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S3 - Pathophysiology > Emphysema, Chronic Bronchitis & Asthma, Lung Parenchyma Disorders, Disease of Pulmonary Vasculature > Flashcards

Emphysema, Chronic Bronchitis & Asthma, Lung Parenchyma Disorders, Disease of Pulmonary Vasculature Flashcards

1
Q

EMPHYSEMA

A

EMPHYSEMA

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2
Q

Does COPD describe a single pathology?

A

No, it is an umbrella term for 3 different pathologies.

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3
Q

What 3 pathologies are under COPD?

A
  • Emphysema
  • Chronic Asthma
  • Bronchitis
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4
Q

COPD is the _____ leading cause of death in America. Often, patients with emphysema have __________. ____ million US adults are estimated to have COPD. ____ million US adults have reported a physician diagnosis of chronic bronchitis.

A
  • fourth
  • lung cancer
  • 12.7
  • 10.1
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5
Q
  • What is the most common risk factor of COPD?

- What are some others?

A

-SECONDHAND SMOKE

  • exposure to air pollution
  • occupational dusts and chemicals
  • heredity
  • Hx of childhood respiratory infections and socioeconomic factors
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6
Q

The 3 pathologies of COPD (emphysema, chronic obstructive bronchitis, chronic asthma) _______ air flow. These may occur ____________ or in combination with one another.

A
  • obstruct

- independently

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7
Q

Is COPD a specific diagnosis?

A

NO

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8
Q

What are the presenting signs of COPD?

A
  • dyspnea
  • sputum production
  • chronic cough
  • reduced function
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9
Q
  • What is the most basic and frequently performed test of pulmonary function?
  • Emphysema is diagnosed when the FEV1/FVC ratio is
A
  • Spirometry

- 0.70

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10
Q

What is Emphysema?

A

Pathological accumulation of air in the lungs.

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11
Q

Emphysema is a disease of ________ and is characterized by ___ _________ in the lungs.

A
  • exhalation

- air trapping

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12
Q

Emphysema causes an ________ in residual volume (RV) and total lung capacity (TLC), and a decrease in the ____/_____ ratio.

A
  • increase

- FVC1/FVC

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13
Q

What is the genetic cause of Emphysema?

A

1

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14
Q

Alpha-1 Antitrypsin:

  • Alpha-1 antitrypsin (A-1AT) is a protein found in the ______ and synthesized in the _______.
  • A-1AT protects the lungs from the degrading actions of powerful enzyme called ________ ________ (↑ elastin degradation) and other proteases. This elastase is produced and released by neutrophils.
  • A-1AT coats cells and provides protection against the neutrophil elastase.
  • Serum concentrations of A-1AT can rise many fold during periods of acute __________ providing protection from inflammatory damage.
A
  • blood, liver
  • neutrophil elastase
  • inflammation
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15
Q

Cigarette smoke ___________ A-1AT leaving the lung susceptible to damage. Smoking causes a ____________ state which means that neutrophils are busy, lots of elastase and reduced effectiveness of A-1AT.

A
  • inactivates

- hyperinflammatory

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16
Q

A-1AT Deficiency and Cigarette Smoking:

  • Destruction of individual _______
  • Development of “_____” alveoli
  • Destruction of _____ supports for the very smallest airways allowing them to collapse during expiration
A
  • alveoli
  • “super”
  • CT
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17
Q

1 in ___ cases of Emphysema are not linked to tobacco use.

A

7

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18
Q

Emphysema:

  • Creates ________ lungs with _______ alveoli (super alveoli)
  • __________ becomes problematic
  • Forced expiration causes smaller airways to _________ during expiration
  • Leads to “___ _______” in the alveoli
  • Results in ↓ alveolar ____
  • ________ disease
  • FEV1/FEV < .5 = ___ ______
A
  • hyperinflated lungs with enlarged alveoli
  • Exhalation
  • collapse
  • air trapping
  • PO2
  • Progressive
  • bad news
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19
Q
  • What is the first complaint that presents itself in Emphysema?
  • What are some other clinical manifestations?
A

-SOB at rest

  • Apprehensive, anxious, addicted to O2
  • Thin, cachectic
  • Deformed chest with prolonged expiration
  • Absent or non-productive cough
  • Mild disease (mild hypoxemia)
  • With progression hypoxemia worsens and CO2 is retained
  • Chronic pulmonary metabolic acidosis
  • Deconditioning
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20
Q

Emphysema patients can have accompanying ________ problems, more specifically ____ _______.

A
  • cardiac

- cor pulmonale

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21
Q

Emphysema has a _____ prognosis. It is ________, ____________, and debilitating. It may present with lung _______.

A
  • poor
  • chronic, progressive
  • lung cancer
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22
Q

Is PT of benefit to patients with Emphysema?

A

Yes

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23
Q

6 Emphysema Treatments Implications for the PT.

A

1) reducing airway edema secondary to inflammation and bronchospasm
2) facilitating the elimination of bronchial secretions
3) preventing and treating respiratory infection
4) increasing exercise tolerance
5) avoiding airway irritants and allergens
6) relieving anxiety and treating depression

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24
Q

Emphysema Medications.

A
  • β2 agonists or anticholinergics
  • Antiinflammatory agents
  • Antibiotics
  • Mucolytic expectorants
  • Mast cell membrane stabilizers
  • Antihistamines
  • Glucocorticoids
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25
Q

In Emphysema, patients with PaO2 of 55 or less, or a resting O2 sat of 88% (2x 3 weeks apart) or less may be on long term ____ therapy.

A

O2

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26
Q

Emphysema Implications for the PT:

  • Always use ______ __
  • Monitor __, __ and __ frequently
  • The first heart sound (closing of the tricuspid and mitral valves) is best heard under the sternal area. Hyper inflated lungs causes the heart to elongate, displacing the left ventricle downward and medially.
A
  • pulse ox

- HR, RR, and BP

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27
Q

Those who retain CO2 may have a ________ hypoxic drive i.e. very low PO2 needed to help drive the respiration.

A

-decreased

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28
Q

What is a Metered-Dose Inhaler (MDI)?

A

Used to deliver drugs to the lungs.

  • Users take in slow deep breath over 10s while maintaining seal and pressing on the device
  • Evaluate the ability of the child or adult to correctly use the MDI
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29
Q

CHRONIC BRONCHITIS AND ASTHMA

A

CHRONIC BRONCHITIS AND ASTHMA

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30
Q

Emphysema = “____ _______”

Chronic Bronchitis = “______ ________”

A
  • pink puffer

- blue bloater

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31
Q

What is Chronic Bronchitis?

A

Productive cough lasting at least 3 months per year for 2 consecutive years.

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32
Q

A FEV1/FEV

A

75%

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33
Q

What is Chronic Bronchitis characterized by?

A
  • Inflammation
  • Excessive mucous production
  • Scarring of lining of the bronchial tubes
  • Obstruction of bronchial air flow is caused by increased mucous production/reduced mucous clearance
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34
Q
  • Chronic Bronchitis is caused by _______ exposure to irritants causes mucus hypersecretion and hypertrophy of mucous producing glands in the larger bronchi.
  • It involves the destruction of ciliary cells lining ______.
  • It is associated with _______ r4!
A
  • chronic exposure
  • airways
  • decreased
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35
Q
  • Chronic Bronchitis often begins with recurrent ______ ______ that brings mucus from the lungs. This increases over the course of the day and as the disease worsens.
  • _________ is associated with narrowed airways.
  • Symptoms are typically ___________.
A
  • morning cough
  • wheezing
  • progressive
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36
Q

What can cause exacerbations of Chronic Bronchitis?

A
  • Triggered by upper- or lower-airway infections.

- Triggered by exposure to environmental irritants such as dust, fumes, or air pollution.

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37
Q

Chronic Bronchitis patients tend to be polycythemic. What is this and why?

A
  • Increased concentration of hemoglobin in the blood.

- If they are hypoxic, make more to transport more O2.

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38
Q
  • Chronic Bronchitis patients tend to have _____, prolonged ________, persistent _________ with expectoraton, and recurring _________.
  • These patients also tend to be _______.
A
  • SOB, prolonged expiration, persistent cough, recurring infection
  • obese
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39
Q

Blue Bloaters:

  • Decreasing ___________
  • Increasing ___ and decreasing expiratory flow
  • Dreadful / mismatch with much shunting.
  • Hypoxemia, hypercapnia, cyanosis, polycythemia
  • ____ ________ secondary to chronic pulmonary HTN
  • Pulmonary Rehabilitation Programs
A
  • ventilation
  • RV
  • V/Q
  • cor pulmonale
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40
Q

Chronic Bronchitis PT Implications:

  • Reduce exposure to irritants
  • Bronchodilators (- ________)
  • Mucolytics
  • NSAIDs
A

B-2 Agonists

41
Q

Chronic Bronchitis or Emphysema?

  • Recurrent Cough
  • Thin Appearance
  • CO2 Retention
  • Cyanosis
A
  • Recurrent Cough = Chronic Bronchitis
  • Thin Appearance = Emphysema
  • CO2 Retention = Emphysema
  • Cyanosis = Emphysema
42
Q

Asthma is a _________, reversible, __________ lung disease characterized by _____________ resulting from exaggerated __________ response of the airway smooth muscles to various stimuli.

A
  • episodic
  • obstructive
  • bronchospasms
  • inflammatory
43
Q

Asmtha = Bronchial ______reactivity

44
Q

What are the clinical manifestations of Asthma?

A
  • episodic dyspnea

- coughing and wheezing

45
Q
  • What are the 2 main types of Asthma?
  • Which is a result of an allergic reaction to specific triggers?
  • Which has no known allergic cause or trigger and has an adult onset?
A
  • Extrinsic and Intrinsic
  • Extrinsic
  • Intrinsic
46
Q

Intrinsic asthma is most often secondary to chronic or recurrent _________ of the bronchi, sinuses, or tonsils and adenoids.

47
Q

Asthma Pathogenesis:

  • An ____________ response consisting of cellular infiltration, epithelial disruption, mucosal edema, and mucous plugging airways.
  • Inflammatory ____________ produces bronchial smooth muscle spasm; vascular congestion; increased vascular permeability; edema formation; production of thick, tenacious mucus; and impaired mucociliary function.
A
  • inflammatory

- mediators

48
Q

What is the clinical course of Asthma?

A
  • Attack characterized by dyspnea with wheezing
  • Upper airway obstruction occurs
  • Difficulty with expiration
  • Air trapping occurs in distal alveoli and hyperinflation
  • Hypercapnia, acidotic
  • Repeated attacks cause airway remodeling, chronic air trapping, proliferation of submucosal glands, and hypertrophied smooth muscle
49
Q

Asthma Treatment:
-Identifying and avoiding ________ and __________
Use of ___________ (B2 agonists) and _____-___________ agents
Low dose _____________

A
  • triggers and allergens
  • bronchodilators and anti-inflammatory
  • corticosteroids
50
Q

_______ ________ Bronchospasm is an acute, reversible, and self terminating that develops 5-15 minutes after vigorous intensity exercise and subsides in 30-60 minutes.

A

Exercise Induced Bronchospasms

51
Q

LUNG PARENCHYMA DISORDERS

A

LUNG PARENCHYMA DISORDERS

52
Q

When does pulmonary edema occur?

A

When the pulmonary vasculature fills with fluid that leaks into the IS spaces or the vasculature becomes very leaky allowing fluid to escape into the IS space.

53
Q

Once fluid leaks into the IS spaces, fluid can then move into the ________ spaces, what does this do?

A
  • alveolar spaces

- decreases the space available for gas exchange

54
Q

Pulmonary Edema Develops as a Result of:

  • ______ overload
  • decreased ________
  • _________ obstruction
  • increased capillary ___________
A
  • fluid
  • albumin
  • lymphatic
  • permeabilty
55
Q

The early stages of pulmonary edema present as persistent _______, slight __________, _________, and intolerance to exercise.

A
  • cough
  • dyspnea
  • diaphoresis (sweating)
56
Q

As Pulmonary Edema worsens, what happens?

A
  • dyspnea becomes more acute
  • respirations increase in rate
  • audible wheezing
  • cough becomes productive-frothy sputum tinged with blood, giving it a pinkish hue
57
Q

What is treatment of Pulmonary Edema aimed at?

A
  • enhancing gas exchange
  • reducing fluid overload
  • strengthening and slowing the heartbeat
58
Q
  • What does the prognosis of pulmonary edema depend on?

- Is the presence of pulmonary edema a medical emergency?

A
  • Depends on the underlying condition

- Yes

59
Q

What is Acute Respiratory Distress Syndrome (ARDS)?

A

A condition that causes fluid to leak into your lungs, limiting the movement of air into the alveoli (hypoxemia!!)

60
Q
  • Most people who get ______ are already in the hospital for something else such as sepsis, accidents, or pulmonary toxic molecules.
  • ARDS occurs when a pulmonary or extrapulmonary insult causes the release of __________ mediators.
A
  • ARDS

- inflammatory

61
Q

ARDS is characterized by what?

A

Widespread inflammation in the lungs.

62
Q
  • ARDS results in impaired gas exchange within the lungs at the level of the __________.
  • ARDS causes rapidly progressing _______, _________ and _________.
  • ARDS is associated with a high mortality rate between __ and __%.
A
  • alveoli
  • dyspnea, tachypnea, and hypoxemia
  • 20-50%
63
Q

What are some of the complications that ARDS creates?

A
  • Atelectasis
  • Pneumothorax
  • Widespread organ damage/failure
  • Kidney failure
  • Cardiogenic shock
  • Long term scarred lungs and ICU acquired weakness
64
Q
  • What is atelectasis?

- What is pneumothorax?

A
  • collapsed lung

- accumulation of air in pleural space

65
Q

._________ is the COLLAPSE of normally expanded and aerated lung tissue at any structural level

A

Atelectasis

66
Q

What are the 3 categories of Atelectasis?

A
  • Obstructive-absorptive
  • Non-obstructive
  • Compressive
67
Q

The primary cause of _______-________ Atelectasis is obstruction of the bronchus serving the affected area. Describe it.

A

Obstructive-absorptive

  • communication between the alveoli and the trachea is obstructed
  • air in the alveoli is not replaced
  • air diffuses into the blood
  • alveoli collapse
68
Q

____-_________ Atelectasis is an interference with the natural forces that drive lung expansion. Describe it.

A

Non-obstructive

  • hypoventilation associated w/ decrease pulmonary motion
  • failure to breath deeply post-op because of pain leading to muscle guarding and splinting
  • oversedation, coma, immobility
  • loss of surfactant
69
Q

___________ Atelectasis is caused externally (pneumothorax, hemothorax (blood), hydrothorax (fluid) in pleural cavity).

A

Compressive

70
Q

Compression of the lungs implications for the therapist?

A
  • Frequent gentle position changes, deep breathing, coughing, ambulation sooner rather than later.
  • These interventions promote ciliary clearance, mucus clearance, enhanced lung expansion.
71
Q

____________ is the abnormal collection of air in the pleural space.

A

Pneumothorax

72
Q
  • Pneumothorax is typically __________. The air may be removed with a syringe or a chest tube.
  • Can it resolve without treatment?
A
  • unilateral

- Yes, small spontaneous pneumothorax will typically resolve without treatment.

73
Q

Pneumothorax can only develop if air is allowed to enter the pleural through damage to the _________ or the _____ itself.

A
  • chest wall

- lung

74
Q

What are the 2 types of Lung Cancer?

A
  • Small cell lung cancer (SCLC)

- Non-small cell lung cancer (NSCLC)

75
Q

Small Cell Lung Cancer (SCLC):

  • Cells become so dense that there is almost no cytoplasm present and the cells are compressed into an ovoid mass
  • SCLC tends to be located ________, most often near the hilum of the lung
  • __________ and distant _______ are usually present at the time of diagnosis
  • Occurs most frequently in smokers
  • Very __________, typically metastasizes before diagnosed
A
  • centrally
  • lymphatic and distant metastases
  • aggressive
76
Q

Non-Small Cell Lung Cancer (NSCLC):

  • Acccounts for about __% of all lung cancers
  • Spread of the primary cancer to other locations
  • Involves lymph and blood vessels
  • Metastases: ______, ______ and ______
  • __________ of the kidney, breast, pancreas, colon, and uterus are likely to metastasize to the lung
A
  • 85%
  • brain, bone, and liver
  • Carcinomas
77
Q

How are most lung cancers diagnoses?

A

Routine chest X-rays

78
Q

What are the clinical manifestations of Lung Cancers?

A
  • cough, sputum production and dyspnea
  • anorexia, fatigue, weakness, weight loss
  • recurring bronchitis or pneumonia
  • difficulty swallowing
  • cardiac and esophageal compression
79
Q

DISEASES OF THE PULMONARY VASCULATURE

A

DISEASES OF THE PULMONARY VASCULATURE

80
Q
  • What is Pulmonary Hypertension (PH)?
  • What is normal pulmonary mmHg?
  • What is considered PH?
A
  • High BP in the pulmonary arteries
  • 15-18 mmHg
  • 5-10 mmHg above normal
81
Q
  • ________ PH is rare and may be idiopathic.

- Who is PH most common in?

A
  • Primary

- young and middle aged women

82
Q

PH is characterized by diffuse __________ or the pulmonary arterioles caused by _________ of _______ muscle in the vessel walls and formation of ________ lesions in and around vessels.

A
  • narrowing
  • hypertrophy of smooth muscle
  • fibrous lesions
83
Q

The pathology of PH is ____________.

A

vasoconstriction (r4!!)

84
Q

What are some underlying causes of PH?

A
  • CHF
  • blood clots in lungs
  • HIV
  • cocaine or meth use
  • liver disease
  • lupus, scleroderma, RA, other autoimmune diseases
  • lung diseases like emphysema, chronic bronchitis, or pulmonary fibrosis
  • congenital heart diseases
85
Q

Pulmonary Hypertension treatment is predicated on ______.

  • Right sided Heart failure
  • Hypoxia due to chronic lung disease
  • Sleep apnea
  • Autoimmune diseases
86
Q

Primary PH pharmacologic management includes what?

A
  • Prostoglandins
  • Viagra
  • Traclee
  • Letairis
87
Q

PH is _________ to diagnose and there is a delay of __-__ years between onset of symptoms and diagnosis.

A
  • difficult

- 1-2 years

88
Q

What tests can be used to diagnose PH?

A
  • Pulmonary function tests
  • Oximetry
  • V/Q scan
  • blood tests
  • exercise capacity tests
  • R heart catheterization
89
Q

Pulmonary Hypertension results in impaired _______ capacity with CV pump dysfunction or failure.

A

aerobic capacity (endurance)

90
Q

The mean life expectancy after prognosis of PH is - years and _____.

A
  • 2-3 years

- poor

91
Q

What are the risk factors for Pulmonary Embolism?

A
  • Prolonged immobility (bed rest)
  • Hypercoagulability (meds, smoking, polycythemia, cancer, surgery)
  • Damage to the walls of the veins
92
Q

A patient with a cancer diagnosis has a _x chance of having a PE or DVT.

93
Q

Symptoms of PE?

A
  • chest pain
  • dyspnea
  • apprehension
  • cough
  • hemoptysis
  • diaphoresis
  • syncope
  • cardiopulmonary arrest
  • palpitation
  • chest tightness
94
Q

Signs of PE?

A
  • tachypnea
  • tachycardia
  • hypotension
  • gallop
  • rales
  • temp
  • edema
  • cyanosis
95
Q

3 Clinical Classifications of PE?

A 
Low Risk PE
-normotensive
-no RV dysfunction
-normal biomarkers
Intermediate Risk PE
-normotensive
-RV dysfunction/dilation
-Myocardial necrosis
High Risk PE
-Hypotension
-Pulselessness
-Profound bradycardia
96
Q

Pulmonary Embolism:

  • ______ that may occur suddenly
  • Sudden, sharp chest pain that may become worse with deep breathing or coughing
  • ______ heart rate
  • Rapid breathing
  • Sweating
  • Anxiety
  • Coughing up blood or pink, foamy mucus
  • Fainting
A
  • SOB

- rapid

97
Q

Is a lung a difficult organ to harvest?

A

Yes, 15% of cadaveric lungs are recovered

-severe shortage

98
Q

Lung Transplant are given anti-rejection drugs such as what?

A
  • Cyclosporine
  • Tacrolimus
  • Antimetabolites
99
Q

Lung Transplantation:

  • Patients are badly __________
  • Wound management
  • Initiating airway _________ techniques
  • Patient has lots of lines and wires
  • Slow progression/improvement
  • Exercise
  • Want to monitor O2 sats, vital signs & breathing patterns
A
  • deconditioned

- clearance

S3 - Pathophysiology (14 decks)

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