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N351: Pathophysiology I > Module 6 > Flashcards

Module 6 Flashcards

1
Q

Pneumonia

A

Acute inflammation of parenchymal tissues (functional parts like alveoli and bronchioles) in the lungs

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2
Q

Alveolitis

A

Inflammation of Alveoli

Another name for Pneumonia

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3
Q

Percent of Population that gets Pneumonia Yearly?

A

1 % (4 million)

12 cases per 1000

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4
Q

Pneumonia is the ___ leading cause of death

A

6th

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5
Q

Most common cause of death from infectious disease comes from?

A

Pneumonia

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6
Q

Host Resistances Against Pneumonia?

A

Nasopharyngeal Defenses
Glottic and Cough Reflexes
Mucociliary Blanket
Pulmonary Macrophages

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7
Q

Nasopharyngeal Defenses as Host Defenses

A

Removes particles from the air and destroys invading organisms

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8
Q

Risk Factors that are Detrimental to Nasopharyngeal Defenses?

A

Hay Fever
Common Cold
Nasal Trauma

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9
Q

Glottic and Cough Reflexes as Host Defenses

A

Prevent aspiration into the tracheobronchial tree

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10
Q

Risk factors that are detrimental to glottic and cough reflexes?

A

Stroke
Abdominal or Chest Surgery
Sedastion/Anesthesia
NG tube (increases aspiration pneumonia risk

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11
Q

Mucociliary Blanket as Host Defenses

A

Removes secretions, microorganisms, and particles out of the airway

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12
Q

Risk factors that are detrimental to the mucociliary blanket?

A

Smoking
Inhalation of Irritating Gases

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13
Q

Pulmonary Macrophages as Host Defenses

A

Removes microorganisms

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14
Q

Risk factors that are detrimental to the pulmonary macrophages?

A

Alcohol Intoxication
Smoking

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15
Q

Those most Susceptible to Pneumonias

A
  1. Age (Very young and Elderly)
  2. Antibiotic Therapy (leading you susceptible)
  3. Chronic Diseases (Diabetes, cardiac, respiratory, ETOHism - since it causes physiologic stress)
  4. Smoking
  5. Post-operative Patients (if they do not deep breath or cough out of pain or fear)
  6. Immunosuppression (AIDS, organ transplant, chemo)
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16
Q

Complications due to Pneumonia

A
  1. Bacteremia / Septicemia (bact is localized with competent immune system, but Septicemia is systemic spread with a compromised immune system - via blood)
  2. Empyema
  3. Lung Abscesses
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17
Q

Empyema

A

Pus formation in the pleural cavity

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18
Q

What may need to be done to Lung Abcesses?

A

They may need to be Incised and Drained since it can infect nearby tissue once the walled off area becomes sealed off and necrotic

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19
Q

Etiologies of Pneumonia

A
  1. Infectious Agents via Droplet Inhalation
  2. Smoke Inhalation
  3. Aspiration of food contents, gastric contents, NG tube, or stroke
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20
Q

Most common infectious agent of pneumonia?

A

Gram Positive Bacteria

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21
Q

Infectious Agents that can cause Pneumonia?

A
  1. Bacterial (streptococcus pneumonia G(+)/diplococcus pneumoniae G (+) - staphylococcus aureus, streptococcus pyogenes /or/ gram negative - Kibsiella pneumoniae, pseudomonas aeruginosa, E coli, Haemophilus influenzae, Legionella pneumophila)
  2. Viral - influenza, parainfluenza, RSV, CMV (=90% mortality)
  3. Mycoplasma Pneumoniae / Other
  4. Fungal - Candida, Mucor, Aspergillus, Histoplasmosis, Coccidiomycosis, Blastomycosis
  5. Protozoal/Fungal - Pneumocystis Carinii
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22
Q

What causes community based pneumonia?

A

Gram Positive Pneumonia

This has a les than 5% mortality rate - often not in the hospital

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23
Q

Mortality of Gram Negative Pneumonia?

A

20-50% so many pneumonia from this occur nosocomially in the hospital

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24
Q

Legionella

A

Gram negative bacteria that can cause pneumonia

Is found in cooling systems, condensers, water reservoirs, shower heads - any place with lots of water

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25
Q

Who is parainfluenza virus pneumonia most deadly for?

A

Infants and Premature Infants

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26
Q

CMV

A

Cytomegalovirus that has a 90% mortality rate from causing pneumonia in those who got transplants, are immunocompromised, elders, and infants

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27
Q

Atypical Pneumonia is caused by …

A

Mycoplasma pneumoniae

It does not appear in the aveolar sacs and does NOT cause the characteristic productive cough of normal pneumonia

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28
Q

Histoplasmosis

A

fungal infectious agent that grows in soil enriched by bird feces that can cause pneumonia

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29
Q

If aspiration occurs due to gastric contents, what can happen to the lungs?

A

they can get burned - thus causing pneumonia

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30
Q

American Thoracic Society on Community-Acquired Pneumonias?

A

they have created a decision tree of categories on those with pneumonia who need to be in the hospital, not in the hospital, ICU, or medical unit

It tells the location or treatment and treatment of choice for different pneumonia patients

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31
Q

Subjective Manifestations of Pneumonia

A
  1. Lassitude and severe malaise
  2. Chest pain that increases with inspiration
  3. Dyspnea
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32
Q

Lassitude

A

no energy to do anything

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33
Q

Objective Manifestations of Pneumonia

A
  1. Increased Temperature (106) and shaking chills (indicating hypothalamus reset)
  2. Increased Respiration Rate, Use of Accessory Muscles
  3. Orthopnea
  4. Productive cough with Sputum
  5. Gray Complexion
  6. Rales and Rhonchi
  7. Decreased breath sounds over consolidation
  8. Friction Rub (Pleuritic Pain)
  9. Dull on Percussion
  10. Changes in having them say E –> A in a stethoscope
  11. Increased HR
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34
Q

Orthopnea

A

Having to sit up to breathe, cannot do it lying down

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35
Q

Sputum colors are not ___ of pneumonia

A

diagnostic

*they just give a good picture and guess - need sputum culture to diagnose

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36
Q

Pneumococcal Pneumonia Sputum

A

Purulent and Rusty

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37
Q

Staphylococcal Pneumonia Sputum

A

Yellow and Blood Streaked

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38
Q

Klebsiella Pneumonia Sputum

A

Red and Gelatinous

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39
Q

Mycoplasma Pneumonia Sputum

A

Non-productive that advances to mucoid (atypical pneumonia)

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40
Q

What is a gray complexion indicative of in pneumonia?

A

toxic and dangerous pneumonia that required immediate medical attention

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41
Q

Rales

A

Fine inspiratory crackles from fluid in the alveoli

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42
Q

Rhonchi

A

Coarse inspiratory and expiratory crackles from mucus in the bronchi

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43
Q

What is consolidation in pneumonia?

A

Not being able to hear exchange of gasses because there is so much buildup that leads to exchange being unable to occur - very dangerous

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44
Q

How to tell the difference between heart and lung pleuritic pain?

A

If they hold their breath and you still hear the friction rub then it is heart pleurisy.

If they hold their breath and you can no longer hear the friction rub then it is Respirophasic

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45
Q

Diagnostics of Pneumonia?

A
  1. increased WBC and Erythrocyte Sedimentation Rate
  2. Chest X Ray
  3. Sputum and Blood Cultures
  4. ABGs
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46
Q

What does a CXR show when someone has pneumonia?

A

patchy or lobar pulmonary infiltrates

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47
Q

When do sputum and blood cultures get taken when a person has pneumonia?

A

BEFORE they get antibiotics

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48
Q

What do ABGs reveal/diagnose in regard to pneumonia?

A

Hypoxemia and Respiratory Alkalosis

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49
Q

Hypoxemia

A

Below normal level of oxygen in the blood (specifically the arteries) and it indicates a problem related to breathing or circulation - thus possibly resulting in symptoms like SOB

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50
Q

Respiratory Alkalosis

A
  • Secondary to hyperventilation

-pH of blood rises (basic) because hyperventilation gives off too much of the volatile acid CO2

  • Occurs in pneumonia
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51
Q

Important indications of Pneumonia in the Elderly?

A
  1. Sudden onset of confusion
  2. Weakness and lethargy
  3. Suddenly falling when the person usually does not fall (could also be falling due to a UTI)
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52
Q

Pathologic Changes / Pathogenesis of Classical Pneumonia

A
  1. Congestion
  2. Red Hepatization
  3. Gray Hepatization
  4. Resolution
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53
Q

Congestion Stage of Pneumonia

A

Starts in 4 to 24 hours

Serous exudate from the initial inflammatory response pours into the alveoli

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54
Q

Red Hepatization Stage of Pneumonia

A

Starts after 48 hours

Extravasation (leakage) of RBCs, fibrin, PMNs into the alveoli

Tissue turns firm and red

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55
Q

Gray Hepatization Stage of Pneumonia

A

Starts after 72 hours and Persists for about 1 Week

Fibrin accumulates and granulates

RBCs and PMNs start disintegrating

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56
Q

Resolution Stage of Pneumonia

A

Starts 1 Week or 12 days (without antibiotics); Occurs in about 48 hours (with antibiotics)

Enzymes lyse the consolidation

Macrophages phagocytize inflammatory cells

Exudate is Expectorated

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57
Q

Treatment of Pneumonia

A
  • Use a culture and sensitivity test (blood and sputum)( to determine the organism and appropriate antibiotic therapy to use

-It takes 48 hours for results, so it may be treated empirically (best guess) with Rocephin for most (gram positive) pneumonias/classic pneumonias

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58
Q

Rocephin

A

Cetriaxone

Antibiotic empirically used while waiting for culture test results for most pneumonia

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59
Q

Pneumococcal Pneumonia is often treated with

A

Penicillin and Cephalosporins

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60
Q

Gram Negative Pneumonia is often treated with

A

Gentamycin or Tobramycin

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61
Q

When administering antibiotics its important to keep what in mind?

A

Allergies

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62
Q

Nursing Care for Pneumonia

A
  1. Monitor VS (T, RR, HR)
  2. Medication Administration
  3. Observe for signs of Resp. Distress
  4. Encourage Cough and Deep Breathing
  5. Observe Sputum
  6. Chest PT, Postural Drainage, Suction
  7. Oxygen Therapy
  8. Pulse Oximetry
  9. Proper Positioning
  10. Plan Activities
  11. Plan Diet
  12. Plan Fluids
  13. Listen to Anxiety Expressions
  14. Cover Mouth and nose when Coughing
  15. Proper Oral Care
  16. Monitor Lab Studies
  17. Evaluate client outcomes (Evaluation of nursing Process)
  18. Teach prevention of pneumonia
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63
Q

Position for Pneumonia Patients

A

Semi Fowlers

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64
Q

What is important to plan in regard to activity for pneumonia patients?

A

Rest periods

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65
Q

What sort of diet is important for pneumonia patients?

A

High calorie and high protein diets

Lots of fluids (3-4 L L/Day PO and IV Fluids)

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66
Q

Why is great oral care important for pneumonia patients?

A

it gets secretions out and cleans part of the respiratory system

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67
Q

Why is chest PT important to pneumonia?

A

It vibrates mechanically to break up congestion, but this is a temporary relief and must be paired with postural drainage and suctioning

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68
Q

What Prevention Measures can be used against Pneumonia?

A
  1. Pneumococcal Vaccine
  2. Stop Smoking
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69
Q

Obstructive Respiratory Disorder

A

Disorder where air can get in, but not out

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70
Q

Restrictive Respiratory Disorder

A

Disorder where you cannot get air in but can get air out

The key to this one is that the lungs cannot expand/stretch for some reason

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71
Q

Obstructive Airway Disorders

A

Asthma
Chronic bronchitis
Emphysema
COPD
Cystic Fibrosis

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72
Q

Restrictive Airway Disorders

A

Pleural Effusion
hemothorax
Pneumothorax
Pneumoconioses
Thoracic Cage Disorders
Adult Respiratory Distress Syndrome

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73
Q

Pleural Effusion

A

fluid in the thoracic space stopping lung expansion

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74
Q

Hemothorax

A

Blood in the thoracic space stopping lung expansion

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75
Q

Pneumothorax

A

Collapsed lung as a result of air leaking into the space between the lung and chest wall

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76
Q

Pneumoconiosis

A

Black Lung Disease

Scarring from fine particles stops the lung from stretching

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77
Q

Thoracic Cage Disorder

A

the thoracic cage / chest wall cannot move thus making lung expansion difficult

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78
Q

ARDS

A

Adult Respiratory Distress Syndrome

Interstitial edema gets hard and prevents the lungs from stretching

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79
Q

Asthma

A

Hyper-responsive, reversible form of airway disease caused by restriction in airway size from bronchospasm, chronic inflammation, and increased airway secretions

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80
Q

If asthma has been triggered before…

A

it will respond even faster in subsequent events (but can be reversed somewhat/mitigated)

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81
Q

Bronchospasm

A

restricting the airway due to some trigger

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82
Q

What are the causes of the bronchospasm, chronic inflammation, and airway secretions in asthma?

A

Bronchial and bronchiolar narrowing from increased smooth muscle tone

mucosal edema

hypersecretion of mucus

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83
Q

We are NOT ____ asthma

A

solving/curing

there are so many triggers making this impossible

84
Q

Asthma is increasing in ___, ___, and ___

A

incidence, prevalence, and mortality

85
Q

The most common cause of chronic illness in children under the age of 17 is ?

A

Asthma

86
Q

Types of Asthma

A

Type 1 - Extrinsic Atopic
Type 2 - Intrinsic (Non-atopic) Idiopathic
EIA (Exercise induced asthma)
ASA Triad
Bronchial Asthma (another name for asthma)

87
Q

Type 1 Asthma

A

Extrinsic Atopic

Immediate hypersensitivity response mediated by IgE

Mast cells release histamine and prostaglandins on exposure to allergens (damage to the cell membrane had occurred, so prostaglandins cause pain and fever)

Usually there is a family history of allergies, uticaria, or hay fever

Usually affects children

Has a good prognosis (complete remission in adolescence)

88
Q

What is seen in a blood culture of a Type 1 Asthma attack>?

A

Increase in IgE and Eosinophils (eosinophils due to delayed reaction)

89
Q

Type 2 Asthma

A

Intrinsic Idopathic, Non Atopic (We do not know why it happens but it is not due to prior allergy

Onset in Adulthood (30 y/o and greater)

Chronic Mucopurulent (pus) Bronchitis

More serious, more difficult to control, poorer prognosis of recovery

90
Q

Atopic

A

Allergy

91
Q

Idiopathic

A

Unsure why it occurs

92
Q

EIA

A

Exercise Induced Asthma

40-90 % of asthma

Triggered by cold air not being warmed and humidified fast enough leading to low CO2 due to hyperventilation (which in turn causes Hypocapnia/Hypocarbia), and Hypocapnia

93
Q

ASA Triad

A

Aspirin Triad Asthma

The person has nasal polyps and a diagnosis of asthma

When they take aspirin or NSAIDs it causes a unique delayed hypersensitive asthmatic reaction hours after ingestion

Often accompanied by severe Rhinitis

94
Q

Two categories of Asthma Triggers

A

Bronchospastic Triggers

Inflammatory Triggers

95
Q

Bronchospastic/Bronchoconstriction Triggers of Asthma

A
  1. Cold air (loss of heat and water)
  2. Exercise (cause unclear)
  3. Emotional Upset (Vagal pathway activation)
  4. Exposure to bronchial irritants (irritant receptors and vagal reflex)
96
Q

Examples of Bronchial Irritants

A

Cigarette Smoke
Pollutants
Gases
Dust
Strong Odors

97
Q

Inflammatory Triggers of Asthma

A

Exerts effects through the inflammatory Response

  • IgE mediated response to allergens (i.e. dust mite and cockroach excrement, molds, mildew, animal dander)
98
Q

Early Response of Asthma

A
  • Immediate bronchoconstriction on exposure to inhaled irritant or antigen
  • symptoms appearing within 10-20 minutes

-recovery within 60-90 minutes

-early response caused by release of chemical mediators from IgE coated mast cells on the mucosa

99
Q

Late Response of Asthma

A

-Develops 3-5 hours after exposure to trigger and may last for days or weeks

  • involves inflammation and increased airway responsiveness

-caused by chem mediators from mast cells/macrophages/epithelial cells (which induce migration and activation of other inflammatory cells)

  • produces epithelial edema and injury, changes in mucociliary function, reduced clearance of secretions, and increased airway responsiveness
100
Q

Inflammatory response in asthma occurs as a ___ response

A

late

101
Q

Inhaler Types

A

Rescue Inhaler
Steroid Inhaler

102
Q

Rescue Inhaler

A

Very good to work on the early asthma response (ok for late response as well)

Only used somewhat allows you to have good control. only when needed is it used

103
Q

Steroid Inhaler

A

Corticosteroids work on the late response of asthma to control inflammation (not helpful for early response)

It does not rescue, you must use it daily no matter how you feel to treat underlying inflammation

104
Q

Manifestations due to Asthma

A
  • bronchi widen and lengthen on inspiration BUT collapse on expiration (this is why its hard to get air out and accessory muscles may be used)
  • expiration becomes difficult from edema, airway narrowing, and mucus obstruction

-primary issue is getting air out - hyperinflated lungs

-expiration needs use of accessory muscles

-decreased FEV1 and PEFR

-Dyspnea - Orthopnea

-Tachypnea

-Wheezing Especially on expiration

-PaO2 is 60-72 mmHg

-PaCO2 low initially due to increased respiratory response but increases over time due to decreased alveolar ventilation

-V/Q Mismatch

-Cyanosis

-Intercostal Retraction

-Fatigue

105
Q

Why is it hard to get air out in asthma?

A

bronchi widen and lengthen on inspiration BUT collapse on expiration (with potentially hyper inflated lungs)

106
Q

FEV1

A

Forces expiratory volume in 1 second

107
Q

PEFR

A

Peak Expiratory Flow Rate

lower than 75% means danger

108
Q

Pulsus Paradoxus

A

BP increase on inspiration and drastic decrease on expiration (below 50% of normal lung function)

109
Q

Below 25% PEFR indicates?

A

Respiratory Failure

110
Q

What is the partial pressure of O2 in asthma?

A

60-72 mmHg

111
Q

What occurs to the partial pressure of CO2 in asthma?

A

it will initially decrease due to hyperventilation initially, but increase as a result of decreased alveoli capability to exchange gases (alveolar ventilation)

112
Q

V/Q Mismatch in Asthma

A

*more common in chronic bronchitis, but can occur here

Hypoxemia and Hypercapnia unoxygenated blood returns to the L atriu, which causes pulmonary artery vasoconstriction and pulmonary HTN leading to R ventricular failure

113
Q

Hypocapnia

A

low CO2 in the bloodstream

114
Q

Hypercapnia

A

excessive CO2 in the bloodstream

115
Q

Intercostal Retraction

A

Reduced air pressure in your chest causing intercostal muscles to be sucked inward between the ribs when you breath

this indicates a blocked airway (trachea or bronchioles)

easier to see in children and infants

116
Q

Important Facts to know about Bronchial Asthma in Children

A
  • It is the most frequent admitting diagnosis in childrens hospitals
  • more common in boys
  • 1/3 have onset by age 1, but most occurences occur by age 4-5
  • 1 parent with it has a 25% of passing it on, and 2 have a 50% change of passing it on (BUT there are polygenic/multifactorial reasons/determinants other than just genetics)
117
Q

Pharmacologic Treatments for Asthma

A
  1. Beta 2 Adrenergic Bronchodilator
  2. Anticholinergic Bronchodilators
  3. corticosteroids
  4. Leukotriene Receptor Antagonists
  5. Mast Cell Stabilizers
118
Q

What pharmacologic treatment for asthma is for Prevention only?

A

Mast Cell Stabilizers (Cromolyn Sodium [intal])

they prevent release of histamine and prostaglandin thus getting in the way of inflammation and bronchoconstriction in the first place

119
Q

Leukotriene Receptor Antagonists

A

pharma treatment for asthma

they inhibit bronchoconstriction by blocking the inflammatory response that is due to leukotrienes

120
Q

Corticosteroids and Asthma

A

Can be inhaled, taken orally, or by IV

ex: Hydrocortisone, Methylprednisolone (IV), and Beclomethasone (Vanceril)

Work in the late stage of asthma against inflammation

Must be used on a normal schedule, DOES NOT RESCUE AT ALL (Steroid Inhaler)

121
Q

Anticholinergic Bronchodilators

A
  • pharma treatment of asthma

ex: ipratropium (Atrovent)

  • inhibits bronchoconstriction in asthma
122
Q

Beta 2 Adrenergic Bronchodilators

A

Pharma treatment of asthma

ex: Albuterol, Epinephrine (status asthmaticus choice), Xanthines

Adrenergic means SNS - so these are Rescue Inhalers working on B2 receptors of the SNS to cause bronchodilation

ex: Albuterol is a rescue inhaler; EP is an emergent treatment for life threatening asthma; Xanthines relax the smooth muscles and are a blood level rescue medication (so don’t use too much) that cause bronchodilation

123
Q

Nursing Care of Asthma

A
  1. Monitor VS (RR, HR)
  2. Administer Meds (Bronchodilators/Corticosteroids)
  3. Observe for Signs of Resp. Distress
  4. Chest PT, Postural Drainage, Suction
  5. PURSED LIP BREATHING observation
  6. Monitor urinary output (UO), I and O (input and output), and daily weight
    7/ Get sputum culture to determine any bacterial cause
  7. monitor thera drug levels (theophylline [xanthine])
  8. monitor lab studies
  9. Administer oxygen therapy
  10. Pulse Ox
  11. Positioning, Activity, Diet, Fluid, Anxiety, Oral Care Determinations
  12. Prep for Mechanical Ventilation if needed
  13. Evaluate treatment response
  14. Promote prevention measures
124
Q

How can stress exacerbate asthma attacks?

A

stimulate vagal pathways thus causing bronchoconstriction

125
Q

Prevention Measures for Asthma?

A

Stop Smoking
Reduce Stress
Desensitize with “Allergy Shots”
Environmental control

126
Q

Oxygen Therapy Recommendations for Asthma

A

2-3 L/min (28-30%) O2 via Venturimask

127
Q

When should oxygen therapy for asthma not be used?

A

in prolonged/severe attacks

128
Q

Positioning for Asthma Patients

A

High Fowlers

129
Q

Diet for Asthma Patients

A

High calorie and protein with small and frequent feedings

130
Q

Fluids for Asthma Patients

A

PO 3-4 L/day and IV fluids

131
Q

PFT

A

Pulmonary function test spirometry

the spirometer measures maximum air flow, lung volume, and other parameters which are important in understanding the individuals pulmonary (lung) function

132
Q

What are VC and FEV1 levels in Obstructive Respiratory Disorders?

A

VC is normal, but there is a decrease in FEV1 since they cannot get air out of the lungs (thus making 75-80% of the vital capacity getting out [FEV1])

133
Q

What are the VC and FEV1 levels in Restrictive Respiratory Disorders?

A

FEV1 is relatively the same in reference to VC, but the VC is lowered since air cannot get in (so there’s not enough air in the lungs even if 75-80% of what is there can still get out)

134
Q

COPD

A

Chronic Obstructive Pulmonary Disease (or chronic Obstructive Lung Disease (COLD), or Chronic Airway Obstruction (CAO))

It is a group of diseases that result in the obstruction of airflow (cannot get out air)

135
Q

What diseases does COPD include?

A

Chronic Bronchitis

Emphysema

136
Q

Describe Chronic Bronchitis

A

Inflammation of Bronchial Walls with hypertrophy of the mucous goblet cells

it is characterized by a chronic productive cough with copious mucus

often has frequent and recurrent respiratory infections

137
Q

Describe Emphysema

A

distended, inelastic, destroyed alveoli with bronchiolar obstruction and collapse

138
Q

Etiologies of COPD

A

Air Pollution
Smoking
Chronic Respiratory infections
Exposure to Molds and Fungi
Allergic Reactions

139
Q

Blue Bloater

A

Chronic Bronchitis

Oxygenation is difficult leading to cyanosis, and pressure in the lungs rise leading to the right ventricle having trouble pushing blood to the lungs leading to swelling

140
Q

Pink Puffer

A

Emphysema

Because it is hard work to breath, does not have blue tinge or hypoxia since theres hard amoung of work breathing, but they do breath hard and faster (puffer) and are typically very thin, SOB, find it hard to eat, use accessory muscles when breathing, and use up Calories trying to breath

141
Q

Diagnosis requirements for Chronic Bronchitis

A

Presence of chronic productive cough and bronchial wall inflammation for at least 3 months of a year OR 2 months per year for 2 successive years

142
Q

Why is there tons of mucus in chronic bronchitis?

A

the goblet cells hypertrophied leading to this

143
Q

Etiology of Chronic Bronchitis

A

Cigarette Smoking

Inhalation of Industrial Gases and Other Toxic Substances

144
Q

Why do the etiologies of chronic bronchitis cause the symptoms/signs of it?

A

Smoke and gases cause:

Inhibition of cilia and macrophages

inflammation of major and small airways

hypertrophy mucosal glands (causing excessive secretions)

narrowing and constriction of smooth muscle (leading to bronchoconstriction, airway alteration, and air flow changing)

145
Q

Manifestations of Chronic Bronchitis

A

Dyspnea on Exertion
Decreased PaO2
Increased PaCO2
Decreased Alveolar Ventilation
V/Q Mismatch
Scattered rhonchi and rales on Forced Expiration
Abnormal ABGs
Chronic Cough
Copious Yellow green Sputum
Exercise Intolerance
Polycythemia
Clubbing of fingers

146
Q

DOE

A

Dyspnea on Exertion - trouble breathing while doing something

147
Q

Decrease Alveolar Ventilation in Chronic bronchitis leads to…

A

decreased O2 and retained CO2 leading to acidosis (decreased pH)

148
Q

V/Q Mismatch value in chronic bronchitis?

A

Will be lower than 0.8 because lower ventilation leads to a smaller value (ex: 3/5L = 0.6)

149
Q

Hypoventilation of Alveoli occurs due to Air trapping hypoxemia, hypercapnia cyanosis (“blue bloater)… why is this?

A

Unoxygenated blood goes to the L atrium causing pulmonary artery vasoconstriction then pulmonary HTN, ultimately causing R ventricular failure leading to potential pedal edema, ascites, JVD, peripheral edema, or cor pulmonale

150
Q

How does the kidney react to Chronic Bronchitis?

A

Kidney sense hypoxia, so it secretes erythropoietin –> causing increased erythrocytosis –> thus causing cyanosis due to more blood with less oxygen on the Hgb

151
Q

Vasoconstriction leads to pulmonary hypertension in chronic bronchitis, thus causing what?

A

a pressure of 25/10 (high) that the R ventricular wall is not used to pushing against it causing blood backflow leading to edema, ascites, etc

152
Q

Pedal Edema

A

fluid in feet and ankles due to backflow in chronic bronchitis

153
Q

Ascites

A

fluid extravasation into the peritoneal cavity due to backflow in chronic bronchitis

154
Q

JVD

A

Jugular Vein Distension occurring due to chronic bronchitis

155
Q

Cor Pulmonale

A

A problem with the heart due to a lung disease

156
Q

Shunting

A

Where blood goes to areas in the pulmonary circuit where it CAN exchange with alveoli, and away from those that it cannot

This leads to patchy ventilation, aterial constriction, high lung pressure, right side lung failure

157
Q

Rhonchi occurs in ___ airways, and Rales occur in ____ airways

A

large; small

158
Q

If a chronic bronchitis patient can cough and clear a lung noise, it is probably…

A

a rhonchi since its easier to clear / expel those large airways

159
Q

Abnormal ABG values of chronic bronchitis patients and what they mean?

A

pH does not change, PaCO2 and HCO3- are high, and pO2 is low

Normal pH in this means theres compensation where HCO3- compensates for the high CO2 levels since it is a base - this can cause acidosis

160
Q

Fully Compensated Respiratory Acidosis

A

acidosis occurring in chronic bronchitis patients since bicarbonate must compensate for high CO2 leading to the kidney keeping extra bicarbonate to maintain a normal pH

161
Q

Clubbed Fingers indicate…

A

long hypoxemia (like in chronic bronchitis)

162
Q

Polycythemia can occur in what respiratory disease?

A

too many RBC, high Hct, High RBC rates

Chronic Bronchitis

163
Q

Emphysema

A

Obstructive resp disease different from bronchitis because it is due to the destruction of walls of alveoli (lack of elastic recoil)

dilation and loss of elasticity of airspaces distal to terminal bronchioles and loss of normal elastic recoil occurs

164
Q

In emphysema, expiration is ____

A

active (uses ATP)

Active occurs for both inhalation and expiration when expiration is normally passive

165
Q

Interestingly, the lack of a warm, moist environment for emphysema patients leads to…

A

decreased rates of infection, but they cannot cough the secretions out meaning the infections are more fatal when they do occur

166
Q

In early stages of emphysema, what can the patient do to prevent CO2 buildup?

A

stay well oxygenated with accessory muscle use to breathe

167
Q

What happens to larger airways in emphysema?

A

they become thinned and atrophied causing them to become more collapsible

168
Q

Because there is not higher pressure in the lungs for emphysema patients, there is no…

A

Cor Pulmonale or Peripheral Edema occurring

169
Q

Etiologies of Emphysema

A
  1. Cigarette Smoking (main overarching reason)
  2. Often autosomal recessive genetically determined
170
Q

Genetic Emphysema

A

Autosomal Recessive

Early onset (about 30 y/o) with severe progression

Deficiency of alpha antitrypsin, which normally inhibits proteolytic enzymes of leukocytes during inflammation of respiratory infections, occurs

This deficiency leads to a loss of inhibition of the enzymes causing digestion of the lung tissue alongside the bacteria

171
Q

Alpha 1 Antitrypsin

A

inhibits proteolytic enzymes to prevent alveolar degradation in the lungs

172
Q

How does smoking interact with Alpha 1 Antitrypsin?

A

it inactivates it too, causing the breakdown in emphysema from this etiology as well

173
Q

2 Types of Emphysema

A
  1. Centrilobular
  2. Panacinar
174
Q

Centrilobular Emphysema

A

emphysema associated with smoking

affects the resp bronchioles and alveolar ducts

unevenly distributed amongst the lungs BUT affects the upper and posterior portions more severely

175
Q

Panacinar Emphysema

A

destruction and enlargement of alveoli distal to the terminal bronchioles

emphysema associated with genetic abnormality or progression of chronic bronchitis

lower portions of the lung more affected

176
Q

Manifestations of Emphysema

A

Dyspnea even at rest

Tachypnea

V/Q NOT present

Respiratory Alkalosis from Hyperventilating or Normal ABGs

Little cough or sputum

Barrel chest

Inability to eat and weight loss

slowly debilitating

177
Q

Blebs

A

air filled areas where the alveoli have dilated in a person with emphysema

if near the lung wall they can rupture and lead to pneumothorax

tend to run in families

178
Q

Why is there dyspnea even at rest for emphysema?

A

because both inspiration and expiration become an active process

179
Q

Why is there NOT a V/Q mismatch in emphysema patients?

A

they lose function of both ventilation and perfusion due to the alveolar capillary network, so the value is relatively the same simply because both values lowered

180
Q

Why does respiratory alkalosis occur in emphysema?

A

because hyperventilation causes loss of a lot of CO2 (acid) leading to a higher / basic pH

181
Q

Barrel chest

A

hyperinflation of the lungs leading to a 1:1 thoracic ratio

indicative of emphysema

182
Q

How slowly can emphysema progress?

A

over 20-30 years - it is slowly debilitating

183
Q

Chronic Bronchitis v Emphysema: Barrel Chest

A

CB - May be present
Emp - Dramatic presence

184
Q

Chronic Bronchitis v Emphysema: Weight Loss

A

CB - infrequenty
Emp - may be severe in advanced disease

185
Q

Chronic Bronchitis v Emphysema: SOB

A

CB - Predominant early symptom
Emp - may be absent early in the disease process

186
Q

Chronic Bronchitis v Emphysema: Decrease Breath Sounds

A

CB - Variable
Emp - Characteristic of

187
Q

Chronic Bronchitis v Emphysema: Wheezing

A

CB - variable
Emp - usually absent

188
Q

Chronic Bronchitis v Emphysema: Rhonchi

A

CB - Often prominent
Emp - usually absent or minimal

189
Q

Chronic Bronchitis v Emphysema: Sputum

A

CB - frequent early symptom
Emp - may be absent or develop late

190
Q

Chronic Bronchitis v Emphysema: Cyanosis

A

CB - often dramatic
Emp - often absent even late in disease

191
Q

Chronic Bronchitis v Emphysema: Smoking History

A

CB - Usual
Emp - Usual

192
Q

Chronic Bronchitis v Emphysema: Age of Onset

A

CB - 30 to 40
Emp - 40 to 50

193
Q

Chronic Bronchitis v Emphysema: Blood Gases

A

CB- hypercapnia and hypoxemia may be present
Emp- relatively normal until late in disease

194
Q

Chronic Bronchitis v Emphysema: Cor Pulmonale

A

CB- frequent with peripheral edema occurring too
Emp- only in advanced cases

195
Q

Chronic Bronchitis v Emphysema: Polycythemia

A

CB- frequent
Emp- only in activated cases

196
Q

Chronic Bronchitis v Emphysema: Prognosis

A

CB- numerous life threatening episodes
Emp- slowly debilitating disease

197
Q

Treatment for COPD (Chronic Bronchitis and Emphysema)

A
  • control of environmental irritants and infection
    -nutritional support
    -exercise training
    -breathing exercises and retraining
    -managing secretions (more for chronic bronchitis)
    -pharmacologic treatment
    -oxygen therapy
    -psycho emotional support
198
Q

What is meant by treating COPD through control of environmental irritants and infection?

A
  • avoid cig smoke, pollutants, occupational exposures and individuals with known respiratory infections

-immunizations for flu and pneumococcal (pneumonia) infection

-early reporting of signs and symptoms

199
Q

How should COPD be treated with nutritional support?

A

Small, frequent, nutritional meals

ex: Pulmocare which is a high protein drink that takes less energy to digest - VERY important for emphysema which has pain eating and has active expiration

200
Q

Why is exercise important for COPD patients?

A

so they learn to use abdominal muscles (belly breathing) to breath and do exercise to keep themselves as fit as possible within disease parameters

201
Q

What is breathing exercises and retraining for COPD?

A
  1. Resistive loading inspiratory muscle training
  2. Pursed lip breathing and ab muscle assistance during expiration
202
Q

Pursed Lip Breathing

A

kiss shaped and blowing hard breathing that pops the alveoli open to breath easier

*more important for emphysema patients

203
Q

Pharmacologic Treatments for COPD?

A

Beta adrenergic agonists
Anticholinergic agents
Xanthines
Corticosteroids

*This is more important for asthma and chronic bronchitis rather than emphysema

204
Q

Anticholinergic Agents is used more for …

A

Chronic bronchitis than asthma or emphysema

205
Q

Oxygen Therapy for COPD Patients?

A
  • continuous LOW flow rate: 1-3 L/min
    -this is because the CO2 receptors may be tired from CO2 high pressure from being unable to breath out efficiently - so the O2 receptors are the impetus to breath, so low O2 flow gets them to breath in less and prevent acidosis or cessation of breathing

N351: Pathophysiology I (11 decks)

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