COPD NCLEX Review Notes

This is an NCLEX review for COPD (chronic obstructive pulmonary disease). Patients who have
COPD are experiencing limiting airflow and decrease elasticity of the aveolar sacs. COPD leads to
impaired gas, hyperinflation of the lungs, and other complications such as heart failure.

In the previous review, I covered other respiratory disorders of the respiratory system. So, if you are
studying for NCLEX or your nursing lecture exams be sure to check out that section.

When taking care of a patient with COPD it is very important the nurse knows how to recognize the
typical signs and symptoms seen in this condition, how it is diagnosed, nursing interventions, and
patient education.

Don’t forget to take the COPD quiz.

In this NCLEX review for COPD, you will learn the following:

 Definition of COPD
 Types of COPD
 Pathophysiology of COPD
 Complication of COPD
 Signs and Symptoms of COPD
 How COPD is Diagnosed
 Nursing Interventions for COPD
 Medications used to treat COPD
NCLEX Review on COPD
Definition: pulmonary disease that causes chronic obstruction of airflow from the lungs

Keys Point for COPD:

 Limited Airflow (due to thick and swollen bronchioles that have become deformed with
excessive sputum production and this narrows the airways)
 Inability to fully exhale (due to loss of elasticity of the alveoli sacs from damage and the sacs
start to develop air pockets)
 Irreversible once developed…cases vary among people from mild to severe…managed with
lifestyle changes and medications.
 Happens gradually….most people start to notice signs and symptoms middle-aged and will
present with dyspnea with activity they could normally tolerate, recurrent lung infections, chronic
cough etc.
 COPD is a term used as a “catch all” for diseases that limit airflow and cause dyspnea.
Types of COPD include:

 Emphysema “pink puffers”

  Chronic bronchitis “blue bloaters”
Pathophysiology of COPD
Normal breathing:

Inhaled oxygen travels down through the trachea which splits at the carina into bronchial tubes
starting with the primary bronchus then into smaller airways called secondary and tertiary bronchi
which divide into bronchioles and the oxygen goes into the alveolar sacs where gas exchange
happens. As the alveoli inflate and deflate with ease, inhaled oxygen attaches to the red blood cells
and carbon dioxide enters the respiratory system to be exhaled.

What happens in breathing with COPD?

In conditions such as chronic bronchitis “blue bloaters”:

The name “blue bloaters” is due to cyanosis from “hypoxia”

and bloating from edema AND increase in lung volume. The
bloating is from the effects of the lung disease on the heart
which causes right-sided heart failure.

In chronic bronchitis, the bronchioles become damaged that

leads them to be thick and swollen and deformed. This is
accompanied by more sputum production. This limits the
ability of the person being able to completely exhale the air
taken in. So, when they take another breath in, it will
increase the air volume even more (because they have
retained air from the previous breath), and this leads to
hyperinflation.

Also, less oxygen is getting into the blood and more carbon dioxide is staying in the blood. This leads
to low blood levels and high carbon dioxide levels. Patients will have cyanosis due to a
decreased oxygen level. To compensate, the body increases RBC production and cause blood to
shift elsewhere which increases pressure in the pulmonary artery leading to pulmonary
hypertension. Pulmonary hypertension leads to right-sided heart failure (which is why you will start
to see bloating..edema in the abdomen and legs)

In conditions such as emphysema “pink puffers”:

The name comes from hyperventilation (puffing to breathe) and pink complexion (they maintain a
relatively normal oxygen level due to rapid breathing) rather than cyanosis as in chronic bronchitis.

In emphysema, the alveoli sacs lose their ability to inflate and deflate due to an inflammatory
response in the body. So, the sac is unable to properly deflate and inflate. Inhaled air starts to get
trapped in the sacs and this causes major hyperinflation of the lungs because the patient is retaining
so much volume.

Hyperinflation causes the diaphragm to flatten. The diaphragm plays a huge role in helping the
patient breathe effortlessly in and out. Therefore, in order to fully exhale, the patient starts to
hyperventilate and use accessory muscles to get the air out now. This leads to the barrel chest
look and during inspect it may be noted there is an INCREASED ANTEROPOSTERIOR DIAMETER.
The damage in the sacs cause the body to keep high carbon dioxide levels and low blood oxygen
levels. Inhaled oxygen will not be able to enter into the sacs for gas exchange and carbon dioxide
won’t leave the cells to be exhaled.

The body tries to compensate by causing hyperventilation (increasing the respiratory rate…hence
puffer) and the patient will have less hypoxemia “pink complexion” than chronic bronchitis who have
the cyanosis because pink puffers keep their oxygen level just where it needs to be from
hyperventilation.

Signs & Symptoms of COPD

Remember: Lung Damage

Lack of energy

Unable to tolerate activity (shortness of breath)

Nutrition poor (weight loss) due to energy used breathing especially with emphysema

Gases abnormal (high PCO2 >45 and low PO2 <90)..respiratory acidosis

Dry or productive cough constant (productive with chronic bronchitis)

Accessory muscle usage during breathing, Abnormal lung sounds: diminished, coarse crackles
(chronic bronchitis) or wheezing

Modification of skin color from pink to cyanosis in lips, mucous membranes, nail beds (“blue bloaters”)

Anteroposterior diameter increased (barrel chest)….emphysema “pink puffers”

Gets in the Tripod Position during dyspnea (stands leaning forward while supporting body with hands
on knees or an object)

Extreme dyspnea

In turn over time, people with COPD will be stimulated to breathe due to low oxygen levels
RATHER than high carbon dioxide levels.

Complications of COPD
 Heart Disease (remember heart and lungs work together in replenishing the body with oxygen)
…heart failure
 Pneumothorax (spontaneous due to forming of air sacs)
 Risk for Pneumonia
 Cancer (especially lung)
How is COPD Diagnosed?
Spirometry: A test where a patient breathes into a tube that measure how much volume the lungs
can hold during inhalation and how much and fast air volume is exhaled.
  Measuring the FVC (Forced Vital Capacity): a low reading shows restrictive breathing….it
measures the largest amount of air a person exhales after breathing in deeply in one second.
 Forced Expiratory Volume: measures how much air a person can exhale within one second. A
low reading shows the severity of the disease.
Nursing Interventions for COPD
Monitor Respiratory System:

 Assess lung sounds (may need suction) and sputum production…obtain a culture if ordered…at
risk for pneumonia
 Keep oxygen saturation (88%-93%) why between this range?

 Patients with COPD are stimulated to breathe due to LOW OXYGEN SATURATION rather
than high carbon dioxide levels….which is the opposite for people for healthy lungs. If they
are given too much oxygen it will reduce their need to breathe…causing hypoventilation
and carbon dioxide levels will increase to toxic levels.
 Given oxygen as prescribed in low amounts 1-2 liters
 Monitor effort of breathing and teach about pursed-lip and diaphragmatic breathing
 Pursed-lip breathing: used for when patient starts to get dyspneic. This technique increases
the oxygen level and encourages them to breath out longer (remember these patient don’t fully
exhale very well). It is similar to like blowing out a birthday candle.
 Diaphragmatic breathing: uses abdominal muscles for breathing rather than accessory
muscles
 helps make diaphragm stronger which is weak
 slows down breathing rate to allow breathing to be easier
 decreases energy used to breathe
 used along with pursued breathing technique
 Administering breathing treatments as needed: bronchodilators, nebulizer etc. Respiratory
therapy helps play a role in this as well (medications are discussed in more detail below)
Patient Education for COPD
 Nutrition needs: eating high calorie, protein rich meals that are small but frequent and staying
hydrated if not contraindicated….avoid large heavy meals due to compression on the lungs from
the stomach
 Avoiding sick people, irritants, hot humid (smothering) or very cold weather
 Stop smoking or being around people who smoke
 Vaccination up-to-date: annual flu shot and Pneumovax every 5 years because it is very hard
for people with COPD to recover from illnesses
 Pursed lip and diaphragmatic breathing techniques
 Administering medications: be familiar with groups, side effects, and patient teaching
Medication Regime for COPD
Remember the mnemonic: Chronic Pulmonary Medications Save Lungs

Corticosteroids: decreases inflammation and mucous production in airway… given: oral, IV, inhaled
and used in combination with bronchodilator like:

 Symbicort: combination of steroid and long acting bronchodilator

 Other corticosteroids: Prednisone, Solu-medrol, Pulmicort
 Side effects: easy bruising, hyperglycemia, risk of infection, bone problems (long term use)

 Patient education: rinse mouth after using inhaled corticosteroids…can develop thrush,
use corticosteroid inhaler AFTER using bronchodilator inhaler
Methylxanthines: Theophylline (most commonly given orally) type of bronchodilator used long term in
patients who have severe COPD

 Remember: Narrow therapeutic range of 10 to 20 mcg/mL

 Increases risk for digoxin toxicity and decreases the effects of lithium and Dilantin
Phosphodiestrace-4 inhibitors: “Roflumilast” used for people who have chronic bronchitis and it
works by decreasing COPD exacerbation…not a bronchodilator

 Side effects: can cause suicidal thoughts (remember the word “last” in the drug’s name…it
could be the patient’s last days if they are not assessed for this side effect) and can cause
weight loss.
Short-acting bronchodilators: relaxes the smooth muscle of the bronchial tubes and are used in
emergency situations where quick relief is needed

 Albuterol (beta 2 agonist) and Atrovent (anticholinergic)

Long-acting Bronchodilators: relaxes the smooth muscle of the bronchial tubes (same as short-acting
bronchodilators BUT their effects last longer) used over a longer period of time….taken once or twice
a day

 Beta 2 agonist: salmeterol, anticholinergics: Spiriva

 Patient education: let them know which drug is short and long-acting, how to use inhaler and to
use bronchodilator inhaler BEFORE steroid inhaler (wait 5 minutes in between)

 WHY? TO OPEN UP THE AIRWAYS SO THE STEROID CAN GET IN THERE AND DO
ITS JOB
 Side effects of beta 2 agonist: increased heart rate, urinary retention
 Side effects of anticholinergic: dry mouth, blurred vision
sthma NCLEX Lecture
What is it? Asthma is a chronic lung disease (no cure) that causes narrowing and inflammation of the
airways (bronchi and bronchioles) that leads to difficulty breathing.

How does it happen?

First, let’s talk about what should happen

normally with breathing! Normally, when
you breathe in air, it travels down
through your upper airway to your lower
airway, which is the trachea, bronchi,
bronchioles, and alveoli (where gas
exchange happens). The oxygen you
breathe in crosses over into your blood
stream and the carbon dioxide in your
blood crosses over into the airway to be
exhaled.

What is happening in patients with

asthma?

In patients with asthma, the bronchi and

bronchioles are chronically
inflamed and can become so inflamed
that it leads to an asthma attack. This
will cause the patient to experience
wheezing, chest tightness, shortness of
breath, and coughing. An asthma attack
occurs due to a trigger of some type
(discussed later).
Key Players of an Asthma Attack:

Bronchi and Bronchioles

 What surrounds these structures? Surrounding the bronchi and bronchioles are smooth
muscles that wrap around the airway. This muscle helps with dilating and constricting the
airway.

 During an asthma attack, these smooth muscles constrict. This causes chest
tightness and difficulty breathing.
 What is inside these structures? Inside these structures is a mucosa lining which contains
special cells called goblet cells. Goblet cells produce mucous, which helps trap the irritants and
bacteria we breathe in and prevent these substances from entering further into our respiratory
system.
 During an asthma attack, the mucosa becomes very inflamed (this narrows the
airway…decreasing air flow and air becomes trapped in the alveoli). The goblet
cells (due to the inflammatory response) produce excessive amounts of mucous.
Hence, leading to further decrease in air flow: coughing, wheezing (as air tries to
flow through the narrow airway and around the mucous it makes a musical
whistling sound).
 During this, air is becoming trapped in the alveoli . Therefore, gas exchange is not taking
place and low amounts of oxygen are entering the blood (the patient will have decreased
oxygen saturation) and carbon dioxide is staying in the blood (patient will have the buildup
of CO2…..respiratory acidosis). The patient will feel like they can’t exhale all the way.
Now asthma attacks vary in severity among patients. It is important for the patient to recognize
the triggers and early signs and symptoms of a pending asthma attack (discussed below).
These early signs and symptoms are different for every patient, but as the nurse you will need to
teach the patient how to recognize them. They will usually have these signs and symptoms 1 to 2
days before an attack. In addition, the patient will need to follow an asthma action plan created by the
MD and the patient.

What is an asthma action plan? It is a plan created to help the patient control their asthma based
on the patient’s current signs and symptoms, along with using a peak flow meter. The asthma action
plan has three zones (green, yellow, and red) and based on the patient’s signs and symptoms, they
will treat their asthma with the prescribed medications. See a sample action plan below.

The cause of asthma is unknown (may be genetic or environmental) but certain “triggers” can lead to
an asthma attack:

What can trigger asthma?

 Environment: smoke, pollen, pollution, perfumes, dander, dust mites, pests (cockroaches), cold
and dry air, mold
 Body Issue: respiratory infection, GERD, hormonal shifts, exercise-induced
 Intake of Certain Substances: drugs (beta adrenergic blockers that are nonselective), NSAIDS,
aspirin, preservatives (sulfites)
How is it diagnosed? pulmonary function test (PFT)

Another thing is to educate the patient about early warning signs:

 starting to become short of breath easily

 easily fatigued with physical activity
 frequent coughing (mainly at night) and trouble sleeping at night
 symptoms similar to a cold: sneezing, scratchy throat, tired, headache
 irritable
 wheezing with activity
 reduced peak flow meter reading
Signs and Symptoms of Asthma Attack
 Chest Tightness
 Wheezing (auscultate…expiratory wheezing and can program to inspiration in severe cases)
 Coughing
 Difficulty Breathing (***especially exhaling)
 Increased respiratory rate
Can progress to: where rescue inhaler won’t work, can’t talk easily, chest retractions (stomach
sucked in, chest sticking out along with collarbone with each breath…this means the patient is not
getting enough air into the lungs), cyanosis of the lips and skin, sweaty…need medical intervention
fast!!

Nursing Interventions for Asthma

Presenting with an asthma attack:

 Baseline vital signs

 Keep patient calm and comfort the patient
 Position in high Fowler’s to help with ease of breathing
 Administer bronchodilators as ordered by MD
 Administer oxygen (oxygen saturation 95-99%)
 Assess peak flow meter reading (watch for numbers less than 50% of the patient’s personal
best reading)
 Auscultate lung sounds throughout: (decrease in wheezing?….patient breathing easier?
respiratory rate normal?)
 Monitor skin color and for any retractions of the chest, can they talk to you with ease now or is it
still difficult for them to talk?)
 Current peak flow meter reading numbers (if the patient uses this device…ask patient (if they
know) their personal best reading and current readings, and medications they’ve taken
What is a Peak Flow Meter: it shows how controlled a patient’s asthma is and if it is getting worse
(lets a patient know if an attack is pending…several hours to days before one)

How does the patient use a peak flow meter? As represented in the picture above, the patient will
exhale as hard as they can onto the device. The device will then measure how much air was exhaled
out of the lungs.

 Many times a peak flow meter is used with an asthma action plan created with MD. As stated
above, the device measures the airflow out of the lungs (large airways) not small (so the patient
needs to know early warning signs too). It helps the patient know when they need to take a
short-acting bronchodilators and when they should go to the hospital for treatment.
 When a patient starts using a peak flow meter, they need to FIRST figure out their personal
best peak flow meter reading. This will be the highest number reached over a period of time.
 It will be the number used to compare against other reading numbers, which will allow the
patient to know if their asthma is under good control.

 How is the personal best peak flow meter reading figured out? The patient will use the
peak flow meter to figure out their best peak flow reading when their asthma is under
good control, and measure it once in the morning and once at night for 3 weeks
usually and record the numbers BEFORE TAKING MEDICATION. The highest number
they obtain over this period of time will be their personal best reading.
 Then they will need to continue to use the peak flow meter at the same time every day, either in
the morning or at night BEFORE TAKING MEDICATION, and compare it with the personal best
reading. If the reading is 80% or less than their personal best, they need to follow the action
plan created with their doctor.
You will be providing them with education on how to follow their prescribed asthma action plan (quiz
the patient to ensure they understand how to follow the plan).

Help the patient identify triggers (educate them on the triggers), how to avoid (except exercise-
induced) and those early warning signs.

What if a trigger is exercised-induced? The patient doesn’t need to quit exercising (important for
overall health). To help decrease the chances of an attack they can:

 warm up before exercising for 10-15 minutes

 administer short acting beta agonists before exercising
 breathe through nose instead of mouth during cold windy days to warm the air before it enters
the lungs (cold air can make the smooth muscles around the airway constrict)
 avoid exercising when sick with a respiratory illness
Medications used to treat Asthma
Bronchodilators: opens the airways to increase air flow….different types

Bronchodilators types used for Asthma: Beta-agonists* and Anticholingerics*, Theophylline

*commonly given as inhaled routes for asthma…theophylline is oral

Short-acting beta agonist (Albuterol):

 inhaler or nebulizer: used as the fast acting relief during an asthma attack or prior to
exercise for asthma that is exercise-induced NOT for daily treatment
 ***(if patient is using their inhaler more than 2 times a week, then the patients asthma plan
needs to be readjusted because their asthma is not under good control).
Long-acting beta agonists (Salmeterol, Symbicort…this drug is a combination of a long-acting beta
agonist AND corticosteroid):

 NOT for an acute asthma attack

****Side effects of these medications: tachycardia, feeling nervous/jittery, monitor heart rhythm for
dysrhythmia
Anticholinergics:

 Ipratropium: a bronchodilator that also is short-acting and relaxes airway….used when a

patient can’t tolerate short-acting beta agonist.
 Tiotropium: a bronchodilator that is long-acting
 These drugs can cause dry mouth….. “sugarless candy helps with this”
Theophylline: given PO

 not as common because of possible toxicity and maintaining blood levels of 10-20 mcg/mL
 AVOID consuming products with caffeine while taking this medication…WHY? Caffeine has the
same properties as Theophylline, which can increase the toxic effects of the medication.
*****Always administer the bronchodilator FIRST and then 5 minutes later the corticosteroid.

If not responding to treatment, may need intubation and mechanical ventilation.

Anti-inflammatories: decreases swelling and mucus production…used as long-term treatment to

control asthma not an acute attack.

Anti-inflammatories used to treat asthma include: “Corticosteroids, Leukotriene Modifiers,

Immunomodulators, Cromolyn”

Inhaled corticosteroids: “Fluticasone”, “Budesonide”, “Beclomethasone”

 watch for thrush (use spacer with inhaler and rinsing mouth after administration)
 risk for osteoporosis and cataracts (cloudy lens on the eyes)
 May be given IV or PO for severe asthma attack.
Leukotriene Modifiers (oral): “Montelukast”

 blocks the function of leukotriene which causes the smooth muscle on the airways to constrict
and plays a role in mucus production. When this function is blocked it leads to the relaxation of
the smooth muscle and decreased mucous production…NOT for an acute attack
Immunomodulator (subq): “Omalizumab”

 blocks the role of the immunoglobulin IgE, which will decrease the allergic response…hence
asthma attacks
 given subcutaneously
 used when patient’s asthma is poorly controlled and other treatments are not working
 NOT used as a quick relief
 NO LIVE vaccines while receiving
Nonsteroidal Anti-Allergy: “Cromolyn” (inhaled)

 long term use….not for quick relief in emergency situations

 stops mast cells from secreting histamine. This decreases inflammation.
  While receive the patient may temporarily experience sneezing, burning in nose, itchy/watery
eyes, bad taste in mouth.
ARDS NCLEX Review
What is ARDS (acute respiratory distress syndrome)? It’s a type of respiratory failure that occurs
when the capillary membrane that surrounds the alveoli sac becomes damaged, which causes fluid to
leak into the alveoli sac.

Result? Impaired gas exchange! Gas exchange doesn’t occur properly due to many reasons, such
as: fluid in the alveoli sac, collapsed alveoli sacs, and a decrease in lung compliance (hence the
lungs are becoming less elastic….”stiff”).

This will lead to oxygen not being able to cross the alveolar capillary membrane to go back in the blood to
oxygenate it, which will result in hypoxemia. In turn, the organs of the body will suffer due to this and death
can occur if treatment does not happen. In majority cases of ARDS, the patient will need respiratory assistance
via a ventilator with PEEP (discussed in detail below).

Quick Facts about Acute Respiratory Distress Syndrome (ARDS)

 It has a fast onset!

 It tends to occur in people who are already sick (hospitalized) and develops as a complication.
For example, a patient who has experienced severe burns is at risk for ARDS due to the
systemic inflammation present in the body.
 ARDS has a high mortality rate!
What can cause the capillary membrane to become more permeable and leak fluid? Usually
events that lead to major systemic inflammation in the body, which can be indirectly damage the
capillary membrane or directly damage the capillary membrane.

Indirect vs. Direct Injury to the Capillary Membrane

Indirect (source isn’t the lungs): the capillary membrane is INDIRECTLY damaged. There is a
systemic inflammatory response system (SIRS) by the immune system.

Common Causes:

 *Sepsis (most common and there is a very poor prognosis if the patient has a gram-negative
bacteria)
 Burns
 Blood transfusion (multiple)
 Inflammation of the pancreas (pancreatitis)
 Drug overdose
Direct (source is the lungs)….capillary membrane is DIRECTLY damaged

 Pneumonia
 Aspiration
 Inhaling a toxic substance
  Significant drowning event
 Embolism
How it happens? Pathophysiology: Phases (varies on severity…this is worst case scenario)

Exudative Phase: occurs about 24 hours after injury to the lung (directly or indirectly)

What happens during this phase?

 Damage to the capillary membrane that leads to pulmonary edema. This causes the leaking of
fluid, proteins, and other substances into the interstitium and then into the alveoli sac. It is very
important to note this fluid contains a LOT of protein. Significance? Remember proteins regulate
water pressure, oncotic pressure! So, if the fluid is high in protein it’s going to draw even MORE
fluid into the interstitium and then the alveoli sac.
 Cells that produce surfactant become overwhelmed and damaged.

 Role of surfactant: decreases surface tension in the lungs. In other words, the alveoli sacs
stay stable. Therefore, when a person exhales the sac does NOT collapse.

 A decrease in surfactant creates an unpredictable alveoli sac that can easily

collapse. This leads to:

 ATELETASIS will occur (collapse of the lung tissue)

 To make matters worse: a membrane that is made up of dead cells and other
substances start to collect on the alveoli. This is called a hyaline membrane. This
membrane will continue to develop in the next phase and will cause the lungs to
become LESS elastic and can further impair gas exchange!
End Result? With all the fluid in the alveoli sac (pulmonary edema), development of a hyaline
membrane, collapsing of the sacs, decreased surfactant = inadequate ventilation where alveoli sacs
are NOT getting enough air (leading to V/Q mismatch) AND a hallmark sign and
symptom: REFRACTORY HYPOXEMIA

Refractory hypoxemia is where the patient will maintain a low blood oxygen level even though
they are receiving high amounts of oxygen!

Early: Due to all this the patient will experience an increase in breathing (still have hypoxemia).
WHY? The body is trying to increase the oxygen level, but it won’t be able to! This will cause the
patient to blow off too much carbon dioxide (CO2 can still cross the membrane but O2 can’t)
….respiratory ALKALOSIS will develop BUT in the late phase (as the patient progresses to the
2nd and 3rd phases (late), carbon dioxide levels start to rise. This is because the hyaline membrane
continues to develop leading to carbon dioxide not being able to cross over to be exhaled, and the
patient will no longer be able to maintain breathing due to weak respiratory muscles. Respiratory
acidosis will start to develop later on.

Proliferative Phase: occurs about 14 days after the injury (grow or reproduce new cells quickly)

 repair structures, fluid in the sac is reabsorbed, but lung tissue becomes very dense and
fibrous….lung compliance and hypoxemia becomes even worse
Fibrotic Phase: occurs about 3 weeks after injury….major fibrosis of the lung tissue, decreases lung
compliance and hypoxemia with dead space filling the lungs.

Patients who enter the fibrotic phase will have major lung damage and poor recovery.

Pathophysiology of ARDS in a Nutshell

Atelectasis (alveolar sac fill with fluid and collapse…pulmonary edeam)

Refractory Hypoxemia

Decrease in lung compliance (lung aren’t as elastic or stretchable….hyaline membrane develops)

Surfactant cell damaged (decrease in surfactant production)

Signs and Symptoms of ARDS

In the very early phase: sign and symptoms are hard to detect. At first the fluid is leaking in the
interstitum so lung sounds may be normal or random a crackle here or there. But as it progresses the
patient will have difficulty breathing and be “air hunger”. There will be an increased respiratory rate,
low oxygen in the blood and respiratory alkalosis.

Then as time goes on:

 Symptoms of full respiratory failure: tachypnea, difficulty breathing, major hypoxemia even
though receiving a high about of oxygen (refractory hypoxemia), cyanosis, low oxygen
saturation, mental status change (tired, confused), tachycardia, chest retractions, decrease lung
compliance, lung sound: crackles throughout, low Pao2, high PaCo2 x-ray with white-out of
bilateral lung infiltrates

Nursing Interventions for ARDS (acute respiratory distress syndrome)

Maintain airway/respiratory function:
Most patients with ARDS will need: mechanical ventilation with PEEP (positive end-expiratory
pressure)

 The patient will need high amounts of PEEP because of the collapsed sacs, stiffening of the
lung, and pulmonary edema. Usually the pressure is anywhere from 10 to 20 cm of water. This
high amount of pressure will open the sacs, improve gas exchange, and help keep them clear of
fluid.

 Nurse: high PEEP can cause issues with intrathoracic pressure and decrease cardiac
output (watch out for a low blood pressure) along with hyperinflation of the lungs
(possible pneumothorax or subq emphysema…this is where air escapes into skin from a
lung leaking air)
Monitoring ABGs

Positioning to help with respiratory function:

Prone Positioning: turning the patient from supine to prone (putting the patient on their belly)

 This helps improve oxygen levels without actually giving the patient a high concentration of
oxygen! Remember in this position the heart will shift forward and not compress the back of the
lungs and it will help drain areas of the lungs that normally can’t be drained in the supine
position. So, this will:

 Help with perfusion and ventilation (helping with correcting the V/Q mismatch)
 Help move secretions from other areas that were fluid filled and couldn’t move in the
supine position
 Help improve atelectasis.
How does the MD know if this is pulmonary edema caused by a cardiac issue like heart
failure or due to a leaking capillary membrane? A pulmonary artery wedge pressure can help
with that!

 This is where a pulmonary catheter with a balloon is inserted into the pulmonary arterial branch

 If the reading is less than 18 mmHg it indicates ARDS, but if it’s greater than this number it
indicates a cardiac problem.
Assessing other systems of the body to make sure they are getting enough oxygen: mental status,
urine output, heart (blood pressure and cardiac output with PEEP)

Preventing complications: pressure injury, blood clots, infection related to ventilator, nutrition,
pneumothorax

Administering drugs: corticosteroids (help with inflammation), antibiotics (preventing and treating
infection), fluids colloids or crystalloids solutions if cardiac output decreased along with drugs like that
have an inotropic effect (helps with heart muscle contraction), GI drugs for stress ulcers
Cystic Fibrosis NCLEX Review
What is cystic fibrosis? It’s a genetic
disorder that causes the EXOCRINE
glands to work incorrectly. This leads to
some major complications that can affect
the respiratory (both upper/lower),
digestive (pancreas, liver, intestines),
integumentary, and reproductive systems.

What are exocrine glands? These are

glands that produce and transfer it’s
secretions (ex: mucous, tears, sweat,
digestive enzymes) via DUCTS to its
intended area of the body rather than
directly into the bloodstream like endocrine
glands.

In cystic fibrosis, a gene that makes up the

exocrine glands is mutated and this prevents the exocrine glands from working properly. The gene
that is mutated is called the CFTR gene!

The CFTR gene, which stands for cystic fibrosis transmembrane regulator, is a protein that
controls the channels of sodium and chloride. In other words, it controls the sodium and water
transport in and out of the cell.

Therefore, these channels that are within the membrane of exocrine cells that makes our sweat,
mucous, tears, and digestive enzymes don’t work properly. So, the substances produced by the
exocrine glands don’t look and work like they are supposed to.

For example: How is mucous supposed to be? Thin and slippery which helps lubricate the
structures. However, this is the problem in patients with cystic fibrosis.

 In patients with CF the mucous is THICK and STICKY (rather than thin and slippery) and
this affects the following structures:

 Lungs (upper and lower):

 upper sinuses and formation of polyps (leading to snoring, nasal stuffiness)

 blockage of the airways: overtime leads to obstructive pulmonary diseases
like emphysema …..air trapping can occur which causes hyperinflation

 Or bleds can develop and rupture leading to a pneumothorax

 Pulmonary hypertension which can lead to heart failure in the long term
 Clubbing of the nails due to the lack of oxygen in the blood
 Hemoptysis: coughing up blood either due to infection or severe damage to
lung tissue (mainly in older patients rather than children)
 Very susceptible to lung infections that can create permanent damage to the
lungs
 Thick, sticky mucous creates perfect conditions for bacteria to thrive and
survive! These patients are at risk for pseudomonas aeruginosa,
staphylococcus aureus etc.

 There is a risk of the development of antibiotic resistance or allergies to

antibiotics, which can make treating the infection very hard.
 Gastrointestinal (blockage of passage ways within the body)
 Pancreas (this structure makes pancreatic enzymes):

 PAL: protease, amylase, lipase: These substances are secreted

via the pancreatic duct into the duodenum and this helps digest
proteins, fats, and vitamins.
 However, these enzymes are not accessible for proper usage
because of the mucous blocking the pancreatic duct. Hence, they
will stay in the pancreas and this inflames the structure and can
cause fibrosis of the pancreas. In addition, the patient can
develop cystic fibrosis related diabetes. Therefore, when a
patient is not receiving pancreatic enzymes they will experience:

 weight loss, malabsorption, nutrition major issue, delayed

puberty, GREASY, ODOROUS STOOL, BLOATNG,
ABODOMINAL PAIN
 Many patients will need a feeding tube to help with
nutrition, PANCREATIC ENZYMES SUPPLEMENTS, fat-
soluble vitamins like D E A K
 Liver: mucous blocks biliary ducts which causes the bile to become
thick and gallstones can develop along with gallbladder
inflammation.
 Distal Intestinal Obstruction Syndrome (DIOS): blockage
in the intestine….intestines can also make thick mucus like
the lungs and pancreas and when thick mucus and stool get
together it can lead to a blockage in the gut.

 Meconium ileus (infants): sticky meconium becomes

stuck in the ileum of the intestine
 Infertility in males and females: most people who have cystic
fibrosis are unable to have children because of the thickness
of mucous. For example, women have troubling conceiving
because the cervical mucous is not friendly towards sperm,
and males tend to be sterile because there are issues with the
vas deferens duct that helps sperm go for the testicle to the
urethra (thick mucus blocking it or the duct is not formed
correctly).
 Integumentary: sweat glands produce too much salt.
Therefore, the sweat/tears are very salty. The patient is at risk
for electrolyte complications and dehydration. However, the
salty sweat is helpful with diagnosing CF (sweat chloride test).
Quick Facts about Cystic Fibrosis:
 Most common is Caucasians and males, but can affect any race or gender.
 NIH (National Institute of Health) statistics: life expectancy in 1960 was age 10. Today the
median life expectancy is age 37 (“NIH Fact Sheets – Cystic Fibrosis”, n.d.).
 This is most commonly detected during the 1st year of life…child will have GI and respiratory
issues (ex: infant may have a meconium ileus).
 Severity depends (not all patients are 100% alike in their severity)
 It’s an autosomal recessive disorder….which means the child had to receive one mutated
gene from both parents. In most cases, the parents are carriers of the disease but don’t have
symptoms of CF.

 Diagnosed: Sweat Test: painless test that measures the amount of salt in the sweat

 Pilocarpine and electric current is applied to the skin to help it sweat (usually on the arm).
A gauze is used to collect the sweat which is sent to a lab to measure the salt in the sweat

 Results:

 39 mmol/L or less negative for cystic fibrosis

 40 to 59 mmol/L needs further testing, not conclusive
 60 mmol/L or more POSITIVE for cystic fibrosis
Nursing Interventions and Treatments for Cystic Fibrosis
Nursing Focus: Mucous, Nutrition, Treatment for infection (most patients will die due to a lung
infection or issue of some type), preventing blockages in GI system

Patients who have CF are on a wide variety of medications like the following:

 stool softeners
 pancreatic enzymes
 nasal sprays
 vitamins
 antibiotics
 anti-inflammatories (inhaled or oral)
 mucolytics (oral or nebulizer)
 bronchodilators (oral or inhaled)
Mucous: Huge part of the everyday routine treatment and this includes: Chest PT, postural drainage,
using PEP devices and nebulizers along with huff coughing

 Chest physiotherapy (Chest PT): helps drain the airways of that thick sticky mucous

 It is done with postural drainage along with percussion and vibration to facilitate the
draining of mucous from the lung lobes followed by huff coughing (THIS IS A HUGE
PART OF treatment for CF patients!!!!)
Chest PT: percussion (cupping hands and percussing of the over the lung fields and take special care
when percussing over spine, stomach, breast bone, organs to avoid injury), some patients use
vibration with a special vest and then huff coughing is performed

**Patient usually performs this 2-4 times per day or more depending on if they are fighting a lung
infection. Sessions vary: 20 minutes to an hour.

TEST!!! When should you perform chest PT on a patient? Perform when the stomach is empty to
prevent reflux of food and vomiting……1-2 hours after meals (hence in between meals). NOT after
(reason: regurgitation) or before (reason: risk of decreasing the appetite because coughing up thick
sticky mucous can taste bad which can decrease a person’s appetite).

Airway Clearance devices: PEP (positive expiratory pressure): Helps with clearing the airway

 PEP devices: assists with moving mucous from the lungs…..person breathes in and out of
device (resistance when breathing out and this helps even more to move mucous)….creates a
vibration (performs several times) and then huff cough to expel mucous. Device names: Flutter
valve or Acapella
Prevent infection: wearing a mask due flu times or when sick, hand hygiene, avoid sick people, and
stay up-to-date with vaccinations, lung transplant possible if lung problems severe

Exercise: regular aerobic exercise to help keep lungs healthy and clear secretions. Educate to
monitor sweating because of the risk of losing too much salt (may need salt supplements and
increase caloric needs when exercising)
GI: pancreatic enzymes, fat-soluble vitamins, high calories, high protein and high fat diet

Pancreatic enzymes:

TEST!!! Swallow them! Don’t chew or crush them! If person can’t swallow the capsule, you can open
it and put it in an ACIDIC FOOD like apple sauce. Do not mix in an alkaline-based food like yogurt,
pudding or ice cream because this will inactive the enzyme.

How do you know the patient is receiving an adequate amount of enzymes? The patient’s stool is
NOT greasy or odorous and they are free from abdominal bloating or pain.

TEST!!! When would you administer these enzymes? Administer before all meals and snacks.
Example of these enzymes are: Pancrelipase, Pancreatin

Some patients have feeding tubes because their caloric intake is very high, especially during illness
or during the late stages of the disease. High protein and high calorie and fat diet with vitamin
supplements like the fat-soluble: DEKA

Obstruction and Constipation Prevention

 Drink a lot of water to keep mucous in gut thin, use Miralax Polyethylene Glycol (common) daily
as prescribed by MD to prevent constipation
 Monitor for bowel obstruction: signs: no bowel movement, pain, can’t pass gas etc.
Cystic Fibrosis Diabetes Mellitus: pancreas is damaged….monitor blood sugar (can drop or be
high)…may need insulin
Pneumonia NCLEX Review Notes
Definition: a lower respiratory tract infection that causes inflammation of the alveoli sacs

Key Players:

 Germs: Bacteria, Virus, Fungi

 Lung Parenchyma: Alveoli, Alveolar Ducts, and Bronchioles (the trio in gas exchange)

Process of normal gas exchange: oxygen is inhaled through

the upper respiratory system down through trachea, the bronchus (right and left primary
bronchi) which splits at the carina and enters into the lungs at the hilum and branches into the

 Secondary Bronchi (also called Lobar Bronchi)

 Tertiary Bronchi (also called Segmental Bronchi)
then into smaller branches called bronchioles to the alveolar ducts to the alveolar sacs which
inflate and deflate to allow gas exchange.

During this process, there is the transfer of oxygen from inhalation into the bloodstream and transfer
of carbon dioxide out of the blood through the lungs which is exhaled. This happens in the alveoli
capillary wall. Then the fresh oxygenated blood is taken back to the heart through the pulmonary vein
and is pumped through the heart to the body.

How does Pneumonia develop?

Normally, the respiratory system can “fight off” these type of germs by filtering the air taken in through
the nose and airway BUT certain conditions can damage the body’s ability to do this and make the
body more susceptible to developing PNA.

These risk factors include:

 Prior infection: flu or cold

 Weak immune system: Elderly, infants, HIV, autoimmune medications
  Immobile: strokes or any other condition that causes decrease mental awareness or restrict
ability to move
 Lung problems: COPD, asthma, smokers
 Post-opt patient: not coughing deep breathing
These germs get into the lungs by inhalation, aspiration, or from the blood and attack the alveoli
sacs. These sacs become very inflamed and fill with fluid, body’s immune defense cell RBCs and
WBCs, and bacteria.

This causes the sac to lose the ability to inflate and deflate
which allows proper gas exchange. Therefore, the patient will start to experience HYPOXEMIA (low
oxygen in the blood) because oxygen cannot transfer across capillary wall to attach to RBCs to
supply the body with oxygen and the body keeps the CO2 (carbon dioxide) which leads
to RESPIRATORY ACIDOSIS!

Arterial Blood Gase Values due to Respiratory Acidosis:

 ABGs: PO2: <90 mmHg

 pH: lower 7.35 mmHg
 PCO2: higher than 45 mmHg
 **To compensate for this the Kidneys start to conserve bicarbonate (HCO3) to hopefully
increase the blood’s pH back to normal…..so HCO3 becomes >26 mEq/L
Further look at the Germs that Cause Pneumonia:

 Bacteria: most common cause of pneumonia especially in community-acquired is caused

by Streptococcus pneumoniae
 Atypical Bacteria: Mycoplasma pneumoniae that causes “walking pneumonia” which is a
milder form of pneumonia that isn’t severe enough to require complete bed rest
 Virus: influenza, RSV most common causes of PNA in children
 Fungi: least common…most likely to affect people with severe suppressed immune system and
typically is contracted from outside in nature from plants, animals etc.
Types of Pneumonia
 Community-acquired Pneumonia (most occurring): patient obtains the germs that causes the
pneumonia OUTSIDE of the healthcare system hence in the community.
 Hospital-acquired Pneumonia: patients who are on mechanical ventilation at major risk…it is
hard to treat because the bacteria tend to be resistant to antibiotics and more likely a bacteria
cause. Criteria: patient must have developed 48-72 hours after admission
Diagnosed:
 Notice: abnormal lungs sound when auscultating with stethoscope may hear coarse crackles,
rhonchi (type of wheezing) or bronchial breath sounds which should be noted only in the
tracheal area and this represents lung consolidation.
 Chest x-ray, sputum culture
Signs & Symptoms of Pneumonia
Remember the word: PNEUMONIA

Productive cough, Pleuritic pain (chest pain that is caused by coughing, breathing etc.)

Neuro changes (especially ELDERLY patients…may not even have a fever but fatigue and increased
respiratory rate)

Elevated labs: PCO2 >45 (retaining carbon dioxide because it can’t pass capillary of alveoli sac),
increased WBC (represents infection…body is trying to fight infection off)

Unusual breath sounds: coarse crackles, rhonchi, or bronchial in the peripheral lung fields

Mild to high Fever (bacteria cause produces highest fever….. greater than 104’F)

Oxygen saturation decreased (want >90%) will need supplementary oxygen

Nausea and vomiting (won’t feel like eating)

Increase heart rate and respirations

Aching all over with joint pain, Activity intolerance with shortness of breath

Nursing Interventions for Pneumonia

Monitor respiratory system:

 Lung Sounds
 Respiratory rate/vital signs
 Oxygen Saturation >95%
 ABGS (if ordered)
 Sputum (collect for culture)
  Suction as needed
Encourage usage of incentive spirometer for deep breathing and encourage coughing and deep
breathing

Encourage 2-3 L of fluid (unless on fluid restriction as with patients who have heart failure)…fever
causes dehydration, lose water through breathing (300-400 mL), and patient is too sick to have the
urge to drink

Education on prevention: Up-to-date Vaccinations (Pneumovax every 5 years for patients 65+ and
19-64 years old with risk factors and annual flu shot)

Education about stop smoking, avoid people who are sick, hand-washing

Keeping head of bed elevated greater than 30 degree for immobile patients to prevent aspiration
especially while eating and after meals along with frequent turning.

Breathing treatments and other respiratory therapy treatments (usually by respiratory therapy
department). These will be schedule or PRN (as needed).

Treatments include: Bronchodilators, chest percussion etc.

Medications:

Administering per doctor’s order: fluids, antipyretics, antivirals (if a viral cause), and antibiotics (if a
bacterial cause)

Antibiotics Groups for BACTERIAL Pneumonia

Remember the mnemonic: Various Medications Frequently Treat Pneumonia Cases

Antibiotics used depend on the bacteria type that is causing the infection, the patient’s ability to
tolerate etc.

Vancomycin: used to treat severe cases and is one of the few that can treat bacteria that may be
resistant to other antibiotics….watch for HEARING LOSS “ototoxicity”

Macrolides: “Zithromax (Z-Pak)” used in patients with Penicillin allergy….narrow-spectrum targets

mainly gram positive bacteria

Tetracylines: “Doxycycline” broad-spectrum that targets gram positive and negative bacteria. Side
effects: not for pregnant women or 8 years or younger due to growth retardation and teeth
discoloration, photosensitivity of the skin and decreases effectiveness of birth control, no antacids or
milk product while taking this medication because it affects absorption.

Fluroquinolones: “Levaquin” broad-spectrum (targets gram-negative and positive)…treatment for

severe infection that are found in the hospital that are resistant. Side effects: c. diff infection, tendon
rupture, cardiac arrhythmias such as QT interval prolonged

Cephalosporins: “Keflex, Rocephin” watch with patients who are allergic to penicillin (can also be
allergic to cephalosporin)…great for community acquired pneumonia… ( 3rd and 4th generations of
cephalosporins broad-spectrum)
Penicillin: “Penicillin G”…narrow-spectrum…target gram positive bacteria…. monitor if patient is
allergic to cephalosporins, decreases effectiveness of birth control

Education about antibiotics: Take medications as prescribed and don’t stop in the middle of
treatment….even if feeling better which helps decrease resistance

Viral Cases: May be prescribed an antiviral of the virus that is causing the pneumonia ex: Tamiflu

Tuberculosis NCLEX Review

What is Tuberculosis: it’s a contagious bacterial infection caused by mycobacterium
tuberculosis that affects mainly the lungs BUT it can also affect the kidneys, brain, spine, joints, and

liver.

First, let’s talk about mycobacterium tuberculosis:

 It’s acid-fast (it stains bright red with the acid-fast staining smear)
 It’s an AEROBIC bacteria (so it LOVES oxygen and must have it to grow):

 Which is why TB most commonly affects the UPPER part of the lungs because there is a
higher oxygen concentration in the apex of the lungs rather than the base
 Tuberculosis is spread through the air (airborne precautions….wear a respirator at all times
when providing patient care and special ventilation/negative pressure air room must be
used for the patient with an ACTIVE TB infection). The bacteria is very small, so it can
suspend itself in the air….it’s different than droplet type of infections:
 If a person with an ACTIVE infection of TB talks, coughs, sneezes, laughs, yells (all
these actions create droplets that harbor the bacteria) this can be inhaled by others.
 Must be in contact with the person for a period of time to catch tuberculosis, which is why
people who live in close quarters or spend a lot of time together are at risk. Another risk
factor is having a weaken immune system (ex: HIV)….see more risk factors below.
Risk Factors for developing Tuberculosis
“TB Risk” (remember these factors for tests)

Tight living quarters: long-term health care facilities, homeless shelters, prisons etc.

Below or at the poverty line (poor…homeless)

Refugees (high incidence of TB in their home country)

Immune system issues: HIV

Substance abusers (IV drugs, ETOH)

Kids less than the age of 4-5….weak immune systems

As the nurse assess your patient for risk, especially patients who are presenting with
respiratory symptoms (this is best done at admission…..most paperwork will have questions
that are similar to these questions):

 Have you travelled outside of the country or lived outside of the country for a long period of
time? If so, where and how long?
 Where do you live? LTC, homeless, prison etc.
 Use drugs? If so, what type?
 If foreign born, ask is they have ever received the BCG (bacilli Calmette-Guerin) vaccine. This
is a vaccination administered in some countries to prevent TB in children. If the patient has
received this vaccine, they will have a positive TB skin test result (avoid a PPD skin test
because it will give a false positive….needs a blood test instead) and a chest x-ray.
 Are you having the following signs and symptoms: night sweats, cough for 3 weeks or more,
blood in sputum, chest pain, weight loss and loss of appetite etc.?
 Ever have a tuberculin skin test? If so, what where the results?
****Not everyone who is infected with mycobacterium tuberculosis will develop an active
tuberculosis infection. Most of the time when a person inhales the bacteria the immune system
detects it, and it becomes encapsulated (so the immune system keeps it under control). Therefore,
most people will never develop the active disease unless those encapsulated bacteria become active
again.

So, let’s talk about the differences between a latent tuberculosis infection (LTBI) versus an active
TB infection.

Latent tuberculosis infection (LTBI): the mycobacterium tuberculosis bacteria is lying dormant and
being controlled by the immune system….it’s encapsulated

 Therefore, the person is: NOT contagious and does NOT have signs and symptoms, will
have a normal chest x-ray, and negative sputum test

 Only sign the person will have is a positive TB skin test or blood test. This means that the
immune system has responded to the bacteria.
  Still need treatment? YES! This will help prevent an ACTIVE TB infection in the future.
According to the CDC, 5-10% of patients who do NOT receive treatment for latent TB
will develop active TB at some point.
Active TB: the immune system isn’t able to contain the bacteria so it takes over (ex: weaken immune
system due to HIV). Most cases of active TB are due to a latent case that turns into an active case

 Therefore, the person is: CONTAGIOUS AND HAS SIGNS/SYMPTOMS, positive PPD or blood
test, will have an ABNORMAL chest x-ray and positive sputum culture.
 The bacteria can now spread via the lymphatic system throughout the body and affect other
areas of the body like the brain, spine, joints etc.
Signs and Symptoms of Tuberculosis (active)
****remember most patients are asymptomatic until they reach the active stage

 Cough that lasts three weeks or more

 coughing up blood
 fever
 night sweats
 fatigue
 unintentional weight loss
 chills
 loss of appetite
 chest pain, or pain with breathing or coughing
Testing for Tuberculosis
PPD tuberculin skin test (also called Mantoux Test, TST, TB skin test): this is
where purified protein derivative (hence where PPD comes from with the name) is injected with a
tuberculin needle on the inner part of the forearm…after the injection it will look like this:

 It is read in 48-72 hours…..(the patient must come back to have the test read and if the patient
does NOT return within 72 hours the test will have to be repeated)
 A positive result doesn’t necessarily mean the patient has an active infection of TB. It just
means they have been exposed to it.
 Does it tell the difference between a latent vs active infection? NO! The person will need a
chest x-ray and sputum culture to confirm.
As the nurse you will be assessing for induration of the injection site. Induration is a hard or swollen
area that is raised on the skin. This will be measured in millimeters (mm). Redness is not
measured…the induration is measured (for exams remember the criteria for positive results)

 15 millimeters (mm) or more: Positive in all persons (doesn’t matter if the person does not
have any risk factors)
 10 mm or more: positive if the person is an immigrant, IV drug user, working or living in tight
living quarters, child less than 4
 5 mm or more: positive if person have HIV, in contact with someone with TB, organ transplant
patient, or immunosuppressed
Interferon-Gamma Release Assays (IGRA Test): starting to become more popular

Two types currently on the market: QuantiFERON-TB Gold (QFT) and T-Spot

The blood test will check for the immune system’s reaction to mycobacterium tuberculosis.
  Benefits: just one visit (doesn’t have to come back for results to be read and results are
not affected by people who have had the BCG vaccine)
 Downsides: It doesn’t differentiate between latent vs active…again the person will need a
sputum culture and chest x-ray to confirm.
Sputum: (AFB “acid-fast bacilli” Smear): the patient provides the specimen through coughing it up or
a bronchoscopy to collect the sputum. The sputum is stained with a special dye and given an acid
wash. If mycobacterium tuberculosis is present it will stain a bright red color.

 NURSE: collect three different sputum specimens on 3 different days

 It’s best to collect them in the morning before breakfast (most collection of secretions from
overnight)
Chest x-ray: assesses for abnormal infiltrate in the lungs.

Nursing Interventions and Treatments for Tuberculosis

Always screen patients

Initiate airborne precautions:

 Negative pressure room (door closed at all times)

  Must wear a respirator when providing care (fitted yearly for this mask)
 Strict hand hygiene
 How about if the patient has to leave the room for testing? Many procedures can be
performed by the bedside, but if the patient must leave the room they will need to wear
a surgical mask.
Active TB infection education: most patients are treated outpatient because of the duration of
how long they must take medications (6 months to a year)

 Isolation at home: can’t go to work, run errands, school etc. until no longer contagious (can go
to medical appointments only….must wear surgical mask). To be removed from isolation they
will need to be on medications for about 3 weeks, have 3 negative acid-fast sputum
cultures, improvement of signs and symptoms, and be taking medications exactly as ordered
(TB can become drug resistant)
 No visitors, stay in separate rooms from other family member (stay away from young kids), keep
windows and doors closed
 Coughing, sneezing? Do this in a tissue and dispose immediately by flushing or put it an air tight
bag and dispose
Medications for Tuberculosis
Educate patient they will be on medication treatment for several months…6 months to a year
(depending on if they have LTBI or active TB)…..must be compliant (this is very hard for patients due
to the amount of time they must take the medication and the frequency)

DOT (directly observed therapy): CDC recommends this to be used with ALL patient with TB
because it is difficult to determine who will and won’t take their medication correctly.

 This ensures the patient takes the correct medication at the right time and continues therapy. A
trained individual (public health nurse or trained DOT worker) actually observes the patient
swallowing the medication.

 It helps decrease the patient from being noncompliant, monitors the patient for signs and
symptoms related to the medications, and helps prevent resistant cases of TB.
 Family members are NOT candidates for DOT.
Most common drug regime used includes four drugs:

“PERI”: This word means “around or surrounds”. Normally, our body would surround this bacteria and
encapsulate it, but it has failed to do this. Therefore, these medications must do it!

Pyrazinamide: bactericidal effect (kills the bacteria)

 watch in patients who are diabetic or have kidney problems, gout (increases uric acid which can
level to a gout attack)
 Monitor uric acid level, liver and kidney function…can cause liver problems
 GI problems common…take with food
Ethambutol: stop RNA synthesis and is bacteriostatic (stops the bacteria from reproducing)
  Can inflame optic nerve (monitor for blurred or color changes in vision): needs to get eye
checked regularly….always ask patient about vision…notify MD if this occurs
 Peripheral neuropathy (damage to peripheral nerves): report numbness or burning in the hands
or feet….notify MD if this occurs
Rifampin: kills the bacteria by stopping RNA-polymerase

 Educate about turning body fluids orange and can stain soft contact lenses…so wear hard
contact lenses instead
 makes birth control less effective (use back up method), sunburn easily, no alcohol (this drug
can cause liver problems: watch for jaundice, issues bleeding etc.)
Isoniazid (INH): kills the bacteria and stops it growth

 decrease Vitamin B6 levels: monitor for tingling in extremities, tried, irritable, depressed
(peripheral neuropathy)…need supplementation
 monitor liver function and tell patient for monitor for liver problems as well
 neurotoxicity: mental status
Streptomycin: still used for TB, but not as the first line usually

Stops protein synthesis and kills the bacteria…..watch for hearing changes (ringing in the eyes…can
be ototoxicity (eight cranial nerve)
Iron-Deficiency Review Notes
Definition: a type of anemia that is caused by low IRON levels.

What is Anemia? Anemia is a decreased amount of red blood cells or hemoglobin in the body.
These components play a huge role in carrying oxygen throughout the body. If you are low in
RBCs or hemoglobin, your body won’t receive enough oxygen to function properly.

Key Points about Iron-Deficiency Anemia:

 Most common type of anemia (there are various types)

 Body uses IRON to make hemoglobin
 Low levels of iron lead the body to produce fewer red blood cells which leads to less
hemoglobin in the body. Hence, your body receives less amounts of oxygen.
 Signs and symptoms are vague at first and as it progresses the signs and symptoms become
more noticeable
 A blood test such as a CBC (complete blood count) or iron level will help the doctor detect
anemia.
 Women who are childbearing age may be plagued with this due to heavy menstruation or
pregnancy and people with poor digestion (intestinal issue) or poor intake of iron.
 Treatment includes: incorporating more iron in the diet, taking iron supplements, and
prevention.
Pathophysiology of Iron Deficiency Anemia
The red blood cells transport oxygen throughout the body and remove carbon dioxide (a waste
product from metabolism) with the help of hemoglobin.

Hemoglobin is an “ingredient” found in the RBC that is a protein that contains IRON.

 IRON helps make hemoglobin.

 Around 70% of the body’s iron is found in the hemoglobin.
 Function of hemoglobin is to facilitate the transfer of the oxygen and carbon dioxide throughout
the body. It does this with the help of the RBCs.
Remember low IRON levels: mean less production of hemoglobin which means less oxygen to
the body.

Causes of Iron-Deficiency Anemia

 Poor intake of iron through diet (pregnancy…increased demand of iron for fetus, vegetarians)
 Absorption problem: intestinal surgery…gastric bypass, celiac disease, small intestine removal
(most iron is absorbed by the small intestine)
 Losing iron from blood loss (menstruation, GI bleeding…ulcers, hemorrhoids)
Signs and Symptoms of Iron-Deficiency Anemia
Remember the Mnemonic: “Low Iron”

Lethargic

Overexerted easily (may be short of breath)

Weird food cravings (ice, dirt, clay), White-faced (pale)

Inflammation of tongue…will become smooth and turn various colors of red (due to lack of oxygen it
receives), Increased Heart rate (trying to compensate for the low oxygen)

Reduced Hemoglobin level

Observe changes in RBCs with a blood smear test…will appear hypochromic (pale) and microcytic
(small)

Nail changes (Koilonychias….spoon-shaped nails), neuro change (confused, moody)

Diagnosed?
 CBC (to assess red blood cells, hemoglobin levels)…may order a blood smear to assess color
and size of RBCs
 Iron levels
Nursing Interventions for Iron-Deficiency Anemia
 Monitoring, education, and administering medications
 Monitor patient for bleeding and hemoglobin levels and other major signs and symptoms…
assessing diet, menstrual cycles etc.
 Educating how to take IRON supplements:

 Take iron on an empty stomach (increases absorption…may take with small amounts of
food due to stomach upset)
 Take with Vitamin C…glass of orange juice (helps increase absorption)
 Don’t take with any milk products, calcium, or antacids (decreases absorption) and
wait 2 hours in between
 Stools will turn black which is normal while taking iron supplements (tarry stools or having
stools with blood..not normal)
 For liquid preparations: mix in a drink, drink with straw, and brush teeth afterwards (can
stain teeth)
 Side effects: constipation (drink plenty of fluids and take over the counter stool softener if
needed)
 May give IV iron or blood transfusion if severe per md order
 Eat Food High in Iron: Remember the mnemonic “Eat Lots of Iron”
Egg yolks
Apricots

Tofu

Legumes, Leafy green vegetables

Oysters

Tuna

Sardines, Seeds

pOtatoes

Fish (halibut, haddock, salmon)

Iron-fortified cereal and breads

Raisins, Red meats (beef)

pOultry (turkey, chicken)

Nuts

Pernicious Anemia NCLEX Review

What is Pernicious Anemia?

Pernicious anemia is a form of vitamin b 12 anemia that is an autoimmune condition where the body
does not produce intrinsic factor, which plays a role in absorbing vitamin b 12.

Pathophysiology of Pernicious Anemia

The body needs vitamin b 12 to make healthy red blood cells. A protein called intrinsic factor plays
a role in the body’s ability to absorb vitamin b 12. Vitamin b12 is not produced by the body but is
taken in through food with the help of a protein called intrinsic factor. In pernicious anemia, there isn’t
enough INTRINSIC FACTOR to help with absorption of vitamin b 12 in the stomach (total cause
unknown but can be due to stomach surgery or GI disease etc).

How does intrinsic factor help the body absorb vitamin b 12? It attaches to the vitamin B 12
found in the food you consume and releases it into the stomach acid. Then the vitamin b 12 is
absorbed by the ileum. The parietal cells in the stomach produce intrinsic factor and can become
damaged from an autoimmune response in the system. Antibodies attack the parietal cells which
damages them to the point where they cannot produce intrinsic factor. GI disease and stomach
surgery can destroy parietal cells which decrease the production of intrinsic factor.

What happens to the red blood cells in the pernicious anemia? If vitamin b 12 levels are too low
this can lead the body to produce unhealthy red blood cells. Instead of the RBCs being normal sized
and round, they become large and are shaped like an oval (also called macrocytic anemia…
learn about microcytic anemia in iron-deficiency anemia).

This in turn causes the bone marrow (which in responsible for producing RBCs) to produce less of
them and the RBCs have a hard time leaving the bone marrow because they are too big and don’t
divide properly.

Red blood cells play a HUGE role in carrying oxygen throughout the body to organs and
tissues, but if there aren’t enough RBCs the body doesn’t receive enough oxygen. In pernicious
anemia, there are low amounts of RBCs and organ systems start to suffer, especially the heart and
neuro system.

How low vitamin b 12 and low RBCs affect the body?

 Nervous System (majorly affected in pernicious anemia): low vitamin b 12 causes irreversible
damage to nerve cells so the patient can experience paresthesia.
 Heart: it has to work harder to pump blood to get oxygen to the organs and tissue which can
eventually lead to heart failure.
 Intestinal: tongue changes from decreased oxygen and the stomach lining begins to thin which
can cause an upset stomach and increase risk of stomach cancer.
Risk Factors for Pernicious Anemia
 Aging: older adults can experience this due to decreased production of gastric acid and intrinsic
factor.
 Genetic
 Autoimmune disease of the endocrine system: Addison’s, Diabetes Type 1 etc.
How is Pernicious Anemia Diagnosed?
 CBC: to measure RBCs, hgb, hct
 Blood smear to look at RBC (will appear large and oval)
 Vitamin b12 level
 Intrinsic factor antibody assay
 Bone marrow aspiration and biopsy
Signs and Symptoms of Pernicious Anemia
Signs and symptoms may take a while to be noticed by the patient.

*=most common in pernicious anemia

Remember the mnemonic: Pernicious

Pale

Energy gone (very fatigued)*

Red, smooth tongue*

Numbness or tingling in hands and feet*

Intestinal issues (abdominal bloating, diarrhea/constipation, indigestion)

Confusion

Increased sadness (depression)

lOss of appetite (taste changes and weight loss)

Unsteady gait (clumsy)

Shortness of breath with activity

Nursing Interventions for Pernicious Anemia

Goal replace vitamin b 12 (patient can’t receive vitamin b 12 from food…so they will need it a
different route)

 Administer vitamin b 12 injections (intramuscular….not orally because they aren’t absorbing

it in the GI system) as ordered by doctor. Regime is usually weekly at first and then monthly for
maintenance (for lifetime)….if severe anemia will need blood transfusion
 Educated on safety: due to risk of injuries from unsteady gait…more clumsy from the
paresthesia
 Educate about importance of eating enough foods with iron, vitamin C, and folic acid because
these nutrients play a role in red blood cell production as well.
 Maintain good oral hygiene due to changes to tongue.