 if the erythrocyte is again exposed to adequate amounts of required for increased erythropoiesis from hemolysis
oxygen before the membrane becomes too rigid (e.g.,  Transfusion Therapy
when it travels through the pulmonary circulation), it can o RBC transfusions have been shown to be highly
revert to a normal shape. effective
 For this reason, the “sickling crises” are intermittent. o Chronic transfusion therapy may be effective in
 Cold can aggravate the sickling process, because preventing or managing complications from sickle cell
vasoconstriction slows the blood flow. disease by keeping the HbS level to less than 30%.
 Oxygen delivery can also be impaired by an increased o The hemoglobin level is usually kept below 11 to
blood viscosity. keep blood viscosity low.
 This form of the disease is found in about 1 in 500 African  Supportive Therapy
American live births and 1 in 36,000 live Hispanic live births o Supportive care is equally important.
(NHLBI, 2011). o Pain is a significant issue.
 The term sickle cell trait refers to the carrier state for SC o The incidence of painful sickle cell crises is highly
diseases; it is the most benign type of SC disease variable
o many patients have pain on a daily basis.
 if two people with sickle cell trait have children, the children
may inherit two abnormal genes and will have sickle cell
anemia. Nursing Management

 Assess cardiovascular, respiratory, neurologic, GI and

Clinical Manifestations
 Sickled cells are rapidly hemolyzed and thus have a very
short lifespan of 10 to 20 days.
 Anemia is always present
 hemoglobin values range between 7 and 10 g/dL.
 Jaundice (obvious in the sclerae).
 bone marrow expands in childhood in a compensatory
effort to offset the anemia (sometimes leading to
enlargement of the bones of the face and skull)
 The chronic anemia is associated with tachycardia,
cardiac murmurs, and often an enlarged heart
(cardiomegaly).
 Dysrhythmias and heart failure may occur in adults.
 any organ may be affected by thrombosis.
 but the primary sites involve those areas with slower
circulation
o spleen
o lungs
o central nervous system
 All tissues and organs are vulnerable to microcirculatory
interruptions by the sickling process and therefore are
susceptible to hypoxic damage or ischemic necrosis.
 Patients with sickle cell anemia are unusually susceptible to
infection, particularly pneumonia and osteomyelitis.
renal status
 Assess Pain level, administer analgesics as prescribed and
evaluate response
 Monitor and record vital signs, I/O, and laboratory studies
 Encourage increased oral fluid intake
 Administer medications as prescribed
 Apply warm compresses as prescribed
 Allay the patient’s anxiety and provide emotional support
 Avoid
BLEEDING DISORDERS:
IMMUNE THROMBOCYTOPENIC PURPURA
 ITP is a disease that affects people of all ages, but it is
more common among children and young women. Other
names for the disorder are:
o idiopathic thrombocytopenic purpura
o immune thrombocytopenia.
 Primary ITP occurs in isolation; defined as a platelet count
less than 100 × 109/L with an inexplicable absence of a
cause for thrombocytopenia
 Secondary ITP often results from:
o autoimmune diseases (e.g., antiphospholipid
antibody syndrome),
o viral infections (e.g., hepatitis C, HIV)
 o various drugs (e.g., sulfa drugs).
Pathophysiology
 ITP is an autoimmune disorder characterized by a
destruction of normal platelets by an unknown stimulus.
 Antiplatelet antibodies develop in the blood and bind to the
patient’s platelets.
 These antibody-bound platelets are then ingested and
destroyed by the reticuloendothelial system (RES) or tissue
macrophages.
 The body attempts to compensate for this destruction by
increasing platelet production within the marrow.
 However, platelet production may also be impaired as the
antibodies may also induce cell death (via apoptosis) of the
megakaryocytes and thus inhibit platelet production within
the bone marrow
Clinical Manifestations
 low platelet count is an incidental finding (often less than
30,000/mm3; less than 5000/mm3 is not uncommon).
 Common physical manifestations are:
o easy bruising
o heavy menses
o petechiae on the extremities or trunk
 Patients with simple bruising or petechiae (“dry purpura”)
tend to have fewer complications from bleeding than those
with bleeding from mucosal surfaces, such as the GI tract
(including the mouth) and pulmonary system (e.g.,
hemoptysis), which is termed wet purpura.
o Patients with wet purpura have a greater risk
of life-threatening bleeding than do those with
dry purpura;
 Severe thrombocytopenia: (predictive of severe bleeding)
o platelet count less than 20,000/mm3
o a history of prior minor bleeding episodes
o advanced age
 Despite low platelet counts, the platelets are young and
very functional.
o adhere to endothelial surfaces and to one
another, so spontaneous bleeding does not
always occur.
 treatment may not be initiated unless:
o bleeding becomes severe or life-threatening
o platelet count is extremely low (less than
30,000/mm3)
Assessment & Diagnostic Findings
 Patients should be tested for hepatitis C and HIV, if not
previously done to rule out these potential causes
 bone marrow aspirate = increase in megakaryocytes may
be seen
 platelet count that is less than 20,000/mm3 is a common
finding.
Medical Management
 primary goal of treatment = “safe” platelet count
 patient whose count exceeds 30,000/mm3 to 50,000/mm3
may be carefully observed without additional intervention.
 if the count is less than 30,000/mm3 or if bleeding occurs,
the goal is to improve the patient’s platelet count rather
than to cure the disease
 A person with a sedentary lifestyle can tolerate a low
platelet count more safely than one with a more active
lifestyle
 medication known to be associated with ITP = medication
must be stopped immediately
 platelet transfusions are not indicated
 Aminocaproic acid = a fibrinolytic enzyme inhibitor that
slows the dissolution of clots
 Immunosuppressive agents = agents block the binding
receptors on macrophages so that the platelets are not
destroyed
 corticosteroid prednisone at a dose of 1 mg per kilogram
of body weight for 21 days and then tapering the dose until
the patient is off the medication)
o patients cannot take high doses of
corticosteroids
 IVIG = effective in binding the receptors on the
macrophages; however, high doses are required, the drug
is very expensive, and the effect is transient
 anti-D (WinRho) in patients who are Rh (D) positive.
 Splenectomy
 Other management options:
o certain monoclonal antibodies (e.g.,
rituximab).
o thrombopoietin receptor agonists:
 Romiplostim (Nplate) given weekly
as a subcutaneous injection
 eltrombopag (Promacta) is given
orally
Nursing Management
 assessment of the patient’s lifestyle
 A careful medication history
 The nurse must be alert for sulfa-containing medications
 The nurse assesses for any history of recent viral illness
and reports of headache or visual disturbances
 neurologic assessment incorporated into their routine vital
sign measurements
 All injections or rectal medications should be avoided, and
rectal temperature measurements should not be performed
 . Nurses should explore the extent the patient experiences
fatigue and offer strategies to ameliorate this problem.
 Patient education addresses signs of exacerbation of
disease
 The patient is instructed to avoid all agents that interfere
with platelet function, including herbal therapies and over-
the-counter medications.
 The patient should avoid constipation, the Valsalva
maneuver (e.g., straining at stool)
 Patient should avoid vigorous flossing of the teeth
 Electric razors should be used for shaving
 Use soft bristled toothbrushes
 refrain from vigorous sexual intercourse (if Plt is less than
10,000 /mm3)
 Patients who are receiving corticosteroids long term are at
risk for complications including:
o osteoporosis
o proximal muscle wasting
o cataract formation
o dental caries
HYPOPROLIFERATIVE ANEMIA:
APLASTIC ANEMIA
 Aplastic anemia is a rare disease caused by a decrease in
or damage to marrow stem cells, damage to the
microenvironment within the marrow, and replacement of
the marrow with fat.
 Primarily idiopathic cause
Causes:
 Idiopathic
 Congenital or inherited
 Pregnancy
 Infection
 Drug/chemicals
 Radiation
Chemicals/drugs that can cause damage to bone marrow:
 Benzene and benzene derivatives
 Antitumor agents: nitrogen mustard
 Antimetabolites: methotrexate 6-mercaptopurine
 Toxic materials: inorganic arsenic
Others:
 Antimicrobial (chloramphenicol)
 Anticonvulsant (mephenytoin)
 Trimethadione (Tridionel)
 Antithyroid drugs
 Oral hypoglycemic agents ALLERGIC DISORDERS (ARCUINO)
 Antihistamines
 Analgesics B-cells = lymphocyte cells that are important in producing
 Sedatives antibodies
 Phenothiazides T-cells = lymphocyte cells that act as potent vaso-and-
 Insecticides bronchoconstrictor
 Heavy metals
Types of T and B Cells
Clinical Manifestations

 Weakness and fatigue

 Dyspnea, tachypnea
 Multiple infections
 Elevated temperature
 Headache
 Purpura (Bruising), petechiae, ecchymosis
 Pallor
 Palpitations, tachycardia.
 Infection due to leukopenia
 Abnormal bleeding due to thrombocytopenia

Assessment & Diagnostic Findings

 Peripheral blood smear: Pancytopenia

 Hematology: decreased granulocyte, thrombocytes, RBCs
 Bone Marrow biopsy: fatty marrow with reduction of stem Major Classes of Immunoglobulins
cells
 Appears in serum and tissues
(interstitial fluid)
Medical Management
IgG (75% of  Assumes a major role in bloodborne
 Bone marrow transplantation Total and tissue infections
o To provide the patient with undamaged supply of Immunoglobulin)  Activates the complement system
functional hematopoietic tissues  Enhances phagocytosis
 Administration of immunosuppressive therapy with  Crosses the placenta
antithymocyte globulin (ATG)  Appears in body fluids (blood, saliva,
o To remove immunologic function that prolong the tears, and breast milk, as well as
aplasia, thus allowing the patient’s bone marrow to pulmonary, gastrointestinal, prostatic,
recover and vaginal secretions)
 Any offending drug is discontinued IgA (15% of  Protects against respiratory,
 Death usually is caused by hemorrhage or infection. Total gastrointestinal, and genitourinary
 Transfusion therapy: platelets, and packed RBCs Immunoglobulin) infections
 Diet: Well balanced  Prevents absorption of antigens from
 I.V. Therapy: Hydration food
 Oxygen therapy: as needed  Passes to neonate in breast milk for
 Activity: As tolerated, with frequent rest periods. protection
 Monitoring: Vital signs, I/O, and laboratory studies (RBCs,  Appears mostly in intravascular
WBCs, platelets, and stools for occult blood) serum
IgM (10% of
 hematopoietic stem cell transplant (HSCT) for (<60 y.o.)  Appears as the first immunoglobulin
Total
produced in response to bacterial and
Immunoglobulin)
viral infections
Prevention  Activates the complement system
 Prevention of drug-induced aplastic anemia: IgD (0.2% of  Appears in small amounts in serum
o Potentially toxic medication should be used Total  Possibly influences B-lymphocyte
only when alternative therapies are not Immunoglobulin) differentiation, but role is unclear
available  Appears in serum
IgE (0.004% of
o Patient receiving chloramphenicol should be  Takes part in allergic and some
Total
hypersensitivity reactions
monitored in their blood cells counts Immunoglobulin)
 Combats parasitic infections

Nursing Management
Function of Antigens
 Patients with aplastic anemia are vulnerable to problems
ANTIGEN
related to erythrocyte, leukocyte, and platelet deficiencies. EXAMPLES FUNCTION
GROUP
 Assess carefully for signs of infection and bleeding Complete animal stimulate a complete humoral
 Monitor for hypersensitivity reaction while administering protein dander, response.
ATG antigens pollen, and
 If with long-term cyclosporine therapy; horse serum
 they should be monitored for long-term effects including: Low- medications function as haptens (incomplete
o renal or liver dysfunction molecular- antigens), binding to tissue or
o Hypertension weight serum proteins to produce a
o pruritus substances carrier complex that initiates an
o visual impairment antibody response. In an allergic
reaction, the production of
o tremor
antibodies requires active
o skin cancer. communication between cells.
 Chemical Mediators
Hypersensitivity
 is a reflection of excessive immune response to any type of
stimulus.
 hypersensitivity reaction is an abnormal, heightened
reaction to any type of stimulus.
o It usually does not occur with the first exposure to
an allergen. Rather, the reaction follows a re-
exposure after sensitization, or buildup of
antibodies, in a predisposed person.
 most severe hypersensitivity reaction
 unanticipated severe allergic reaction
that is rapid in onset, anaphylaxis is
characterized by edema in many
Anaphylactic
tissues, including the larynx, and is
(Type I)
often accompanied by hypotension,
Hypersensitivity
bronchospasm, and cardiovascular
collapse in severe cases
 immediate reaction beginning within
minutes of exposure to an antigen
Cytotoxic (Type  occurs when the system mistakenly
II) identifies a normal constituent of the
Hypersensitivity body as foreign
Immune  involves immune complexes that are
Complex (Type formed when antigens bind to
III) antibodies
Hypersensitivity
 immune reaction in which T-cell–
dependent macrophage activation and
Delayed- Type
inflammation cause tissue injury
(Type IV)
Hypersensitivity  reaction to the subcutaneous injection
of antigen is often used as an assay for
cell-mediated immunity
Diagnostic Evaluation
 Complete Blood Count With Differential
o The white blood cell (WBC) count is usually
normal except with infection. Eosinophils, which
are granular leukocytes, normally make up 0% to
3% of the total number of WBCs. A level between
5% and 15% is nonspecific but does suggest
allergic reaction.
 Eosinophil Count
o Higher percentages of eosinophils are considered
to represent moderate to severe eosinophilia.
 Moderate eosinophilia is defined as
15% to 40% eosinophils and may be
found in patients with allergic disorders.
 Total Serum Immunoglobulin E Levels
o High total serum IgE levels support the diagnosis
of allergic disease. IgE levels are not as sensitive
as the paper radioimmunosorbent test (PRIST),
the enzyme immunoassay (EIA), or a variant of
this test known as enzymelinked immunosorbent
assay (ELISA).
 Skin Tests
 Provocative Testing
o Provocative testing involves the direct
administration of the suspected allergen to the
sensitive tissue, such as the conjunctiva, nasal or
bronchial mucosa, or gastrointestinal tract (by
ingestion of the allergen), with observation of
target organ response. This type of testing is
helpful in identifying clinically significant allergens
in patients who have a large number of positive
tests.
 Radioallergosorbent Test
o RAST is a radioimmunoassay that measures
allergen-specic IgE. A sample of the patient’s
serum is exposed to a variety of suspected
allergen particle complexes. If antibodies are
present, they will combine with radiolabeled
allergens.
Allergic Disorders
Two Types of IgE-Mediated Allergic Reactions
characterized by a hereditary predisposition
and production of a local reaction to IgE
Atopic antibodies, which manifests in one or more of
Disorders the following three atopic disorders: allergic
rhinitis, asthma, and atopic
dermatitis/eczema.
lack the genetic component and organ
specificity of the atopic disorders. Latex
Nonatopic allergy may be a type I or type IV
Disorders hypersensitivity reaction, although true latex
allergy is considered to be a type I
hypersensitivity reaction.
ANAPHYLAXIS
 Anaphylaxis is a clinical response to an immediate (type I
hypersensitivity) immunologic reaction between a specific
antigen and an antibody. The reaction results from a rapid
release of IgE-mediated chemicals, which can induce a
severe, life-threatening allergic reaction.
Common Causes:
 Foods
 Medications
 Other pharmaceutical/biologic agents
 Insect stings
 Latex
Pathophysiology
Clinical Manifestations
• Peripheral tingling and a sensation of warmth,
possibly accompanied by a sensation of
fullness in the mouth and throat.
Mild
• Nasal congestion, periorbital swelling, pruritus,
systemic
sneezing, and tearing of the eyes can also be
reactions
expected.
• Onset of symptoms begins within the first 2
hours after exposure.
• Flushing, warmth, anxiety, and itching in
addition to any of the milder symptoms.
Moderate • More serious reactions include bronchospasm
systemic and edema of the airways or larynx with
reactions dyspnea, cough, and wheezing.
• The onset of symptoms is the same as for a
mild reaction.
Severe • Abrupt onset with the same signs and
systemic symptoms described previously.
reactions • These symptoms progress rapidly to
bronchospasm, laryngeal edema, severe
dyspnea, cyanosis, and hypotension.
Dysphagia (difficulty swallowing), abdominal
cramping, vomiting, diarrhea, and seizures
can also occur.
• Cardiac arrest and coma may follow.

Medical Management

 Management depends on the severity of the reaction.

 Initially, respiratory and cardiovascular functions are
evaluated.
 If the patient is in cardiac arrest, cardiopulmonary
resuscitation (CPR) is instituted .
 Supplemental oxygen is provided during CPR or if the
patient is cyanotic, dyspneic, or wheezing.
 Epinephrine, in a 1:1,000 dilution, is administered
subcutaneously in the upper extremity or thigh and may be
followed by a continuous intravenous infusion.
 Antihistamines and corticosteroids may also be
administered to prevent recurrences of the reaction and to
treat urticaria and angioedema. Intravenous fluids (e.g.,
normal saline solution), volume expanders, and
vasopressor agents are administered to maintain blood
pressure and normal hemodynamic status. Clinical Manifestations
 Patients who have experienced anaphylactic reactions and
 Typical signs and symptoms of allergic rhinitis include
received epinephrine should be transported to the local
sneezing and nasal congestion; clear, watery nasal
emergency department for observation and monitoring
discharge; and nasal itching.
because of the risk for a “rebound” or delayed reaction 4 to
 Itching of the throat and soft palate is common.
10 hours after the initial allergic reaction.
 Drainage of nasal mucus into the pharynx results in
 Patients with severe reactions are monitored closely for 12
multiple attempts to clear the throat and results in a dry
to 14 hours in a facility that can provide emergency care, if
cough or hoarseness. Headache, pain over the paranasal
needed.
sinuses, and epistaxis can accompany allergic rhinitis.

Nursing Management
 The nurse assesses the airway, breathing pattern, and vital
signs.
 The patient is observed for signs of increasing edema and
respiratory distress.
 Prompt notification of the rapid response team and/or the
provider is required.
 Rapid initiation of emergency measures (intubation,
administration of emergency medications, insertion of
intravenous lines, fluid administration, and oxygen
administration) are important to reduce the severity of the
reaction and to restore cardiovascular function.
 The nurse documents the interventions used and the
patient’s vital signs and response to treatment.
 The patient who has recovered from anaphylaxis needs an
explanation of what occurred, instruction about avoiding
future exposure to antigens, and how to administer
emergency medications to treat anaphylaxis.
 The patient must be instructed about antigens that should
be avoided and about other strategies to prevent
recurrence of anaphylaxis.
 All patients who have experienced an anaphylactic reaction
should receive a prescription for preloaded syringes of
epinephrine.
 The nurse instructs the patient and family in their use and
has the patient and family demonstrate correct
administration.
ALLERGIC RHINITIS
 Allergic rhinitis (hay fever, seasonal allergic rhinitis) is the
most common form of respiratory allergy, which is
presumed to be mediated by an immediate (type I
hypersensitivity) immunologic reaction.
Assessment and Diagnosis
 Findings Diagnosis of seasonal allergic rhinitis is based on
history, physical examination, and diagnostic test results.
Diagnostic tests include nasal smears, peripheral blood
counts, total serum IgE, epicutaneous and intradermal
testing, RAST, food elimination and challenge, and nasal
provocation tests. Results indicative of allergy as the cause
of rhinitis include increased IgE and eosinophil levels and
positive reactions on allergen testing.
Medical Management
 The goal of therapy is to provide relief from symptoms.
Therapy may include one or all of the following
interventions: avoidance therapy, pharmacologic therapy,
and immunotherapy.
Pharmacologic Therapy
 Antihistamines
 Adrenergic Agents
 Mast Cells Stabilizers
 Corticosteriods
 Leukotriene Modifiers
 Immunotherapy
CONTACT DERMATITIS
 a type IV delayed hypersensitivity reaction, is an acute or
chronic skin inflammation that results from direct skin
contact with chemicals or allergens. There are four basic
types: allergic, irritant, phototoxic, and photoallergic.
Clinical Manifestations

 include itching, burning, erythema, skin lesions (vesicles),

Pathophysiology and edema, followed by weeping, crusting, and finally
drying and peeling of the skin. In severe responses,
hemorrhagic bullae may develop. Repeated reactions may
be accompanied by thickening of the skin and pigmentary
 changes. Secondary invasion by bacteria may develop in
skin that is abraded by rubbing or scratching.
ATOPIC DERMATITIS
 a type I immediate hypersensitivity disorder characterized
by inflammation and hyperreactivity of the skin. Other terms
used to describe this skin disorder include atopic eczema,
atopic dermatitis, and atopic dermatitis/eczema syndrome
(AEDS).
Clinical Manifestations
 Pruritus and hyperirritability of the skin are the most
consistent features of atopic dermatitis and are related to
large amounts of histamine in the skin.
 Excessive dryness of the skin with resultant itching is
related to changes in lipid content, sebaceous gland activity,
and sweating. In response to stroking of the skin,
immediate redness appears on the skin.
 Pallor follows in 15 to 30 seconds and persists for 1 to 3
minutes. Lesions develop secondary to the trauma of
scratching and appear in areas of increased sweating and
hypervascularity. Atopic dermatitis is chronic, with
remissions and exacerbations.
Medical Management
 Treatment of patients with atopic dermatitis must be
individualized. Guidelines for treatment include decreasing
itching and scratching by wearing cotton fabrics; washing
with a mild detergent; humidifying dry heat in winter;
maintaining room temperature at 20°C to 22.2°C (68°F to
72°F.
 Using antihistamines such as diphenhydramine (Benadryl);
and avoiding animals, dust, sprays, and perfumes.
 Keeping the skin moisturized with daily baths to hydrate the
skin and the use of topical skin moisturizers is encouraged.
 Topical corticosteroids are used to prevent inammation,
and any infection is treated with antibiotics to eliminate
Staphylococcus aureus when indicated.
 The use of immunosuppressive agents, such as
cyclosporine (Neoral, Sandimmune), tacrolimus (Prograf,
Protopic), and pimecrolimus (Elidel).
Nursing Management
 Patients who experience atopic dermatitis and their families
require assistance and support from the nurse to cope with
the disorder.
 The symptoms are often disturbing to the patient and
disruptive to the family. The appearance of the skin may
affect the patient’s self-esteem and his or her willingness to
interact with others.
 Instructions and counseling about strategies to incorporate
preventive measures and treatments into the lifestyle of the
family may be helpful.
 The patient and family need to be aware of signs of
secondary infection and of the need to seek treatment if
infection occurs.
 The nurse also educates the patient and family about the
side effects of medications used in treatment.
DERMATITIS MEDICAMENTOSA
 a type I hypersensitivity disorder, is the term applied to skin
rashes associated with certain medications.
Clinical Manifestations
 Rashes may be accompanied by systemic or generalized
symptoms. On discovery of a medication allergy, patients
are warned that they have a hypersensitivity to a particular
medication and are advised not to take it again.
Medical Management
 Skin eruptions related to medication therapy suggest more
serious hypersensitivities. Frequent assessment and
prompt reporting of the appearance of any eruptions are
important so that early treatment can be initiated.
 Some cutaneous drug reactions may indicate involvement
of other organs and are known as complex drug reactions.
 Patients who suspect that a new rash may be caused by a
drug allergy (newly prescribed medications, especially
antibiotics such as penicillin or sulfa medications) should
stop taking the medication immediately
URTCARIA (HIVES)
 is a type I hypersensitive allergic reaction of the skin that is
characterized by the sudden appearance of pinkish,
edematous elevations that vary in size and shape, itch, and
cause local discomfort. They may involve any part of the
body, including the mucous membranes (especially those
of the mouth), the larynx (occasionally with serious
respiratory complications), and the gastrointestinal tract.
ANGIONEUROTIC EDEMA (ANGIOEDEMA)
 involves the deeper layers of the skin, resulting in more
diffuse swelling rather than the discrete lesions
characteristic of hives. On occasion, this reaction covers
the entire back. The skin over the reaction may appear
normal but often has a reddish hue.
 regions most often involved are the lips, eyelids, cheeks,
hands, feet, genitalia, and tongue; the mucous membranes
of the larynx, bronchi, and gastrointestinal canal may also
be affected, particularly in the hereditary type.
 Swellings may appear suddenly, in a few seconds or
minutes, or slowly in 1 or 2 hours.
HEREDITARY ANGIOMA
 is a rare, potentially life-threatening condition and is
inherited as an autosomal dominant trait.
 Symptoms are caused by edema of the skin, the respiratory
tract, or the digestive tract. Attacks may be precipitated by
trauma.
Clinical Manifestations
 When skin is involved, the swelling usually is diffuse, does
not itch, and usually is not accompanied by urticaria.
Gastrointestinal edema may cause abdominal pain severe
enough to suggest the need for surgery. Typically, attacks
last 1 to 4 days and are harmless; however, attacks can
occasionally affect the subcutaneous and submucosal
tissues in the region of the upper airway and can be
associated with respiratory obstruction and asphyxiation.
Medical Management
 Attacks usually subside within 3 to 4 days, but during this
time the patient should be observed carefully for signs of
laryngeal obstruction, which may necessitate tracheostomy
as a lifesaving measure. Epinephrine, antihistamines, and
corticosteroids are usually used in treatment.
COLD URTICARIA
 Familial atypical cold urticaria (FACU) and acquired cold
urticaria (ACU) are fairly newly described diseases within
the spectrum of physical urticaria induced by temperature
exposure.
o FACU is an autosomal dominant condition,
inherited from one affected parent, and symptoms
usually begin at birth.
o ACU most frequently affects young adults
between 18 and 25 years of age and is commonly
associated with the more common physical
urticarias. Why a cold stimulus causes the
activation of mast cells and subsequent release
inflammatory mediators and histamine is unknown
 Clinical Manifestations
. time, particularly in children. About one third of proven
 Patients with cold urticaria break out in hives (i.e., urticaria)
when exposed to cold. The urticaria may be prompted by
exposure to cold weather or cold water or after coming in
contact with cold objects. In some patients, holding an ice
cube in the hand can spark the reaction. The clinical
manifestations typically last for 5 to 6 years in ACU. The
condition is diagnosed by physical testing. Ice cube
provocation testing involves applying an ice cube to the
skin of the forearm for 1 to 5 minutes. A positive test results
in development of urticaria at the site in a patient with ACU.
Clinical manifestations of FACU can be precipitated by the
patient merely entering a 4°C (39°F) room.
Medical Management
 Prevention involves avoidance of cold stimuli. Treatment
involves bed rest, warmth, and corticosteroids to treat an
acute attack. All patients with any form of cold urticaria
should carry an EpiPen for emergency use because hives
can progress to anaphylaxis.
FOOD ALLERGY
 IgE-mediated food allergy, a type I hypersensitivity reaction,
occurs in about 2% of the adult population.
 Almost any food can cause allergic symptoms. Any food
can contain an allergen that results in anaphylaxis. The
most common oenders are seafood (lobster, shrimp, crab,
clams, fish), legumes (peanuts, peas, beans, licorice),
seeds (sesame, cottonseed, caraway, mustard, axseed,
sunflower), tree nuts, berries, egg white, buckwheat, milk,
and chocolate. Peanut and tree nut (e.g., cashew, walnut)
allergies are responsible for the most severe food allergy
reactions.
Pathophysiology
 Almost any food can cause allergic symptoms. Any food
can contain an allergen that results in anaphylaxis. The
most common genders are seafood (lobster, shrimp, crab,
clams, sh), legumes (peanuts, peas, beans, licorice), seeds
(sesame, cottonseed, caraway, mustard, axseed,
sunflower), tree nuts, berries, egg white, buckwheat, milk,
and chocolate. Peanut and tree nut (e.g., cashew, walnut)
allergies are responsible for the most severe food allergy
reactions.
Clinical Manifestations
 The clinical symptoms are classic allergic symptoms
(urticaria, dermatitis, wheezing, cough, laryngeal edema,
angioedema) and gastrointestinal symptoms (itching;
swelling of lips, tongue, and palate; abdominal pain;
nausea; cramps; vomiting; and diarrhea).
Assessment & Diagnostic Findings
 A careful diagnostic workup is required in any patient with
suspected food hypersensitivity. Included are a detailed
allergy history, a physical examination, and pertinent
diagnostic tests. Skin testing is used to identify the source
of symptoms and assists in identifying specific foods as
causative agents.
Natural Immunity (Nonspecific)
Medical Management
 Therapy for food hypersensitivity includes elimination of the
food responsible for the hypersensitivity. Pharmacologic
therapy is necessary for patients who cannot avoid
exposure to offending foods and for patients with multiple
food sensitivities not responsive to avoidance measures.
Medication therapy involves the use of H1 blockers,
antihistamines, adrenergic agents, corticosteroids, and
cromolyn sodium. All patients with food allergies, especially
seafood and nuts, should have an EpiPen device
prescribed. Another essential aspect of management is
educating patients and family members about how to
recognize and manage the early stages of an acute
anaphylactic reaction. Many food allergies disappear with
allergies disappear in 1 to 2 years if the patient carefully
avoids the offending food. However, peanut allergy has
been reported to persist throughout adulthood in some
people.
Nursing Management
 In addition to participating in management of the allergic
reaction, the nurse focuses on preventing future exposure
of the patient to the food allergen. If a severe allergic or
anaphylactic reaction to food allergens has occurred, the
nurse must instruct the patient and family about strategies
to prevent its recurrence. Patients’ food allergies should be
noted on their medical records, because there may be risk
of allergic reactions not only to food but also to some
medications containing similar substances.
LATEX ALLERGY
 the allergic reaction to natural rubber proteins—has been
implicated in rhinitis, conjunctivitis, contact dermatitis,
urticaria, asthma, and anaphylaxis.
 Natural rubber latex is derived from the sap of the rubber
tree (Hevea brasiliensis).
 Routes of exposure to latex products can be cutaneous,
percutaneous, mucosal, parenteral, or aerosol. Allergic
reactions are more likely with parenteral or mucous
membrane exposure but can also occur with cutaneous
contact or inhalation. The most frequent source of exposure
is cutaneous, which usually involves the wearing of natural
latex gloves. The powder used to facilitate putting on latex
gloves can become a carrier of latex proteins from the
gloves; when the gloves are put on or removed, the
particles become airborne and can be inhaled or settle on
skin, mucous membranes, or clothing.
 Mucosal exposure can occur from the use of latex condoms,
catheters, airways, and nipples. Parenteral exposure can
occur from intravenous lines or hemodialysis equipment.
Medical Management
 The best treatment available for latex allergy is the
avoidance of latex-based products.
 Antihistamines and an emergency kit containing
epinephrine should be provided to these patients.
Nursing Management
 Patients with latex allergy are advised to notify their health
care providers and to wear medical identification.
 Nurses can be instrumental in establishing and participating
in multidisciplinary committees to address latex allergy and
to promote a latex-free environment.
ALTERED IMMUNITY: IMMUNODEFICIENCY
DISORDERS (ARCUINO)
Types of Immunity
 Present at birth
 co-coordinates the initial response to pathogens
through the production of cytokines and other
effector molecules, which either activate cells for
control of the pathogen (by elimination) or promote
the development of the acquired immune response
 cells involved in this response are monocytes,
macrophages, dendritic cells, natural killer (NK) cells,
basophils, eosinophils, and granulocytes
 mechanisms can be divided into two stages:
o immediate (generally occurring within minutes)
o delayed (occurring within several days after
exposure)
  usually develops as a result of prior exposure to an
antigen through immunization (vaccination) or by Interpretation of Reactions
contracting a disease, both of which generate a
protective immune response. Weeks or months after Negative Wheal soft with minimal erythema
Acquired Immunity (Adaptive; Specific)

exposure to the disease or vaccine, the body 1+ Wheal present (5-8mm) with associated erythema
produces an immune response that is sufficient to 2+ Wheal (7-10mm) with associated erythema
defend against the disease on re-exposure. In Wheal (9-15mm), slight pseudopodia possible with
3+
contrast to the rapid but nonspecific natural immune associated erythema
response, this form of immunity relies on the Wheal (12+mm) with possible pseudopodia ang
4+
recognition of specific foreign antigens. diffuse erythema
 is broadly divided into two mechanisms:
o the cell-mediated response, involving T-cell
PRIMARY IMMUNODEFICIENCIES
activation
o effector mechanisms, involving B-cell Immune Major
Compone Disorder Treatment
maturation and production of antibodies nt Symptoms
 two types of acquired immunity are:  Bacterial,  Antibiotic therapy
o active (immunologic defenses developed by fungal, and and treatment for
the person’s own body) viral viral and fungal

Phagocytic cells
o passive (temporary immunity transmitted from infections infections
a source outside the body that has developed Hyperimm  Deep-  Granulocyte-
immunity through previous disease or unoglobul seated cold macrophage
immunization) inemia E abscesses colony-stimulating
factor (GMSCF)
Response to Invasion  Granulocyte
colony-stimulating
Body’s Three Means of Defense factor (GCSF)
primarily involves the WBCs Sex-linked  Severe  Passive pooled
(1) Phagocytic (granulocytes and macrophages), which agammagl infections plasma or
Immune have the ability to ingest foreign particles obulinemi soon after gamma-globulin
Response and destroy the invading agent; a birth
eosinophils are only weakly phagocytic (Bruton’s
(2) Humoral / begins with the B lymphocytes, which can disease)
B lymphocytes

Antibody transform themselves into plasma cells  Bacterial  Intravenous

immune that manufacture antibodies. infections immunoglobulin
response with Giardia (IVIG)
(3) Cellular involves the T lymphocytes, which can Common lamblia  Metronidazole
Immune turn into special cytotoxic (or killer) T cells variable
 Pernicious (Flagyl)
Response that can attack the pathogens. immunode
anemia  Quinacrine HCl
ficiency
 Chronic (Atabrine)
(CVID)
Stages of Immune Response respiratory  Vit B12
infections  Antimicrobial
 Recognition stage therapy
 Proliferation stage  Ataxia with  Antimicrobial
 Response stage progressive therapy
 Effector stage neurologic  Management of
deterioration presenting
, symptoms
Cellular vs. Humoral Immune Response Ataxia-
telangiectasi  Fetal thymus
telangiect
Humoral Responses (B Cellular Responses (T cells) a (vascular transplant
asia
cells) lesions),  IVIG
 Bacterial phagocytosis  Transplant rejection recurrent
and lysis  Delayed hypersensitivity infections,
 Anaphylaxis (tuberculin reaction) malignancie
 Allergic hay fever and  Graft-versus-host disease s
asthma  Tumor surveillance or  Severe  Antimicrobial
 Immune complex destruction infections, therapy
disease  Intracellular infections malignancie  IVIG
s
B-and-T- lymphocytes

 Bacterial and some viral  Viral, fungal, and parasitic Nezelof’s  Bone marrow
infections infections syndrome transplantation
 Thymus
transplantation
Immunomodulators
 Thymus factors
 also known as a biologic response modifier  Thrombocyt  Antimicrobial
 affects the host via direct or indirect effects on one or more openia therapy
components of the immunoregulatory network resulting in  Splenectomy with
 Natural Immunomodulators: Wiskott- bleeding continuous
o Immunostimulant Aldrich  Infections antibiotic
o Immunosuppressant syndrome  Malignancie prophylaxis
s  IVIG
 Bone marrow
one type of biologic response modifier, is
transplantation
a nonspecific viricidal protein that is
Intererons naturally produced by the body and is  Overwhelmi  Antimicrobial
capable of activating other components of ng severe therapy
Severe
the immune system. fatal  IVIG
combined
a group of naturally occurring infections  Bone marrow
Colony- immunode
glycoprotein cytokines that regulate soon after transplantation
stimulating ficiency
production, differentiation, survival, and birth (also
Factor disease
activation of hematopoietic cells includes
(SCID)
opportunistic
Monoclonal destroy pathologic organisms and spare
infections)
Antibodies normal cells.
(MoAbs)
  Episodes of  Pooled plasma o Identify the source patient, who may need to be tested
edema in  Androgen therapy for HIV, hepatitis B, and hepatitis C.
various o Report as quickly as possible to the employee health
Angioneur parts of the services, the emergency department, or other
otic body,
Complement System

designated treatment facility.

edema including
respiratory
tract and
bowels
 Lysis of  None
erythrocytes
Paroxysm due to lack
al of decay-
nocturnal accelerating
factor on
erythrocytes
10 Warning Signs of Primary Immunodeficiency
1. Four or more new ear infections within 1 year
2. Two or more serious sinus infections within 1 year
3. Two or more months on antibiotics with little effect
4. Two or more pneumonias within 1 year
5. Failure of an infant to gain weight or grow normally
6. Recurrent, deep skin or organ abscesses
7. Persistent thrush in mouth or fungal infection on skin
8. Need for intravenous antibiotics to clear infections
9. Two or more deep-seated infections including
septicemia
10. A family history of PI
SECONDARY IMMUNODEFICIENCIES (HIV & AIDS)
 occur as a result of underlying disease processes or the
treatment of these disorders.
 Common causes of secondary immunodeficiencies include:
o chronic stress
o burns
o uremia
o diabetes
o autoimmune disorders
o viruses
o exposure to immunotoxic medications and
chemicals
o substance and alcohol misuse
HIV Transmission
 Inflammation and breaks in the skin or mucosa result in the
increased probability that an HIV exposure will lead to
infection. Human immunodeficiency virus type 1 (HIV-1) is
transmitted in body fluids (blood, seminal fluid, vaginal
secretions, amniotic fluid, and breast milk) that contain free
virions and infected CD4+ T cells.
 Mother-to-child transmission of HIV-1 may occur in utero, at
the time of delivery, or through breast-feeding, but most
perinatal infections are thought to occur after exposure
during delivery.
 HIV is not transmitted through casual contact.
Prevention
 Preventive education
 Because HIV infection in women often occurs during the
childbearing years, family planning issues need to be
addressed. Attempts to achieve pregnancy by couples in
which only one partner has HIV (known as discordant
couples) expose the unaffected partner to the virus. Nurses
need to educate women who take hormonal contraceptives
to prevent pregnancy about using condoms to prevent HIV
infection and other sexually transmitted infections (STIs)
Post Exposure Prophylaxis for HCPs
 If you sustain an occupational exposure to HIV, take the
following actions immediately:
o Wash the area with soap and water
o Alert your supervisor/nursing faculty, and initiate the
injury-reporting system used in the setting.
o Give consent for baseline testing for HIV, hepatitis B,
and hepatitis C. Confidential HIV testing can be
performed up to 72 hours after the exposure but should
be performed as soon as the health care worker can
give informed consent for baseline testing.
o Start the prophylaxis medications within 2 hours after
exposure. Make sure that you are being monitored for
symptoms of toxicity. Practice safer sex until follow-up
testing is complete. Continue the HIV medications for
the full 4 weeks after exposure. The majority of HIV
exposures will warrant a combination of antiretroviral
agents.
o Follow up with postexposure testing at 1 month, 3
months, and 6 months, and perhaps 1 year.
o Document the exposure in detail for your own records
as well as for the employer.
Combinations that may be prescribed for postexposure
prophylaxis include:
1. zidovudine (ZDV)
2. lamivudine (3TC) or emtricitabine (FTC)
3. stavudine (d4T) and 3TC or FTC
4. tenofovir (TDF) and 3TC or FTC.
Lifecycle of HIV
HIV cannot replicate on its own, must enter and use CD4
mechanisms to make copies of itself
Madam Arcuino’s ppt:
1. HIV attachment
2. Fusing
3. Reverse transcription
4. Integration
5. Transcription
6. Translation
7. Assembly
8. Budding
From the book:
In this first step, the GP120 and GP41
glycoproteins of HIV bind with the host’s
Attachment uninfected CD4+ receptor and chemokine
coreceptors, usually CCR5, which results in
fusion of HIV with the CD4+ T-cell membrane.
Only the contents of HIV’s viral core (two
single strands of viral RNA and three viral
Uncoating
enzymes: reverse transcriptase, integrase, and
protease) are emptied into the CD4+ T cell.
HIV changes its genetic material from RNA to
DNA DNA through action of reverse transcriptase,
synthesis resulting in double-stranded DNA that carries
instruction for viral replication
New viral DNA enters the nucleus of the CD4+
T cell and through action of integrase is
blended with the DNA of the CD4+ T cell,
Integration resulting in permanent, lifelong infection. Prior
to this, the uninfected person has been only
exposed to, not infected with, HIV. With this
step, HIV infection is permanent
When the CD4+ T cell is activated, the double-
stranded DNA forms single-stranded
Transcription
messenger RNA (mRNA), which builds new
viruses.
The mRNA creates chains of new proteins and
enzymes (polyproteins) that contain the
Translation
components needed in the construction of new
viruses
The HIV enzyme protease cuts the polyprotein
Cleavage chain into the individual proteins that make up
the new virus.
New proteins and viral RNA migrate to the
Budding membrane of the infected CD4+ T cell, exit
from the cell, and start the process all over.

Stages of HIV Infection
 period from infection with HIV to the
development of HIV-specific antibodies
Stage 1
 characterized by high levels of viral replication,
–
widespread dissemination of HIV throughout the
Primary
Infection body, and destruction of CD4+ T cells, which
leads to dramatic drops in CD4+ T-cell counts
(normally 500 to 1,500 cells/mm3 of blood).
 occurs when CD4 T-lymphocyte cells are
between 200 and 499 and when the count drops
below 200 cells/mm3 of blood; at this point, the
person is considered to have AIDS. For
surveillance purposes, HIV disease progression
Stage 2 is classified from less to more severe; once a
case is classified into a surveillance severity
stage, it cannot be re-classified into a less
severe stage even if the CD4 T-lymphocytes
increase, which often occurs when a person
receives medications to treat HIV infection.
 classification has implications for services (e.g.,
disability benefits, housing, and food stamps),
because these programs are often linked to an
Stage 3 AIDS diagnosis. The CDC’s 2008 definition also
emphasizes CD4+ percentages, which are less
subject to variation on repeated measurements
than the absolute CD4+ T-cell count.
Assessment & Diagnostic Findings
 During the first stage of HIV infection, the patient may be
asymptomatic or may exhibit various signs and symptoms
such as fatigue or skin rash. Patients who are in later
stages of HIV infection may have a variety of symptoms
related to their immunosuppressed state.
Test Findings in HIV Infection
EIA (Enzyme Immunoassay) Antibodies are detected,
-a variant of this is called resulting in positive results
ELISA (enzyme-linked and marking the end of the
immunosorbent assay) window period
Western blot Also detects antibodies to
HIV
Used to confirm EIA
Viral load Measures HIV RNA in the
plasma
CD4 / CD8 These are markers found on
lymphocytes
HIV kills CD4+ cells, which
results in a significantly
impaired immune system
OraQuick In-home HIV test
Manifestatio
 The following are specific recommendations from the CDC
(2010b) that apply to testing for HIV infection:
o HIV screening is recommended for all persons
who seek evaluation and treatment for STIs.
o HIV testing must be voluntary and free of coercion.
Patients must not be tested without their
knowledge.
o HIV screening after notifying the patient that an
HIV test will be performed (unless the patient
declines) is recommended in all health care
settings.
o Specific signed consent for HIV testing should not
be required. In most settings, general informed
consent for medical care is considered sufficient to
encompass informed consent for HIV testing.
o The use of rapid HIV tests should be considered,
especially in clinics where a high proportion of
patients do not return for HIV test results.
o Positive screening tests for HIV antibody must be
confirmed by a supplemental test before the
diagnosis of HIV infection can be established.
o Providers should be alert to the possibility of acute
HIV infection and perform a viral load test in
addition to an antibody test for HIV, if indicated.
Persons suspected of recently acquired HIV
infection should be referred for immediate
consultation with an infectious disease specialist.
HIV Test Results: Implications
 Interpretation of Positive Test Results
o Antibodies to HIV are present in the blood (the
patient has been infected with the virus, and the
body has produced antibodies).
o HIV is active in the body, and the patient can
transmit the virus to others.
o Despite HIV infection, the patient does not
necessarily have AIDS.
o The patient is not immune to HIV (the antibodies
do not indicate immunity).
 Interpretation of Negative Test Results
o Antibodies to HIV are not present in the blood at
this time, which can mean that the patient has not
been infected with HIV or, if infected, the body has
not yet produced antibodies (window period—may
be between 3 weeks and 6 months).
o The patient should continue taking precautions.
The test result does not mean that the patient is
immune to the virus, nor does it mean the patient
is not infected; it just means that the body may not
have produced antibodies yet.
Clinical Manifestations
Shortness of breath
dyspnea (labored breathing)
Manifestations
cough
Respiratory
chest pain
fever
Symptoms are associated with various opportunistic
infections, such as those caused by P. jiroveci,
Mycobacterium avium-intracellulare,
cytomegalovirus (CMV), and Legionella species.
loss of appetite
Gastrointestinal Manifestations
nausea
vomiting
oral and esophageal candidiasis
chronic diarrhea
Gastrointestinal symptoms may be related to the
direct effect of HIV on the cells lining the intestines.
In patients with AIDS, the effects of diarrhea can be
devastating in terms of profound weight loss (more
than 10% of body weight), fluid and electrolyte
imbalances, perianal skin excoriation, weakness,
and inability to perform the usual activities of daily
living.
greater risk of developing certain cancers, including:
Oncologic
Kaposi’s sarcoma (KS)
lymphoma (especially non-Hodgkin lymphoma and
ns
primary CNS lymphoma)
invasive cervical cancer
profound effects on cognition
motor function
executive function
Neurologic Manifestations
attention
visual memory
visuospatial function
Neurologic dysfunction results from direct eʃects of
HIV on nervous system tissue, opportunistic
infections, primary or metastatic neoplasm,
cerebrovascular changes, metabolic
encephalopathies, or complications secondary to
therapy. Immune system response to HIV infection
in the CNS includes inflammation, atrophy,
demyelination, degeneration, and necrosis.
higher rates of depression
The causes of depression are multifactorial and may
include a history of preexisting mental illness,
Manifestations
Depressive
neuropsychiatric disturbances, and psychosocial
factors. Depression also occurs in people with HIV
infection in response to the physical symptoms,
including pain and weight loss, stigma, and the lack
of someone to talk with about their concerns.
People with HIV/AIDS who are depressed may
 experience:
irrational guilt and shame
loss of self-esteem
feelings of helplessness and worthlessness
suicidal ideation
tend to overestimate disability in their daily
functioning
KS
opportunistic infections (e.g. herpes zoster and
herpes simplex are associated with painful vesicles
that disrupt skin integrity)
Integumentary Manifestations
Molluscum contagiosum is a viral infection
characterized by deforming plaque formation.
Seborrheic dermatitis is associated with an
indurated, diffuse, scaly rash involving the scalp and
face.
Patients with AIDS may also exhibit:
a generalized folliculitis associated with dry, flaking
skin or atopic dermatitis, such as eczema or
psoriasis
patients treated with the antibacterial agent
trimethoprim–sulfamethoxazole (TMP-SMZ) develop
a drug-related rash that is pruritic with pinkish-red
macules and papules.
Medical Management
 Treatment of Opportunistic Infections:
o Despite the availability of antiretroviral
medications, opportunistic infections continue to
cause considerable morbidity and mortality for
three main reasons:
 (1) many patients are unaware of their
HIV infection and present with an
opportunistic infection as the initial
indicator of their disease
 (2) some patients are aware of their HIV
infection but do not take antiretroviral
agents because of psychosocial or
economic factors
 (3) others receive prescriptions for
antiretroviral medications but fail to attain
adequate virologic and immunologic
response as a result of issues related to
adherence, pharmacokinetics, or
unexplained biologic factors
o Laboratory tests should indicate immune function
has improved with initiation of ART, resulting in
faster resolution of the opportunistic infection. This
has been most clearly shown for opportunistic
infections for which effective therapy does not
exist, such as cryptosporidiosis, microsporidiosis,
and PML. These conditions may resolve or at
least stabilize after the institution of ART as well
as resolution of lesions of KS.
 Pharmacologic Therapy:
o REVERSE TRANCRIPTASE = Zidovudine,
Lamivudine
o INTEGRASE = Raltegravir
o PROTEASE = Ritonavir, Indinavir
alaryngeal communication: alternative modes of speaking that
do not involve the normal larynx; used by patients whose larynx
has been surgically removed
aphonia: impaired ability to use one’s voice due to disease or
injury to the larynx
apnea: cessation of breathing
dysphagia: difficulties in swallowing epistaxis: hemorrhage
from the nose due to rupture of tiny, distended vessels in the
mucous membrane of any area of the nose
herpes simplex (cold sore): a cutaneous viral infection with
painful vesicles and erosions on the tongue, palate, gingiva,
buccal membranes, or lips
laryngectomy: surgical removal of all or part of the larynx and
surrounding structures
laryngitis: inflammation of the larynx; may be caused by voice
abuse, exposure to irritants, or infectious organisms nuchal
rigidity: stiffness of the neck or inability to bend the neck
pharyngitis: inflammation of the throat; usually viral or bacterial
in origin
rhinitis: inflammation of the mucous membranes of the nose;
may be infectious, allergic, or inflammatory in origin
rhinitis medicamentosa: rebound nasal congestion commonly
associated with overuse of over-the-counter nasal
decongestants
rhinorrhea: drainage of a large amount of fluid from the nose
rhinosinusitis: inflammation of the nares and paranasal
sinuses, including frontal, ethmoid, maxillary, and sphenoid
sinuses; replaces the term sinusitis
tonsillitis: inflammation of the tonsils, usually due to an acute
infection
xerostomia: dryness of the mouth from a variety of causes
acute lung injury: an umbrella term for hypoxemic respiratory
failure; acute respiratory distress syndrome is a severe form of
acute lung injury
acute respiratory distress syndrome (ARDS): nonspecific
pulmonary response to a variety of pulmonary and
nonpulmonary insults to the lung; characterized by interstitial
infiltrates, alveolar hemorrhage, atelectasis, decreased
compliance, and refractory hypoxemia
asbestosis: diffuse lung fibrosis resulting from exposure to
asbestos fibers aspiration: inhalation of either oropharyngeal or
gastric contents into the lower airways
atelectasis: collapse or airless condition of the alveoli caused
by hypoventilation, obstruction to the airways, or compression
central
cyanosis: bluish discoloration of the skin or mucous
membranes due to hemoglobin carrying reduced amounts of
oxygen
consolidation: lung tissue that has become more solid in
nature due to collapse of alveoli or infectious process
(pneumonia) cor pulmonale: “heart of the lungs;” enlargement of
the right ventricle from hypertrophy or dilation or as a secondary
response to disorders that affect the lungs

empyema: accumulation of purulent material in the pleural
space
fine-needle aspiration: insertion of a needle through the chest
wall to obtain cells of a mass or tumor; usually performed under
fluoroscopy or chest computed tomography guidance
hemoptysis: the coughing up of blood from the lower
respiratory tract
hemothorax: partial or complete collapse of the lung due to
blood accumulating in the pleural space; may occur after
surgery or trauma
induration: an abnormally hard lesion or reaction, as in a
positive tuberculin skin test open
lung biopsy: biopsy of lung tissue performed through a limited
thoracotomy incision
orthopnea: shortness of breath when reclining or in the supine
position
pleural effusion: abnormal accumulation of fluid in the pleural
space
pleural friction rub: localized grating or creaking sound caused
by the rubbing together of inflamed parietal and visceral pleurae
pleural space: the area between the parietal and visceral
pleurae; a potential space
pneumothorax: partial or complete collapse of the lung due to
positive pressure in the pleural space pulmonary edema:
increase in the amount of extravascular fluid in the lung
pulmonary embolism: obstruction of the pulmonary
vasculature with an embolus; embolus may be due to blood clot,
air bubbles, or fat droplets
purulent: consisting of, containing, or discharging pus
restrictive lung disease: disease of the lung that causes a
decrease in lung volumes tension
pneumothorax: pneumothorax characterized by increasing
positive pressure in the pleural space with each breath; this is
an emergency situation, and the positive pressure needs to be
decompressed or released immediately
thoracentesis: insertion of a needle into the pleural space to
remove fluid that has accumulated and decrease pressure on
the lung tissue; may also be used diagnostically to identify
potential causes of a pleural effusion transbronchial: through the
bronchial wall, as in a transbronchial lung biopsy
ventilation–perfusion ratio (V./Q.): the ratio between
ventilation and perfusion in the lung; matching of ventilation to
perfusion optimizes gas exchange
acute coronary syndrome (ACS): signs and symptoms that
indicate unstable angina or acute myocardial infarction
angina pectoris: chest pain brought about by myocardial
ischemia
atheroma: fibrous cap composed of smooth muscle cells that
forms over lipid deposits within arterial vessels and protrudes
into the lumen of the vessel, narrowing the lumen and
obstructing blood flow; also called plaque
atherosclerosis: abnormal accumulation of lipid deposits and
fibrous tissue within arterial walls and the lumen
contractility: ability of the cardiac muscle to shorten in
response to an electrical impulse
coronary artery bypass graft (CABG): a surgical procedure in
which a blood vessel from another part of the body is grafted
onto the occluded coronary artery below the occlusion in such a
way that blood flow bypasses the blockage
high-density lipoprotein (HDL): a protein-bound lipid that
transports cholesterol to the liver for excretion in the bile;
composed of a higher proportion of protein to lipid than low-
density lipoprotein; exerts a beneficial effect on the arterial wall
ischemia: insufficient tissue oxygenation
low-density lipoprotein (LDL): a protein-bound lipid that
transports cholesterol to tissues in the body; composed of a
lower proportion of protein to lipid than high-density lipoprotein;
exerts a harmful effect on the arterial wall metabolic syndrome:
a cluster of metabolic abnormalities including insulin resistance,
obesity, dyslipidemia, and hypertension that increase the risk of
cardiovascular disease
myocardial infarction (MI): death of heart tissue caused by
lack of oxygenated blood flow
percutaneous coronary intervention (PCI): a procedure in
which a catheter is placed in a coronary artery, and one of
several methods is employed to reduce blockage within the
artery
percutaneous transluminal coronary angioplasty (PTCA): a
type of percutaneous coronary intervention in which a balloon is
inflated within a coronary artery to break an atheroma and open
the vessel lumen, improving coronary artery blood flow
stent: a metal mesh that provides structural support to a
coronary vessel, preventing its closure
sudden cardiac death: abrupt cessation of effective heart
activity
thrombolytic: a pharmacologic agent that breaks down blood
clots; alternatively referred to as a fibrinolytic
troponin: a cardiac muscle biomarker; measurement is used as
an indicator of heart muscle injury
allograft: heart valve replacement made from a human heart
valve (synonym: homograft)
annuloplasty: repair of a cardiac valve’s outer ring
aortic valve: semilunar valve located between the left ventricle
and aorta
autograft: heart valve replacement made from the patient’s own
heart valve (e.g., pulmonic valve excised and used as an aortic
valve)
bioprosthesis: heart valve replacement made of tissue from an
animal heart valve (synonym: heterograft)
cardiomyopathy: disease of the heart muscle
chordae tendineae: nondistensible fibrous strands connecting
papillary muscles to atrioventricular (mitral, tricuspid) valve
leaflets
chordoplasty: repair of chordae tendineae commissurotomy:
splitting or separating fused cardiac valve leaflets
heterograft: heart valve replacement made of tissue from an
animal heart valve (synonym: bioprosthesis)
homograft: heart valve replacement made from a human heart
valve (synonym: allograft)
leaflet repair: repair of a cardiac valve’s movable “flaps”
(leaflets)
mitral valve: atrioventricular valve located between the left
atrium and left ventricle
orthotopic transplantation: the recipient’s heart is removed
and a donor heart is grafted into the same site
prolapse(of a valve): stretching of an atrioventricular heart
valve leaflet into the atrium during systole
pulmonic valve: semilunar valve located between the right
ventricle and pulmonary artery regurgitation: backward flow of
blood through a heart valve
stenosis: narrowing or obstruction of a cardiac valve’s orifice
total artificial heart: mechanical device used to aid a failing heart,
assisting the right and left ventricles
tricuspid valve: atrioventricular valve located between the right
atrium and right ventricle valve replacement: insertion of a
device at the site of a malfunctioning heart valve to restore
blood flow in one direction through the heart
valvuloplasty: repair of a stenosed or regurgitant cardiac valve
by commissurotomy, annuloplasty, leaflet repair, or
chordoplasty (or a combination of procedures)
ventricular assist device: mechanical device used to aid a
failing right or left ventricle
absolute neutrophil count (ANC): a calculation of the number
of circulating neutrophils, derived from the total white blood cells
(WBCs) and the percentage of neutrophils counted in a
microscope’s visual field anemia: decreased red blood cell
(RBC) count aplasia: lack of cellular development (e.g., of cells
within the bone marrow)
cytokines: proteins produced by leukocytes that are vital to
regulation of hematopoiesis, apoptosis, and immune responses
erythrocyte: a cellular component of blood involved in the
transport of oxygen and carbon dioxide; (synonym: RBC)
erythroid cells: any cell that is or will become a mature RBC
erythropoietin: hormone produced primarily by the kidney;
necessary for erythropoiesis
haptoglobin: blood protein synthesized by liver; binds free
hemoglobin released from erythrocytes, which is then removed
by the reticuloendothelial system
hemolysis: destruction of RBCs; can occur within or outside of
the vasculature
hemosiderin: iron-containing pigment derived from the
breakdown of hemoglobin
hypochromia: pallor within the RBC caused by decreased
hemoglobin content leukemia: uncontrolled proliferation of
WBCs, often immature
lymphopenia: a lymphocyte count less than 1500/mm3
megaloblastic anemia: a type of anemia characterized by the
presence of abnormally large, nucleated RBCs
microcytosis: smaller-than-normal RBCs neutropenia: lower-
than-normal number of neutrophils normochromic: normal RBC
color, indicating normal amount of hemoglobin normocytic:
normal size of RBC
pancytopenia: abnormal decrease in WBCs, RBCs, and
platelets petechiae: tiny capillary hemorrhages
poikilocytosis: variation in shape of RBCs polycythemia:
excess RBCs reticulocytes: slightly immature RBCs, usually
only 1% of total circulating RBCs
spherocytes: small, spherically shaped erythrocytes
thrombocytopenia: lower-than-normal platelet count
thrombocytosis: higher-than-normal platelet count
allergen: substance that causes manifestations of allergy
allergy: inappropriate and often harmful immune system
response to substances that are normally harmless
anaphylaxis: rapid clinical response to an immediate
immunologic reaction between a specific antigen and antibody
angioneurotic edema: condition characterized by urticaria and
diffuse swelling of the deeper layers of the skin (i.e.,
angioedema)
antibody: protein substance developed by the body in response
to and interacting with a specific antigen
antigen: substance that induces the production of antibodies
antihistamine: medication that opposes the action of histamine
atopic dermatitis: type I hypersensitivity involving inflammation
of the skin evidenced by itching, redness, and a variety of skin
lesions
atopy: term often used to describe immunoglobulin E–mediated
diseases (i.e., atopic dermatitis, asthma, and allergic rhinitis)
with a genetic component
B cells: lymphocyte cells that are important in producing
circulating antibodies
bradykinin: a substance that stimulates nerve fibers and
causes pain
eosinophil: granular leukocyte erythema: diffuse redness of the
skin
hapten: incomplete antigen
histamine: substance in the body that causes increased gastric
secretion, dilation of capillaries, and constriction of the bronchial
smooth muscle
hypersensitivity: abnormal heightened reaction to a stimulus of
any kind
immunoglobulins: a family of closely related proteins capable
of acting as antibodies
leukotrienes: a group of chemical mediators that initiate the
inflammatory response mast cells: connective tissue cells that
contain heparin and histamine in their granules
prostaglandins: unsaturated fatty acids that have a wide
assortment of biologic activity
serotonin: chemical mediator that acts as a potent
vasoconstrictor and bronchoconstrictor
T cells: lymphocyte cells that can cause graft rejection, kill
foreign cells, or suppress production of antibodies urticaria:
hives
candidiasis: fungal infection, usually of skin or mucous
membranes, caused by Candida species
enzyme immunoassay (EIA): a blood test that can determine
the presence of antibodies to HIV in the blood or saliva; a
variant of this test is called enzyme-linked immunosorbent
assay (ELISA)
HIV-1: retrovirus isolated and recognized as the etiologic agent
of HIV disease HIV encephalopathy: clinical syndrome
characterized by a progressive decline in cognitive, behavioral,
and motor functions
immune reconstitution inflammatory syndrome (IRIS): a
syndrome that results from rapid restoration of pathogen-
specific immune responses to opportunistic infections Kaposi
sarcoma: malignancy that involves the epithelial layer of blood
and lymphatic vessels

latent reservoir: the integrated HIV provirus within the CD4+ T

cell during the resting memory state; does not express viral
proteins and is invisible to the immune system and antiviral
medications

Mycobacterium avium complex (MAC): opportunistic infection

caused by mycobacterial organisms that commonly causes a
respiratory illness but can also infect other body systems

opportunistic infection: illness caused by various organisms,

some of which usually do not cause disease in people with
normal immune systems peripheral neuropathy: disorder
characterized by sensory loss, pain, muscle weakness, and
wasting of muscles in the hands or legs and feet

Pneumocystis pneumonia (PCP): common opportunistic lung

infection; pathogen implicated is most commonly a fungus

polymerase chain reaction: a sensitive laboratory technique

that can detect and quantify HIV in a person’s blood or lymph
nodes

post-exposure prophylaxis (PEP): taking antiretroviral

medicines as soon as possible, but no more than 72 hours (3
days) after possible HIV exposure; two to three drugs are
usually prescribed which must be taken for 28 days.

pre-exposure prophylaxis (PrEP): prevention method for HIV

negative people who are at high risk of HIV infection; involves
taking a specific combination of HIV medicines daily; use with
condoms and other prevention tools.

progressive multifocal leukoencephalopathy: opportunistic

infection that infects brain tissue and causes damage to the
brain and spinal cord

retrovirus: a virus that carries genetic material in ribonucleic

acid (RNA) instead of DNA and contains reverse transcriptase

reverse transcriptase: enzyme that transforms single-stranded

RNA into a double-stranded DNA

viral load test: measures the quantity of HIV RNA or DNA in

the blood viral set point: amount of virus present in the blood
after the initial burst of viremia and the immune response that
follows

wasting syndrome: involuntary weight loss consisting of both

lean and fat body mass

HEPARIN = PROTAMINE SULFATE

WARFARIN = VIT. K
MAGNESIUM SULFATE = CALCIUM GLUCONATE
ASPIRIN = SODIUM BICARBONATE
THROMBOLYTICS = AMICAR