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
Who is parainfluenza virus pneumonia most deadly for?
Infants and Premature Infants
26
CMV
Cytomegalovirus that has a 90% mortality rate from causing pneumonia in those who got transplants, are immunocompromised, elders, and infants
27
Atypical Pneumonia is caused by ...
Mycoplasma pneumoniae It does not appear in the aveolar sacs and does NOT cause the characteristic productive cough of normal pneumonia
28
Histoplasmosis
fungal infectious agent that grows in soil enriched by bird feces that can cause pneumonia
29
If aspiration occurs due to gastric contents, what can happen to the lungs?
they can get burned - thus causing pneumonia
30
American Thoracic Society on Community-Acquired Pneumonias?
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
31
Subjective Manifestations of Pneumonia
1. Lassitude and severe malaise 2. Chest pain that increases with inspiration 3. Dyspnea
32
Lassitude
no energy to do anything
33
Objective Manifestations of Pneumonia
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
34
Orthopnea
Having to sit up to breathe, cannot do it lying down
35
Sputum colors are not ___ of pneumonia
diagnostic *they just give a good picture and guess - need sputum culture to diagnose
36
Pneumococcal Pneumonia Sputum
Purulent and Rusty
37
Staphylococcal Pneumonia Sputum
Yellow and Blood Streaked
38
Klebsiella Pneumonia Sputum
Red and Gelatinous
39
Mycoplasma Pneumonia Sputum
Non-productive that advances to mucoid (atypical pneumonia)
40
What is a gray complexion indicative of in pneumonia?
toxic and dangerous pneumonia that required immediate medical attention
41
Rales
Fine inspiratory crackles from fluid in the alveoli
42
Rhonchi
Coarse inspiratory and expiratory crackles from mucus in the bronchi
43
What is consolidation in pneumonia?
Not being able to hear exchange of gasses because there is so much buildup that leads to exchange being unable to occur - very dangerous
44
How to tell the difference between heart and lung pleuritic pain?
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
45
Diagnostics of Pneumonia?
1. increased WBC and Erythrocyte Sedimentation Rate 2. Chest X Ray 3. Sputum and Blood Cultures 4. ABGs
46
What does a CXR show when someone has pneumonia?
patchy or lobar pulmonary infiltrates
47
When do sputum and blood cultures get taken when a person has pneumonia?
BEFORE they get antibiotics
48
What do ABGs reveal/diagnose in regard to pneumonia?
Hypoxemia and Respiratory Alkalosis
49
Hypoxemia
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
50
Respiratory Alkalosis
- Secondary to hyperventilation - pH of blood rises (basic) because hyperventilation gives off too much of the volatile acid CO2 - Occurs in pneumonia
51
Important indications of Pneumonia in the Elderly?
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)
52
Pathologic Changes / Pathogenesis of Classical Pneumonia
1. Congestion 2. Red Hepatization 3. Gray Hepatization 4. Resolution
53
Congestion Stage of Pneumonia
Starts in 4 to 24 hours Serous exudate from the initial inflammatory response pours into the alveoli
54
Red Hepatization Stage of Pneumonia
Starts after 48 hours Extravasation (leakage) of RBCs, fibrin, PMNs into the alveoli Tissue turns firm and red
55
Gray Hepatization Stage of Pneumonia
Starts after 72 hours and Persists for about 1 Week Fibrin accumulates and granulates RBCs and PMNs start disintegrating
56
Resolution Stage of Pneumonia
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
57
Treatment of Pneumonia
- 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
58
Rocephin
Cetriaxone Antibiotic empirically used while waiting for culture test results for most pneumonia
59
Pneumococcal Pneumonia is often treated with
Penicillin and Cephalosporins
60
Gram Negative Pneumonia is often treated with
Gentamycin or Tobramycin
61
When administering antibiotics its important to keep what in mind?
Allergies
62
Nursing Care for Pneumonia
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
63
Position for Pneumonia Patients
Semi Fowlers
64
What is important to plan in regard to activity for pneumonia patients?
Rest periods
65
What sort of diet is important for pneumonia patients?
High calorie and high protein diets Lots of fluids (3-4 L L/Day PO and IV Fluids)
66
Why is great oral care important for pneumonia patients?
it gets secretions out and cleans part of the respiratory system
67
Why is chest PT important to pneumonia?
It vibrates mechanically to break up congestion, but this is a temporary relief and must be paired with postural drainage and suctioning
68
What Prevention Measures can be used against Pneumonia?
1. Pneumococcal Vaccine | 2. Stop Smoking
69
Obstructive Respiratory Disorder
Disorder where air can get in, but not out
70
Restrictive Respiratory Disorder
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
71
Obstructive Airway Disorders
``` Asthma Chronic bronchitis Emphysema COPD Cystic Fibrosis ```
72
Restrictive Airway Disorders
``` Pleural Effusion hemothorax Pneumothorax Pneumoconioses Thoracic Cage Disorders Adult Respiratory Distress Syndrome ```
73
Pleural Effusion
fluid in the thoracic space stopping lung expansion
74
Hemothorax
Blood in the thoracic space stopping lung expansion
75
Pneumothorax
Collapsed lung as a result of air leaking into the space between the lung and chest wall
76
Pneumoconiosis
Black Lung Disease Scarring from fine particles stops the lung from stretching
77
Thoracic Cage Disorder
the thoracic cage / chest wall cannot move thus making lung expansion difficult
78
ARDS
Adult Respiratory Distress Syndrome Interstitial edema gets hard and prevents the lungs from stretching
79
Asthma
Hyper-responsive, reversible form of airway disease caused by restriction in airway size from bronchospasm, chronic inflammation, and increased airway secretions
80
If asthma has been triggered before...
it will respond even faster in subsequent events (but can be reversed somewhat/mitigated)
81
Bronchospasm
restricting the airway due to some trigger
82
What are the causes of the bronchospasm, chronic inflammation, and airway secretions in asthma?
Bronchial and bronchiolar narrowing from increased smooth muscle tone mucosal edema hypersecretion of mucus
83
We are NOT ____ asthma
solving/curing there are so many triggers making this impossible
84
Asthma is increasing in ___, ___, and ___
incidence, prevalence, and mortality
85
The most common cause of chronic illness in children under the age of 17 is ?
Asthma
86
Types of Asthma
Type 1 - Extrinsic Atopic Type 2 - Intrinsic (Non-atopic) Idiopathic EIA (Exercise induced asthma) ASA Triad Bronchial Asthma (another name for asthma)
87
Type 1 Asthma
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
What is seen in a blood culture of a Type 1 Asthma attack>?
Increase in IgE and Eosinophils (eosinophils due to delayed reaction)
89
Type 2 Asthma
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
Atopic
Allergy
91
Idiopathic
Unsure why it occurs
92
EIA
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
ASA Triad
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
Two categories of Asthma Triggers
Bronchospastic Triggers Inflammatory Triggers
95
Bronchospastic/Bronchoconstriction Triggers of Asthma
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
Examples of Bronchial Irritants
``` Cigarette Smoke Pollutants Gases Dust Strong Odors ```
97
Inflammatory Triggers of Asthma
* Exerts effects through the inflammatory Response* | - IgE mediated response to allergens (i.e. dust mite and cockroach excrement, molds, mildew, animal dander)
98
Early Response of Asthma
- 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
Late Response of Asthma
- 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
Inflammatory response in asthma occurs as a ___ response
late
101
Inhaler Types
Rescue Inhaler | Steroid Inhaler
102
Rescue Inhaler
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
Steroid Inhaler
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
Manifestations due to Asthma
- 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
Why is it hard to get air out in asthma?
bronchi widen and lengthen on inspiration BUT collapse on expiration (with potentially hyper inflated lungs)
106
FEV1
Forces expiratory volume in 1 second
107
PEFR
Peak Expiratory Flow Rate lower than 75% means danger
108
Pulsus Paradoxus
BP increase on inspiration and drastic decrease on expiration (below 50% of normal lung function)
109
Below 25% PEFR indicates?
Respiratory Failure
110
What is the partial pressure of O2 in asthma?
60-72 mmHg
111
What occurs to the partial pressure of CO2 in asthma?
it will initially decrease due to hyperventilation initially, but increase as a result of decreased alveoli capability to exchange gases (alveolar ventilation)
112
V/Q Mismatch in Asthma
*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
Hypocapnia
low CO2 in the bloodstream
114
Hypercapnia
excessive CO2 in the bloodstream
115
Intercostal Retraction
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
Important Facts to know about Bronchial Asthma in Children
- 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
Pharmacologic Treatments for Asthma
1. Beta 2 Adrenergic Bronchodilator 2. Anticholinergic Bronchodilators 3. corticosteroids 4. Leukotriene Receptor Antagonists 5. Mast Cell Stabilizers
118
What pharmacologic treatment for asthma is for Prevention only?
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
Leukotriene Receptor Antagonists
pharma treatment for asthma they inhibit bronchoconstriction by blocking the inflammatory response that is due to leukotrienes
120
Corticosteroids and Asthma
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
Anticholinergic Bronchodilators
- pharma treatment of asthma ex: ipratropium (Atrovent) - inhibits bronchoconstriction in asthma
122
Beta 2 Adrenergic Bronchodilators
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
Nursing Care of Asthma
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 8. monitor thera drug levels (theophylline [xanthine]) 9. monitor lab studies 10. Administer oxygen therapy 11. Pulse Ox 12. Positioning, Activity, Diet, Fluid, Anxiety, Oral Care Determinations 13. Prep for Mechanical Ventilation if needed 14. Evaluate treatment response 15. Promote prevention measures
124
How can stress exacerbate asthma attacks?
stimulate vagal pathways thus causing bronchoconstriction
125
Prevention Measures for Asthma?
Stop Smoking Reduce Stress Desensitize with "Allergy Shots" Environmental control
126
Oxygen Therapy Recommendations for Asthma
2-3 L/min (28-30%) O2 via Venturimask
127
When should oxygen therapy for asthma not be used?
in prolonged/severe attacks
128
Positioning for Asthma Patients
High Fowlers
129
Diet for Asthma Patients
High calorie and protein with small and frequent feedings
130
Fluids for Asthma Patients
PO 3-4 L/day and IV fluids
131
PFT
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
What are VC and FEV1 levels in Obstructive Respiratory Disorders?
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
What are the VC and FEV1 levels in Restrictive Respiratory Disorders?
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
COPD
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
What diseases does COPD include?
Chronic Bronchitis Emphysema
136
Describe Chronic Bronchitis
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
Describe Emphysema
distended, inelastic, destroyed alveoli with bronchiolar obstruction and collapse
138
Etiologies of COPD
``` Air Pollution Smoking Chronic Respiratory infections Exposure to Molds and Fungi Allergic Reactions ```
139
Blue Bloater
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
Pink Puffer
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
Diagnosis requirements for Chronic Bronchitis
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
Why is there tons of mucus in chronic bronchitis?
the goblet cells hypertrophied leading to this
143
Etiology of Chronic Bronchitis
Cigarette Smoking Inhalation of Industrial Gases and Other Toxic Substances
144
Why do the etiologies of chronic bronchitis cause the symptoms/signs of it?
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
Manifestations of Chronic Bronchitis
``` 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
DOE
Dyspnea on Exertion - trouble breathing while doing something
147
Decrease Alveolar Ventilation in Chronic bronchitis leads to...
decreased O2 and retained CO2 leading to acidosis (decreased pH)
148
V/Q Mismatch value in chronic bronchitis?
Will be lower than 0.8 because lower ventilation leads to a smaller value (ex: 3/5L = 0.6)
149
Hypoventilation of Alveoli occurs due to Air trapping hypoxemia, hypercapnia cyanosis ("blue bloater)... why is this?
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
How does the kidney react to Chronic Bronchitis?
Kidney sense hypoxia, so it secretes erythropoietin --> causing increased erythrocytosis --> thus causing cyanosis due to more blood with less oxygen on the Hgb
151
Vasoconstriction leads to pulmonary hypertension in chronic bronchitis, thus causing what?
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
Pedal Edema
fluid in feet and ankles due to backflow in chronic bronchitis
153
Ascites
fluid extravasation into the peritoneal cavity due to backflow in chronic bronchitis
154
JVD
Jugular Vein Distension occurring due to chronic bronchitis
155
Cor Pulmonale
A problem with the heart due to a lung disease
156
Shunting
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
Rhonchi occurs in ___ airways, and Rales occur in ____ airways
large; small
158
If a chronic bronchitis patient can cough and clear a lung noise, it is probably...
a rhonchi since its easier to clear / expel those large airways
159
Abnormal ABG values of chronic bronchitis patients and what they mean?
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
Fully Compensated Respiratory Acidosis
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
Clubbed Fingers indicate...
long hypoxemia (like in chronic bronchitis)
162
Polycythemia can occur in what respiratory disease?
*too many RBC, high Hct, High RBC rates* Chronic Bronchitis
163
Emphysema
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
In emphysema, expiration is ____
active (uses ATP) Active occurs for both inhalation and expiration when expiration is normally passive
165
Interestingly, the lack of a warm, moist environment for emphysema patients leads to...
decreased rates of infection, but they cannot cough the secretions out meaning the infections are more fatal when they do occur
166
In early stages of emphysema, what can the patient do to prevent CO2 buildup?
stay well oxygenated with accessory muscle use to breathe
167
What happens to larger airways in emphysema?
they become thinned and atrophied causing them to become more collapsible
168
Because there is not higher pressure in the lungs for emphysema patients, there is no...
Cor Pulmonale or Peripheral Edema occurring
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Etiologies of Emphysema
1. Cigarette Smoking (main overarching reason) | 2. Often autosomal recessive genetically determined
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Genetic Emphysema
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
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Alpha 1 Antitrypsin
inhibits proteolytic enzymes to prevent alveolar degradation in the lungs
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How does smoking interact with Alpha 1 Antitrypsin?
it inactivates it too, causing the breakdown in emphysema from this etiology as well
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2 Types of Emphysema
1. Centrilobular | 2. Panacinar
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Centrilobular Emphysema
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
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Panacinar Emphysema
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
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Manifestations of Emphysema
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
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Blebs
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
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Why is there dyspnea even at rest for emphysema?
because both inspiration and expiration become an active process
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Why is there NOT a V/Q mismatch in emphysema patients?
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
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Why does respiratory alkalosis occur in emphysema?
because hyperventilation causes loss of a lot of CO2 (acid) leading to a higher / basic pH
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Barrel chest
hyperinflation of the lungs leading to a 1:1 thoracic ratio indicative of emphysema
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How slowly can emphysema progress?
over 20-30 years - it is slowly debilitating
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Chronic Bronchitis v Emphysema: Barrel Chest
CB - May be present | Emp - Dramatic presence
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Chronic Bronchitis v Emphysema: Weight Loss
CB - infrequenty | Emp - may be severe in advanced disease
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Chronic Bronchitis v Emphysema: SOB
CB - Predominant early symptom | Emp - may be absent early in the disease process
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Chronic Bronchitis v Emphysema: Decrease Breath Sounds
CB - Variable | Emp - Characteristic of
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Chronic Bronchitis v Emphysema: Wheezing
CB - variable | Emp - usually absent
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Chronic Bronchitis v Emphysema: Rhonchi
CB - Often prominent | Emp - usually absent or minimal
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Chronic Bronchitis v Emphysema: Sputum
CB - frequent early symptom | Emp - may be absent or develop late
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Chronic Bronchitis v Emphysema: Cyanosis
CB - often dramatic | Emp - often absent even late in disease
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Chronic Bronchitis v Emphysema: Smoking History
CB - Usual | Emp - Usual
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Chronic Bronchitis v Emphysema: Age of Onset
CB - 30 to 40 | Emp - 40 to 50
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Chronic Bronchitis v Emphysema: Blood Gases
CB- hypercapnia and hypoxemia may be present | Emp- relatively normal until late in disease
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Chronic Bronchitis v Emphysema: Cor Pulmonale
CB- frequent with peripheral edema occurring too | Emp- only in advanced cases
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Chronic Bronchitis v Emphysema: Polycythemia
CB- frequent | Emp- only in activated cases
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Chronic Bronchitis v Emphysema: Prognosis
CB- numerous life threatening episodes | Emp- slowly debilitating disease
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Treatment for COPD (Chronic Bronchitis and Emphysema)
- 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
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What is meant by treating COPD through control of environmental irritants and infection?
- 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
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How should COPD be treated with nutritional support?
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
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Why is exercise important for COPD patients?
so they learn to use abdominal muscles (belly breathing) to breath and do exercise to keep themselves as fit as possible within disease parameters
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What is breathing exercises and retraining for COPD?
1. Resistive loading inspiratory muscle training | 2. Pursed lip breathing and ab muscle assistance during expiration
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Pursed Lip Breathing
kiss shaped and blowing hard breathing that pops the alveoli open to breath easier *more important for emphysema patients
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Pharmacologic Treatments for COPD?
Beta adrenergic agonists Anticholinergic agents Xanthines Corticosteroids *This is more important for asthma and chronic bronchitis rather than emphysema
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Anticholinergic Agents is used more for ...
Chronic bronchitis than asthma or emphysema
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Oxygen Therapy for COPD Patients?
- 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