Unit 8 Pulmonary Study Guide

Question 1

Atelectasis occurs when lung tissue collapses. It is divided into three different
types:

Answer 1

1. surfactant impairment- decreased lubricant means alveoli are more likely to collapse d/t a higher surface tension when breathing out
2. compression atelectasis- pressure on lung causes alveoli to collapse
3. obstructive atelectasis- alveoli are blocked and don’t receive enough air because it goes into the blood instead.

Atelectasis will cause hypoxia and hypercapnia d/t impaired gas exchange

Question 2

Explain V/Q mismatch.

Answer 2

V is amount of air into alveoli aka VENTILATION, Q is amount of blood that makes it to the capillaries surrounding the alveoli aka PERFUSION. If there is not enough air, then blood cannot be properly oxygenated. V/Q mismatch is an imbalance between ventilation and perfusion. A shunt is a type of V/Q mismatch that is quite bad.

Question 3

Explain how atelectasis can cause a V/Q mismatch or shunt.

Answer 3

When a lung collapses then the amount of oxygenated blood will drop because the alveoli have been damaged, ventilation has decreased, meanwhile, perfusion has not changed. A shunt is the result of an obstructed airway with bronchoconstriction and even fluid in the alveoli.

Question 4

Thoroughly explain the pathophysiology involved with Acute Respiratory Distress Syndrome (ARDS) and how it can proceed to ARF (acute respiratory failure).

Answer 4

ARDS is an acute lung injury caused by alveolocapillary membranes in lungs being injured. This leads to inflammation and pressure in lungs increases and then fluid from capillaries leaks into lungs causing pulmonary edema, shunting, hypoxia (ARF). It has 3 phases
1. exudative: within 3 days of injury, inflammatory response begins, Cytokines released create further damage to alveocapillary membranes. Edema happens here.

2. proliferative: from day 4-21, alveolar exudate turns into cellular granulation tissue which worsens hypoxia.
3. fibrotic: day 14-21 remodeling and fibrosis. Worsnes everything from ventilation, to V/Q mismatch and decreases gas exchange. ARF is when there is decreased gas exchange.

ARF can be hypoxic, hypercapnia, or both.

• potential injury to these membranes: sepsis, aspirating vomit, drowning, inhaling smoke/toxins, severe pneumonia, head injury, COVID-19, etc.

ARF is inadequate gas exchange, leads to hypoxia

Question 5

Describe the pathophysiology behind pulmonary fibrosis.

Answer 5

Scarring of the lung can occur d/t lung disease, autoimmune disorders, and foreign substances that trigger an inflammatory response when inhaled. Fibrosis stiffens lungs, decreases compliance and hypoxia occurs

main symptom: dyspnea when active

lung transfusion may be necessary

Question 6

Describe the pathophysiology and signs and symptoms associated with pulmonary edema (be very thorough)

Answer 6

Pulmonary edema, or fluid in lungs is most commonly caused by LSHF. When left side of heart is not working, capillary hydrostatic pressure in lungs rises and that will force fluid into the interstitial space.

Edema can also be caused by ARDS, where alveoli are damaged, and surgery/tumors/fibrosis, where lymph nodes are blocked and excess fluid cannot be removed.

s/s: dyspnea, hyposmia, labored breathing, crackles, dull lung bases, pink frothy sputum even!

Question 7

Describe the pathophysiology behind asthma (be
sure to discuss what happens to cause the airway
obstruction, airflow resistance, and hypoventilation)

Answer 7

Asthma is a type I hypersensitivity rxn that is triggered when a person (genetically predisposed) is exposed to an allergen. This triggers IgE which triggers mediators like histamine and bradykinin to be released. The airway is inflamed and this leads to hypoventilation.

Question 8

Explain the difference between the typical type of COPD (chronic obstructive pulmonary disease) and the version caused by an inherited deficiency of alpha-1 anti-trypsin.

Answer 8

COPD is usually caused by chronic bronchitis or emphysema. Caused by smoking. An inherited A-1 anti-trypsin mutation also causes COPD, this is a protein that protects lungs, but because they are not shaped right, they are stuck in the liver (where they are made).

Question 9

Explain the difference (including signs and symptoms and pathophysiology) between the Chronic bronchitis and emphysema forms of COPD.

Answer 9

Chronic bronchitis COPD is caused by inflammation of the airway

Emphysema COPD is when the acini are large but the alveolar wall has no scarring. Obstruction comes from changes in lung tissue. “pink puffer”

• s/s: dyspnea, minimal cough, increased minute ventilation, pink skin, pursed lip breathing, accessory muscle use, cachexia, hyperinflation, barrel chest, decreased breath sounds, and tachypnea.

In chronic bronchitis, there is mucus and inflammation, which causes the obstruction. “Blue bloater” from lack of O2.

• s/s: cough, purulent sputum, blood in cough, mild dyspnea, cyanosis, peripheral edema from Cor Pulmonale, crackles, wheezes, prolonged expiration, and obesity.

Question 10

Define the differences between: Community Acquired Pneumonia (CAP), Ventilator Acquired Pneumonia (VAP), and Healthcare Acquired Pneumonia (HAP).

Answer 10

Pneumonia, pneumonia, an infection that leads to inflammation in lungs.

CAP is from the community OUTSIDE of hospital. MOST COMMON d/t several bacteria like Staph and chlamydia.

VAP is from ventilator in hospital, a type of HAP that occurs after 48hr of admission. Infectious bacterium may be aspirated.
HAP

Question 11

11. Explain how aspiration of food or body secretions can lead to pneumonia.

Answer 11

Pneumonia is when there is an infection in the lung that leads to inflammation. In aspiration pneumonia, a food substance enters the airways. This triggers an inflammatory response since the body treats it as any other foreign substance and that can lead to severe infection. An NG tube can illicit the same inflammatory response if contents accidentally go into the lungs.

Question 12

Describe why the presence of a Nasogastric (NG) tube increases the risk for developing aspiration pneumonia and hemorrhagic pneumonitis.

Answer 12

NG tube is a predisposing factor to pneumonia because food particles may be accidentally aspirated.

Question 13

Differentiate (describe the difference between) Pneumothorax and Tension Pneumothorax (be sure to include the signs and symptoms specific to each).

Answer 13

Pneumothorax is air or gas trapped in pleural space that has changed the negative pressure in the pleural space which will prevent the lung from expanding and it will collapse.

Open pneumothorax occurs when air can enter and exit the pleural space and tension PT is when it can enter but not exit. Pressure in the lungs is greater than barometric pressure.

In tension PT, as air enters pleural space, the trachea may be displaced to the injured side, and severe hypoxemia and hypotension may occur.

s/s: pleural pain, tachypnea and dyspnea.

Hyperresonance can be auscultated

Question 14

Describe the pathophysiology and signs and symptoms associated with bronchiectasis.

Answer 14

Bronchiectasis is the permanent dilation of the bronchus. Usually appears with other signs of chronic inflammation of the bronchi.

This is permanent because the inflammation will scar the bronchi.

s/s: cough, lower respiratory tract infections, clubbing, and blood in the cough.

Question 15

Describe the pathophysiology behind Cystic Fibrosis (be sure to identify the chromosome involved, the tests used for diagnosis, and all the body systems that are impacted).

Answer 15

Autosomal recessive mutation of chromosome 7 where an abnormal protein, CFTR, causes several respiratory problems, as well as G.I., and repro tract.

Mucous production is increased and cilia fxn is impaired, which leads to inflammation.

s/s: cough (foul, productive), wheeze, recurring pulmonary infections, G.I. malabsorption, hypoxia, and pulmonary HTN. With time, barrel chest, and clubbing.

The test used is the sweat test which tests for chloride levels greater than 60mEq

Question 16

Define empyema.

Answer 16

Pus in pleural space d/t infection. Usually occurs when pulmonary lymphatics are backed up.
s/s: fever, tachy, cough, pleural space pain, decreased breath sounds

Question 17

Thoroughly explain Cor Pulmonale and the respiratory risks associated with developing it.

Answer 17

Coronary pulmonale can cause right-sided HF. It is hypertrophy of the right ventricle (before diastole). Caused by pulmonary HTN (pressure from lungs). X-ray would reveal enlarged right heart border.

Risk factors: pregnancy, NSAIDs, smoking, air travel, decongestant meds etc.

Tx: diuretics, O2, and anticoagulants.

Question 18

Describe the pathophysiology and signs and symptoms of squamous cell (non-small cell) carcinoma (lung cancer)

Answer 18

Squamous cell carcinoma is a type of non-small cell lung cancer. They are slow growing, and spread slowly.
s/s: cough, bloody cough, saliva production, airway obstructed, too much Ca

Question 19

Describe the pathophysiology and signs and symptoms of Adenocarcinoma non-small cell lung cancer

Answer 19

Adenocarcinoma is a non-small cell lung cancer that has a moderate growth rate and spreads early to lymph nodes, pleura, bone, adrenal glands, and brain.

s/s: pleural effusion

Question 20

Describe the pathophysiology and signs and symptoms of large cell carcinomas of the lung.

Answer 20

Large cell carcinomas have a fast growth rate that spread early and everywhere.

s/s: pain in the chest wall, pleural effusion, cough, sputum, hemoptysis, and airway obstruction that leads to pneumonia.

Question 21

Describe the pathophysiology and signs and symptoms of small-cell lung carcinoma

Answer 21

Small cell carcinoma, aka oat cell, grows fast and spreads early to the mediastinum, lymph nodes, brain, and bone marrow.

s/s: cough, chest pain, dyspnea, hemoptysis, local wheezing, airway obstruction, and excess hormone secretion

Question 22

Describe the pathophysiology and signs and symptoms of bronchial carcinoid tumors

Answer 22

Bronchial carcinoid tumors are a type of neuroendocrine tumor that grows slowly. Form in the bronchial mucosa and make up 1% of all lung tumors. They are unrelated to smoking and arise in childhood.

s/s: cough, chest pain, dyspnea, wheezing

Dx: chest imaging

Question 23

Describe the pathophysiology and signs and symptoms associated with Croup

Answer 23

Croup, aka laryngotracheobronchitis, is an upper airway disorder in children where airflow is decreased and the body has to work harder to breathe. Usually affects 6mos.-5 year-olds.
D/t viral infection (most of the time) that causes subglottic tissues to inflame. The mucous membranes will be loosened and that increases the chance for edema in the mucosal and submucosal linings.

s/s: runny nose, sore throat, fever, barking cough.

Resolves within a few days but epiglottitis can occur if it does not.

If edema happens in the cricoid cartilage, problems occur.

Question 24

Describe the pathophysiology of Tuberculosis (TB) and explain why living in close quarters (like dormitories, prisons, or military barracks) increases the risk for developing this condition.

Answer 24

An infection caused by mycobacterium tuberculosis that affects the lungs primarily. It is very contagious and spread by droplets. It causes inflammation of the lungs. It can multiply within macrophages and resist lysosomal killing, forming tubercules, caseous necrosis occurs.

Living in closed quarters increases TB chances because of the droplets that linger.

Question 25

25. Explain how the caseation of alveoli in TB could potentially result in a V/Q mismatch.

Answer 25

This leads to a low V/Q, with high perfusion, but close to no ventilation, or air entering and exiting alveoli, since there are fewer alveoli. Alveoli die, gas exchange decreases, oxygenated blood decreases, and tissue cant perfuse, that’s a mismatch!

Question 26

Describe the role of Central Chemo receptors (indicate where they are found, what they respond to, and what they do)

Answer 26

Central chemoreceptors:

What? Sense changes CSF pH, which reflects how much CO2 is present. Regulate depth and rate of respiration
Where? Below BBB, near medulla oblongata in the brain
How? Too much CO2 will increase respiration to decrease the concentration of CO2. If the receptor is impaired, or there is excess CO2, then it won’t work correctly and this task will be delegated to the peripheral receptors.

Question 27

Describe the role of peripheral Chemoreceptors
(indicate where they are found, what they respond
to, and what they do)

Answer 27

What? Peripheral chemoreceptors are sorta sensitive to pH and very sensitive to O2 levels in aa. If O2 levels drop tremendously, they will help restore levels during hypoxemic episodes.

Where? near arch of Aorta and the carotid bodies

How? Send signals from carotid bodies to respiratory center to increase ventilation.

Question 28

Explain what the J receptors in the lungs respond to and what they do when stimulated.

Answer 28

What? J-receptors, aka juxtapulmonary capillary receptors, respond to increased pressure in capillary, to juxtapose it, or lower it!

How? J-receptors will send a signal to th edorsal respiratory group of neurons in brainstem to stimulate ANS to lower pressure by having the lungs do rapid, shallow breathing, this will lower BP, and lower HR as well.

Question 29

Explain why someone with COPD cannot stimulate the peripheral chemoreceptors adequately.

Answer 29

Normally, peripheral chemoreceptors will sense if O2 levels are low, and help increase ventilation, however with COPD, there is an obstruction in the airway, so no matter what O2 levels cannot be restored because ventilation has been impaired.

In COPD, peripheral chemoreceptors takeover, since there is chronic hypoventilation and hypercapnia, but because the primary/central chemoreceptors are down (no longer giving a correct read of CO2 concentration), it will trick the secondary chemoreceptors into thinking that O2 levels are not as low as they actually are, so ventilation will not be effective.

Question 30

Explain the role of surfactants in lung health:

Answer 30

Surfactant reduces the surface tension of alveoli, keeping the lung from stiffening, collecting fluid (edema), and collapsing.

Collapse is common in babies because it has just started to produce surfactant.

Question 31

Define the following: Tidal Volume, Inspiratory Reserve Volume, Expiratory Reserve Volume and Residual Volume

Answer 31

1. Tidal volume- amount of air we breath in and out, in one breath cycle = 500mL
2. Inspiratory Reserve Volume- amount of air we can breath in directly after one breath cycle 3,000-3,300mL
3. Expiratory Resolve Volume- amount of air we can breath out after one breath cycle, 100-1,200mL
4. Residual Volume- amount of air left in lungs after we breathe out, 1,200mL

Question 32

Define the following: Total lung capacity, Vital capacity, Inspiratory capacity, Forced residual capacity, and physiologic dead space.

Answer 32

1. Total lung capacity- TLC= VC+RV. Max. air we can breath in. 5,700-6,200mL.
2. Vital capacity- VC. Max exhale after max inhale 80% of TLC (4,500-5,000mL)
3. Inspiratory capacity- Max inhale after max exhale
4. Forced residual capacity- FRP. air left in lungs after one breath cycle
5. Physiologic dead space- air in lungs that does not undergo gas exchange, thus useless

Question 33

Describe what is meant by the term “good lung down.”

Answer 33

In someone with lung disease on ONE side, placing the good lung down will help V and Q, as gravity helps O2 move into blood.

Question 34

Explain the oxyhemoglobin dissociation curve.

Answer 34

Oxygen is transported in the body bound to Hgb.

Hgb releases O2 into the blood for tissue perfusion by desaturation.

When the dissociation between Hgb and O2 is plotted, it creates and S shape.

Shift to the right means it is easier for them to dissociate and O2 can make it into cells easily.

Shift to the left means that it is harder to separate them and O2 to reach cells.

Shift to right is good, shift to left is bad.

Question 35

Explain what happens during conditions where the pulmonary arteries constrict

Answer 35

When pulmonary aa. constrict, it is typically d/t low O2 levels in alveoli, aka hypoxic pulmonary vasoconstriction. It can affect the whole lung or just a portion. When only a segment of the lung is affected, the aa. constrict and that leads to shunting of other portions of the lung.

If the whole lung is affected, vasoconstriction will happen everywhere and that can lead to pulmonary HTN.

Question 36

Explain the changes in the pulmonary system that are commonly seen in older adults.

Answer 36

Elasticity declines with age.

Tissue strength declines.

The surface area of the capillary network declines.

The immune system is compromised and that leads to an increased risk of infection in the lungs.

Question 37

Explain the pathophysiology, signs and symptoms associated with hypoventilation and hyperventilation (be sure to list the causes too)

Answer 37

Hypoventilation is reduced breathing, which results in hypercapnia and low pH with decreased O2. It can be caused by impaired pulmonary mechanics or changes in central chemoreceptors.
- s/s: confusion and sleepiness

Hyperventilation is increased breathing, when the lungs will remove CO2 quickly and an increase in pH. Usually occurs with anxiety, acute head injury and pain.

Both are dx by arterial blood gas analysis

Question 38

Describe Cheyne-Stokes and Kussmaul Breathing and compare these to normal breathing patterns.

Answer 38

Normal tidal volume (volume of air with one breath cycle) is 400-800 mL, with a longer breath out than breath in.

Cheyne-Stokes RR is alternating period of deep and shallow breathing, coupled with apnea lasting 15-60 secs.

Kussmaul breathing is labored breathing with large tidal volumes . Found in acidotic states like DKA or met acidosis. An increased RR without a pause in between.

Question 39

Describe the following terms and what they are
associated with: hemoptysis, cyanosis, clubbing,
hypoxemia, hypoxia, and hypercapnia

Answer 39

Hemoptysis, blood in cough, infection or inflammation

Cyanosis, blue tint, from lack of O2.

Clubbing is from chronic hypoxia

Hypoxemia is reduced O2

Hypercapnia is too much CO2 and linked to resp. acidosis, resulting in electrolyte abnormalities that may cause dysrhytmias.

Question 40

List the color of abnormal sputum that is seen with: asthma, Klebsella pneumonia, pneumococcal pneumonia, stapholococcal pneumonia, bacterial infection, oral anaerobe abscesses.

Answer 40

asthma- grey/white
klebsiella- red
pneumococcal pneumonia- rusty
staph pneumo- salmon
bacterial- purulent
oral anaerobe- purulent with foul odor

Question 41

Describe “flail chest” and why it occurs.

Answer 41

flail chest is a pulmonary disorder of the chest wall. A fracture of 2+ ribs in more than one place or a fracture in the sternum and several consecutive ribs. Chest wall is now unstable, and doing the opp. of what it should be. RR will increase but to no avail because CO2 is not exiting, leading to hypercapnia and RF

Question 42

Describe the types of pneumothorax

Question 43

Describe Pleural effusion (including each type)

Question 44

describe Bronchiectasis

Question 45

Describe Pulmonary Fibrosis

Question 46

Describe Pneumonoconiosis

Question 47

Explain the pathophysiology behind pulmonary edema and the most common causes of it.

Question 48

Explain the pathophysiology behind acute
bronchitis. Be sure to indicate how to tell the
difference between bronchitis and pneumonia.

Question 49

Describe the pathophysiology behind pulmonary embolism and how it is diagnosed. Be sure to include the signs and symptoms you would see.

Question 50

Describe the pathophysiology behind pulmonary artery hypertension (PAH)