Obstructive and Restrictive Lung Disease Flashcards

1
Q

what is Respirtory Lung Dysfunction: aka Restrictive Lung exspanison diminshed

A

RLD: an abnormal reduction in pulmonary ventilation. Lung expansion is diminished. The volume of gas moving in and out of the lungs is decreased.

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2
Q

What things physilogically affect the Respiratory Lung Dysfunction

A

Aspects of ventilation contributing to RLD

Compliance of the lung and the chest wall
Alteration in lung volumes and capacities
Work of breathing

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3
Q

What is Compliance and what happens if it is reduced???

A

Physiological link that establishes a relationship between the pressure exerted by the chest wall and/or the lungs and the volume of air that can be contained within the lungs

In RLD, chest wall and/or lung compliance is reduced.

ranspulmonary gradient needed just to expand the lungs.

Decreased chest wall compliance  limits thoracic expansion and therefore, lung inflation, even if lung compliance is normal.

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4
Q

What is diminshed when Respiratory lung dysfunction occurs???

ERV goes up or down

Tidal volume - goes up or down

IRV- up or down

A

RLD eventually causes all lung volumes and capacities to be reduced.
When the lung becomes less compliant, the IRV is diminished
Tidal volume also decreases as the work of breathing increases
ERV is reduced, this reduction is particularly pronounced if lung compliance is the principle etiology of the RLD.

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5
Q

What the most two common measures used to ID RLD while using spirometer? and What is indicated by a decrease in TLC and FRC ?

Total lung capacity: the volume in the lungs at maximal inflation, the sum of VC and RV.

Vital capacity: the volume of air breathed in after the deepest inhalation

http://en.wikipedia.org/wiki/Lung_volumes

A

Total Lung Capacity and Vital Capacity are the two most common measures used to identify RLD

Decreases in TLC and FRC are a direct result of a decrease in lung compliance

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6
Q

What is the 3 ways that work of breathing increases

A

In RLD, work of breathing is increased.

Work of breathing is increased by:
Increased airway resistance
Increases in flow rates
Decreases in lung or chest wall compliance

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7
Q

Compensatory mechanism

How does the lungs deal with a decreased breathing compliance.

A

To overcome the decrease in pulmonary compliance, the respiratory rate is usually increased
Accessory muscles of inspiration are recruited either at rest or at a lower activity level, in order to assist with chest wall expansion.

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8
Q

How much does a normal person use of VO2 at rest vs. Someone with RLD how much VO2 do they use???

A

In normal persons at rest, the body uses less than 5% of the VO2 (ie 3-14 ml O2/min) to support the work of breathing

With RLD the % of VO2 required to support the work of breathing can be 25% or more

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9
Q

What are the six classic signs of Respiratory Lung Dysfunction

A

Six classic signs often indicate and are consistent with RLD
Tachypnea
Hypoxemia
Alteration in breath sounds on auscultation
Decrease in lung volumes/capacities
Decreased diffusing capacity
Cor Pulmonale

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10
Q

What is tachypnea???

Tidal Volume- by the way is the NORMAL lung volume without any extra effort being made amount of air inhaled and exhaled.

A

An involuntary adjustment is made to increase the respiratory rate to compensate for the decrease in tidal volume thereby maintaining the same minute ventilation

Early in RLD, overcompensation may occur which results in alveolar hyperventilation

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11
Q

What is hypoxemia? How does it come about

A

Ventilation-Perfusion Mismatching
May occur as a result of:
Changes in the collagenous framework of the lung
Scarring of capillary channels
Distortion or narrowing of the small airways
Compression from tumors in the lung
Bony abnormalities of the chest wall

Decreased oxygen in the blood.

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12
Q

What happens with Tidal voulme, IRV, ERV,

A

Decrease in Tidal volume
Decrease in inspiratory reserve volume
Decrease in expiratory reserve volume
Residual volume is decreased, but degree of decrease may not be as dramatic as that seen in the IRV and ERV

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13
Q

Why does the diffusion capacity decrease with RLD? think scarring

A

DLCO is decreased as a result of a widening of the interstitial spaces due to scar tissue, fibrosis of the capillaries, and ventilation-perfusion abnormalities.

In RLD DLCO has been measured at less than 50% of predicted.

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14
Q

What is Cor Pulmonale?

A

Right sided heart failure resulting from hypoxemia, fibrosis, and compression of the pulmonary capillariespulmonary hypertension.
Because the pulmonary capillaries are fibrotic, they are less capable of distending to handle the ordinary increase in cardiac output expected with exercise

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15
Q

Symptoms associated with RLD

A

Dyspnea

Dry non productive cough

Wasted, emaciated appearance

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16
Q

What is the treatment typically for RLD

A

If etiological factors are permanent or progressive, supportive measures are mostly utilized:
Antibiotic therapy
Measures to promote adequate ventilation
Supplemental oxygen
Prevention of accumulation of pulmonary secretions
Nutritional support

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17
Q

What is obstructive lung dysfunction

A

Diseases of the respiratory tract that produce an obstruction to airflow. This obstruction to airflow can ultimately affect both the mechanical and gas exchanging capability of the lungs.

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18
Q

Typical changes seen with Obstructive lung disease

A

Increased mucus production/impaired mucus secretion
Inflammation of the mucosal lining of the bronchi and bronchioles
Mucosal thickening
Spasm of the bronchial smooth muscle

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19
Q

Two ways that the bronchioles shutdown.

A

Narrowing of the bronchial lumen
Increased resistance to airflow

Loss of normal elastic recoil of lung tissuetendency for the airways to collapse
hyperinflation

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20
Q

What does the work rate of breathing increase

A

Respiratory muscles must work harder to overcome the increased airway resistance
Diaphragm excursion may be limited due to hyperinflation of the lungs
Alveolar ventilation is reduced
Alveolar-capillary membrane surface area may be reduced.

To determine the diaphargmatic distance you can tap on the chest to hear the hollowness upon tapping on it. Also in an X-ray if the lungs are flat then then they are pushing down on the diapharggm and the diaphragm is not expanded

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21
Q

Clinical manisfestations or Signs of Obstructive Lung Disease or OLD

A
Signs
Hypoxemia
Increased production of mucus/impaired clearance
Pulmonary Hypertension
Polycythemia
Cor Pulmonale
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22
Q

External signs of OLD

A

Chronic cough
Expectoration of mucus
Wheezing
Dyspnea on Exertion

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23
Q

Classfications of Obstruction

A

Bronchi or airways with cartilage in their walls (>2mm in diameter)

Bronchioles or airways without cartilage in their walls (<2mm in diameter)

Lung parenchyma (alveolar units): portion of the lung involved in gas exchange.

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24
Q

What are some enviormental factors that can lead to Obstructive Lung Disease and what decade of life does it usally come about???

A
Environmental factors
Pollution
Noxious gases
Occupational exposures
Cigarette smoking

Functionally, not notable until the sixth or seventh decade of life

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25
Q

When does compliance start to decrease in an individual and why does compliance start to decrease.

A

Compliance of the pulmonary system starts to decrease at about age 20

Thorax undergoes changes
Decalcification of ribs
Calcification of costal cartilage

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26
Q

Why does control of ventilation start to decrease what receptors start to lose their abilities

A

Control of ventilation undergoes significant change
Peripheral chemoreceptors are not as responsive to hypoxia
Central receptors are not as responsive to acute hypercapnea- the dam nigger meant to say hypercapnia which is a increase in CO2 in the body and the body losses its ability to detect after a certain amount of time.

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27
Q

what do EEG studies show about OLD.

A

Lung tissue itself shows enlargement of the air spaces owing to enlargement of the alveolar ducts and terminal bronchioles
Alveolar surface area decreases
EEG studies have shown that total nocturnal sleep time is shorter with more frequent awakenings.

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28
Q

What happens with old age

Does TLC change??

Does RV change??

VC?

MVV?

Flow rates??

A
PFTs (Things with old age) 
TLC (total lung capacity are usually unchanged
RV is increased
VC is decreased by about 25% by age 70
Flow rates are decreased
MVV is decreased by about 30%
Diffusing capacity is decreased
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29
Q

Do chest x-rays show bony changes within the thorax after old age?

ABG- Does PaO2 decrease by age 70? What about CO2 does it increase or decrease

A

CXR can show a variety of changes in the bony thorax and in the lung parenchyma

ABGs: the PaO2 is normally decreased to about 75mm Hg at age 70; PaCO2 is normal or slightly elevated

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30
Q

What about cardiovascular changes with old age

Does SV, CO, HRmax decrease or increase

A

Breath sounds: auscultation often reveals slightly diminished breath sounds

CV findings:
HRmax decreases
SV decreases
CO decreases

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31
Q

Why don’t adults realize the decreased lung capacity with old age??? (2 ) reasons

A

Pulmonary reserve is quite large, so that individuals do not usually note changes until the 7th decade.
Often individuals become more sedentary, especially those with comorbidities in other systems.

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32
Q

How much can a sedentary person improve his or her cardiovascular capabilites once starting a new exercise routine.

A

A sedentary elderly person beginning a regular exercise routine can improve their maximal oxygen consumption by 5-25%

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33
Q

Idiopathic Pulmonary Fibrosis what is?

A

An inflammatory process involving all the components of the alveolar wall that progresses to gross distortion of the lung architecture.

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34
Q

Etiology of idiopathic Pulmonary Fibrosis speculated theroies

A

Unknown. May be viral, genetic, or auto-immune. Process seems to begin with inflammation, but then the response to the inflammation continues to generate further abnormalities

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35
Q

patholophysiology of idiopathic pulmonary fibrosist

What happens with the Pulmonary capabilties such as RV, TV, etc..

What do the breathe sounds like??

Can this essentially lead to cor pulmonale

A

Lung involvement shows patchy focal lesions scattered throughout both lung fields
Lesions first show inflammatory changes and then scar and become fibrotic, distorting the capillary network and alveolar septa.

PFTs
Decreased TLC, VC, FRC, and RV
Normal or slightly decreased flow rates
Diffusing capacity is decreased
As the disease progresses the VT decreases and the RR increases

Breath sounds: auscultation reveals bibasilar end-inspiratory dry rales and possibly decreased breath sounds.

CV findings: as the pulmonary capillary bed is destroyed, pulmonary hypertension develops. This can lead to cor pulmonale due to the strain on the right ventricle.

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36
Q

What are some symptoms of idiopathic pulmonary fibrosis think like dyspnea, weight loss, anorexia etc..

A
Symptoms:
Dyspnea
Repetitive non productive cough
Weight loss
Anorexia
Sleep disturbances
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37
Q

What is the typical treatment for idiopathic pulmonary fibrosis

A

Corticosteroids are frequently used in treatment to combat the inflammatory process to help vasodilate I believe.

Supportive measures such as maintaining adequate oxygenation with supplemental oxygen, ventilatory support, and nutritional support.

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38
Q

Bronchiolitis Obliterans what is?

A

A fibrotic lung disease that affects the smaller airways. It can produce both restrictive and obstructive lung dysfunction

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39
Q

Etiology of Bronchiolitis Obliterans??

A

Adult form of disease occurs in those ages 20-80
Causes:
Toxic fume inhalation
Viral, bacterial or mycobacterial infectious agents (particularly mycoplasma pneumoniae)
Associated with connective tissue disorders
Related to organ transplantation (graft vs h

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40
Q

Whats the pathophyisology of the Bronchiolitis obliterans “starts with nercosis”

A

Characterized by necrosis of the respiratory epithelium in the affected bronchioles
Necrosis allows fluid and debris to enter the alveolipulmonary edema and partial or complete obstruction of the airway
With complete obstruction, the trapped air is absorbed and the alveoli collapseatelectasis

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41
Q

Symptoms of the BO what happens to RR, Flow Rate, Lung volume, ??? everything doesn’t decrease.

A

Diffusing capacity is reduced
Lung volumes may be normal or decreased
RR is increased
Flow rates are frequently WNLs, but may be decreased

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42
Q

What does the Chest X-ray look like with this disease

What is the ABG like??? Areterial blood gas PaCO2 does it increase the arterial PH??

A

CXR: may show pulmonary edema; bilateral patchy infiltrates
Later in clinical course, a nodular pattern, consistent with fibrotic changes may be seen

ABGs: hypoxemia is present in most patients; An elevated PaCO2 may result in respiratory acidosis

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43
Q

what does the chest sound like in BO

What are the symptoms : hacking???

A

Breath sounds: Rales and often expiratory wheezing are heard on auscultation. Areas of decreased breath sounds is also common

Symptoms:
Dyspnea
Increased RR
Hacking, non productive cough

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44
Q

What is the treatment for BO????

very similair to idiopathic pulmonary fibrosis??

but watch fluid balance??

A

Corticosteroids may be used, especially in those cases resulting from toxic fume inhalation, or associated with connective tissue disease
Supportive measures such as supplemental oxygen and maintaining proper fluid balance

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45
Q

What is pneumonia???? what are its two ways to be caught?

A

An inflammatory process of the lung parenchyma. This inflammation usually begins with an infection of the lower respiratory tract.
Two categories
Community acquired
Nosocomial or hospital acquired

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46
Q

Etiology how does the virus, and community based pneumoia occur???

What percent does a virus affect???

How do humans usally get rid of the illness???

A

Community acquired pneumonias
Bacteria account for the majority of these pneumonias
Viruses account for about 1/3 of these pneumonias

Although there are many infectious agents in the environment, few pneumonias develop due to the efficient defense mechanisms of the lung

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47
Q

What are the ways that a patient may acquire pneuomia in the hospital??? Think tubes

A

Hospital acquired pneumonias
Defined as infections in the LRT with an onset of 72 hours or more after hospitalization
Generally occur in the sickest patients
Risk factors: nasogastric tube placement, intubation, dysphagia, tracheostomy, mechanical ventilation, Thoracicabdominal surgery, lung injury, diabetes, h/o smoking

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48
Q

What part of the lungs usally gets infected first with pneumoia, and does it and how does our body combat the pneuomia??

A
Bacteria and other microbes commonly enter the LRT.
Defense mechanisms
Cough
Bronchoconstriction
Angulation of the airways
Mucociliary escalator
The immune defenses
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49
Q

What is the most common pathway for pneumoia

What does a patient usally present when he or she has pneumoia??

A

Most common pathways are inhalation and aspiration
Bacterial pneumonias usually have an abrupt onset. Characterized by lobar consolidation, high fever, chills, dyspnea, tachypnea, productive cough, pleuritic pain, and leukocytosis

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50
Q

How does Viral Pneumonia come about????

Does it cause Edema and hemorrhage??

A

Viral pneumonias first localizes in the destruction of the mucosal surface.
If viral infection reaches the level of the alveoli, there may be edema, hemorrhage, hyaline membrane formation
Viral pneumonia has an insidious onset, patchy diffuse infiltrates, moderate fever, dyspnea, tachypnea, nonproductive cough, myalgia, and abnormal WBC

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51
Q

What happens with Lung voulme and pneumoia

What about lung compliance

Gas exchange

RR

Work of breathing

A
PFTs
Decreased lung volumes
Decreased lung compliance
Decreased gas exchange
Increased RR
Increased work of breathing
52
Q

Chest ex-ray for pneumonia

Bacteria pneumonia- what does it look like where is the problem on the x ray what part of the lung

Viral Pneumoia- what does the x-ray look like

A

Bacterial pneumonias show a lobar consolidation

Viral pneumonias show a diffuse scattered fluffy shadows, patchy alveolar infiltrates which follow the distribution of the central conducting airways
When cavities are seen in addition to the other findings above, the pneumonia is described as necrotizing pneumonia

53
Q

What the breath sounds like with pneumoia, What about PaCO2 does it increase or decrease

A

Most patients are hypoxemic
PaCO2 may be reduced as most patients are tachypneic

Breath sounds: Vary, bubbling rales, rhonchi, bronchial breath sounds, decreased or absent breath sounds, pleural ru

54
Q

Symptoms of Pneumoia is tachycardia one of them what about myalgia, and what if its a high is it bacterial or viral what about a moderate fever???

A

CV findings: tachycardia

Symptoms:
High fever (bacterial); moderate fever (viral)
Chills
Dyspnea
Productive cough
myalgias
55
Q

What are some treatments think like precussion its not just corticosterioids and supplemental oxygen there are some other alte whrnatives for pneumoia.

A
Drug therapy
Antibiotics for bacterial pneumonias
Oxygen supplementation
Chest PT 
Postural drainage
Percussion
vibration
Hydration
Nutritional support
56
Q

Streptococcus Pneumoniae who is it most common in?????

What color is the septum in this case

liver dysfunction????

A
More common in :
the elderly
Alcoholics
People with multiple myeloma
CHF
COPD
Specific signs/Sx:
Rusty colored sputum
Hemoptysis
Bronchial breath sounds
Egophony
Pleural effusion in 25% of patients
Slight liver dysfunction
57
Q

Legionella Pnuemophila? what is the main anitbiotic for this disease

A

Can occur in epidemic proportions because the organism is water borne an can emanate from air conditioning equipment
The antibiotic of choice is erythromycin

58
Q

Haemophilus Influenzae what medication do they give you???

Who is most common in????

A

Signs/Sx:
Sore throat
Empyema

Preferred antibiotic is ampicillin

More common in:
Alcoholics
COPD
elderly

59
Q

Klebsiella pneumoniae and how is it acquired in a community based area

And who is more prevelant in a hospital or nosocomial based areas

A
Community acquired
More common in:
Men 
Alcoholics
COPD
DM
Nosocomial 
More common in:
Debilitate patients
Alcoholics
DM
Malignancy
Chronic Renal Disease
Cardiopulm disease
60
Q

Pseudomonas Aeruginosa –> is this the most common of the nosocimal hospital diseases

What are its signs think confusion is one of them

A

Most common cause of nosocomial pneumonias

This necrotizing pneumonia causes alveolar septal necrosis, microabscesses and vascular thrombosis

Signs/Sx:
Confusion
Bradycardia
Hemorrhagic pleural effusion

Treatment always involves two drugs

61
Q

Staphylococcus aureus

Who is it seen in??? Childern age 2?

Whats the signs whats the treatments

A

Causes approximately 5% of community acquired pneumonias

Usually seen in:
children < 2yrs
Patients with CF
Patients with COPD

Signs/Sx
Insidious onset
Cough 
Fever
Dyspnea

Treatment with antistaphylococcal penicillin, cephalosporin, and vancomycin

62
Q

Mycoplasma Pneumoniae are they bacteria or viral “trick question”

A

Class of organisms which is intermediate between bacteria and viruses
They have no rigid cell wall (like bacteria)
They do not require host cell mechanisms to replicate (viral)

Course of the disease is approximately 4 weeks

Treatment with erythromycin or tetracycline

63
Q

Cytomegalovirus

A

Most common in immunocompromised hosts

Persons most at risk
Underlying Cardiopulmonary disease
Immunosuppressed
Pregnant

Treated with dehydroxyphenylglycol

64
Q

Pneumocystis Carinii

what is this disease usally associated think aids and how is it treated really complicated drug name

A

Parasitic protozoa which causes pneumonia

Most commonly associated with AIDS

Treated with trimethoprim-sulfamethoxazole
or pentamidine

65
Q

Psittacosis Pneumonias who usally gets pisittacossi

What is the treatment think tetra__________?

A

Causes approximately 12% of community acquired pneumonias in students and 6% in the elderly

and Treatment is with tetracycline or chloramphenicol

66
Q

Adult Respiratory Distress Syndrome

What is this disease

How does it come about think more external like drug abuse, shock not just virus

A

A clinical syndrome caused by acute lung injury. Characterized by severe hypoxemia and increased permeability of the alveolar capillary membrane.

Trauma: fat emboli, lung contusion, heart-lung transplantation
Aspiration: drowning or gastric contents
Drugs: heroin, barbituates, narcotics
Inhaled toxins: smoke, high oxygen concentrations
Shock
Massive blood Transfusion: sepsis

Metabolic: acute pancreatitis, uremia
Primary pneumonias: viral, bacterial, p. carinii
Other: intracranial pressure, post cardiopulmonary bypass, amniotic fluid embolism, ascent to high altitudes

67
Q

Pathphysiology of Adult Respiratory Distress Syndrome think premability is the big thing here

What about the acute phase may it reslove itself???

A

Primary pathological change is an increase in the permeability of the pulmonary capillary membrane
The excess fluid and plasma proteins are allowed to move into the interstitial tissue and then cross into the alveoli
This change from an air-filled to a fluid filled organ markedly decreases the compliance of the lung

Acute phase may resolve completely so that the patient regains normal lung function

If patient enters a subacute phase, alveolar fibrosis and capillary obliteration develop within the lung which leads to chronic restrictive dysfunction

68
Q

What happens to the FRC, VC RR, Flow rate, VT within Adult respiratory distress syndrome

A

PFTs
FRC, VC and VT are all decreased
Due to the decreased compliance of the lung, the work of breathing is increased and the RR is increased
Flow rates may be normal or somewhat decreased
Diffusion capacity is decreased

69
Q

How does the CXR- symetrical for ARDS, is PaO2 decreased what about PaCO2 ???

A

CXR: symmetric, bilateral, diffuse, fluffy infiltrates

ABGs:
PaO2 by definition is less than 60mm Hg
PaCO2 is usually decreased
In cases of CO2 retention, PaCO2 will be elevated

70
Q

Symptoms of ARDS

Breath Sounds: Do they sound wet, rales, wheezing, stridor are all these present?

What about CV findings is pt. tachycardia and arrythmia

A

Breath sounds: decreased breath sounds are heard over fluid filled areas of the lungs; wet rales are a common finding; wheezing and rhonchi may also be found depending on the precipitating cause of ARDS
CV findings:
Tachycardia
Arrythmias

71
Q

What are the symptoms of ARDS think like headache rapid shallow breathing

etc…

A
Symptoms:
Dyspneic at rest
Rapid shallow breathing pattern
Headache
Impaired mental status
cyanosis
72
Q

How to treat ARDS think supplmental oxygen pretty sevre disease. Remember electrolytes

A

Treat the precipitating cause of ARDS
Support adequate gas exchange and tissue oxygenation until ARDS resolves
Supportive management of nutritional status and fluid/electrolyte balance
Prevent and treat complications of the patient’s condition

73
Q

Sarcoidosis

A

A multisystem disease that is characterized by the presence of noncaseating epitheloid granulomas in many organs. Clinically, the lung is the most involved organ

74
Q

Who acquires scaroidosis? black male 20-40

A
Unknown
Most common in young adults ages 20-40
More common in women than men
Incidence is 10x more prevalent in blacks as compared to whites (american)
Rare in native american indians
75
Q

Patho of Scarodolosis what the three trademark signs

A

Three distinctive features:
Alveolitis
formation of well-defined round or oval granulomas (collection of marcophages)
pulmonary fibrosis

Disease progression is very variable

76
Q

What does the Chest x-ray look like is it symetrical

What happens to TLC, and all lung volumes

V/Q ratio lung complance

A

PFTs
TLC and all lung volumes are reduced
Lung compliance is decreased
Diffusing capacity is decreased primarily due to V/Q mismatching

CXR: bilateral hilar lymphadenopathy is common; lung parenchyma shows diffuse infiltrates

77
Q

What happens to PaO2 late in the disease with Sacodolosis

Breathe Sounds: what about the apicies

A

ABGs: WNLs until late in the disease when PaO2 may decrease

Breath sounds: commonly reveals bibasilar rales , decreased breath sounds in the apices due to bullae; possibly wheezes from bronchial obstruction

78
Q

Sacrodoloasis

CV findings:

Symptoms: vague retrosternal discomfort

Direct effects on the heart: think CHF etc.. remember its a mutilple system disease

Symptoms: where is the discomfort sometimes

A

CV findings: Pulmonary Hypertension develops in 15% of patients
Direct effects on the heart from sarcoidosis include dysrythmias, CHF, papillary muscle dysfunction

Symptoms: dyspnea; cough; vague retrosternal discomfort

79
Q

What is the treatment for Sacrodoloasis: only mentions one to help decrease the alveolitis

A

Corticosteroids to suppress the alveolitis and granuloma formation

80
Q

How does the spinal cord get damaged two ways:

A

Can result from acute trauma or from a pathological process that invades the spinal cord and damages it.

81
Q

What happens over time when a patient has a SCI

think avelovi deflation

A

Paradoxical breathing
Over time the pulmonary compliance is decreased due to the shallow breathing and atelectasis within the lung
Chronic state of hypoxemia

82
Q

SCI
What happnes to TLC, VC, IC

ERV - decreases if???

RR-

RV-

Tidal volume

A
TLC, VC, IC are decreased
ERV is eliminated if there are no active expiratory muscles
RV = FRC
RV is increased
Flow rates are decreased
RR is increased
Tidal volume is diminished
83
Q

SCI

What happens to ribs over time

Breathe sounds

CV findings

Auntnomic Dysreflexia - occurs in lesions above T7

A

CXR: Ribs become more horizontal over time
ABGs: hpoxemia is normal is high cervical lesions
Breath sounds: diminished breath sounds
CV findings: lesions above T7 may have episodes of autonomic dysreflexia

84
Q

SCI

whats autonomic dysreflexia good review

Symptoms include: fatique, dyspnea, irritable

A

Autonomic dysreflexia: vasoconstriction below the level of the injury which causes hypertension. The CNS above the level of the lesion tries to compensate by causing vasodilation and bradycardia.
Symptoms: fatigue, dyspnea, inability to cough, irritable (due to hypercapnia)

85
Q

Treatment for SCI think of gary from Helen Hayes Hospital???

Assited Cough, what else think everything a PT could do????

A
Strength  and endurance training of the respiratory muscles
Active and passive chest wall stretching
Assisted cough
Postural drainage
Chest PT
Suctioning
86
Q

What is ALS good review

A

A progressive degenerative disease of the nervous system that involves upper and lower motor neurons, causing both flaccid and spastic paralysis

Flaccid usally in the legs and Spasms in the upper pathways??

87
Q

How is generally affected by ALS?

Males more than Females????

A

Unknown
Onset is usually >40yrs age
Males are affected 1.7x as often as females

88
Q

With ALS are males affected more than females?? What causes ALS?

A

Unknown
Onset is usually >40yrs age
Males are affected 1.7x as often as females

89
Q

Where does ALS usally affect??? what part of the spinal column

A

Anterior horn cells of cervical, thoracic, and lumbosacral spinal segments are usually the most involved

Following onset of neurological symptoms, the average life expectancy is 3.6 years

90
Q

TLC, IC, VC, ERV are decreaseds

RV is usally increased because the air is typically trapped

CXR: how does that appear

ABG’s : is Pa02 decreased and PaCO2 is increased

A

TLC, IC, VC and ERV are all decreased
RV is usually increased
RR usually increases and VT is decreased

CXR: WNL or may show infiltrates
ABGs: PaO2 is decreased and PaCO2 is increased due to alveolar hypoventilation

91
Q

How do the breath sounds? Sound like???

A

Breath sounds: very decreased breath sounds; possible rales or rhonchi
Symptoms: weakness or wasting of muscles; muscular fasciculations

92
Q

What is the treatment for ALS remember its very progressive disease..

A

the only therapy is supporitive therapy

93
Q

What is poliomyleitis? describe it

A

viral disease that attacks the motor nerve cells of the spinal cord and brain stem and can result in muscular paralysis

94
Q

How does polymyelitis about?

Etiology?

Pathophysiology two stages: preparalytic and paralytic:

A

Etiology: acute viral infection

Lesions are patchy and asymmetric
Microscopically healthy and diseased cells can be seen side by side
Two stages
Preparalytic stage characterized by fever, HA,
Malaise
Paralytic stage tenderness of muscles, swollen painful joints, flaccid paralysis

95
Q

What about the Clinical Mainfestations of Polyio,

Tidal voulme, Diffusing capacity,

RR:

CXR: shows what think avelovi deflation

A

All lung volumes are decreased
RR is increased
Tidal volume is decreased
Diffusing capacity is decreased due to V/Q mismatching and alveolar hypoventilation
CXR: may show atelectasis or infiltrates; if diaphragm is involved it will appear elevated

96
Q

PaO2 is increased or decreased PaCO2

CV: rise in systolic and diastolic

What are the symptoms of Polio

A

ABGs: PaO2 is decreased; PaCO2 is elevated
Breath sounds: usually diminished; rhonchi may be present
CV findings: may be transient rise in SBP/DBP
Symptoms: dyspnea; weak cough

97
Q

Can poliomyleitis can be prevented by the use of a vaccine???

What to do in ventilatory therapy: just think like postioning, etc…

A
No specific treatment
Prevention through use of vaccine
Supportive therapy
Positioning
Ventilatory support
Strengthening exercises after acute phase
Bracing
98
Q

What is Gullian-Barre Syndrome: ?????????

Similair to ALS

A

A demyelinating disease of the motor neurons of the peripheral nerves

99
Q

Pathophysiology of Gullian Barre Syndrome think

PFT: all RV is decreased

RR is increased

What does the chest x-ray look like: atelectasis, inflrates

A

Rapid bilateral ascending flaccid motor paralysis
May leave the patient so involved that they require mechanical ventilation (10-20%)

All the dynamic lung volumes are reduced
RV is usually within normal limits
RR is usually increased
Diffusing capacity may be decreased due to increase in V/Q mismatching and alveolar hypoventilation
CXR: vary widely; atelectasis, infiltrates

100
Q

What is the CV findings: think like autonomic disorders or postural hypotension

Symptoms: of Gullian Barre: weakness, decreased endurance

Treatment: .

A

: hypoxemia and hypercapnia are both common
Breath sounds: diminished breath sounds
CV findings: autonomic abnormalities may occur—arrythmias, hypertension, or postural hypotension
Symptoms: weakness, dyspnea, ineffective cough, decreased endurance

: hypoxemia and hypercapnia are both common
Breath sounds: diminished breath sounds
CV findings: autonomic abnormalities may occur—arrythmias, hypertension, or postural hypotension
Symptoms: weakness, dyspnea, ineffective cough, decreased endurance

Plasmapheresis- lasmapheresis (from the Greek πλάσμα—plasma, something molded, and ἀφαίρεσις—aphairesis, taking away) is the removal, treatment, and return of (components of) blood plasma from blood circulation. It is thus an extracorporeal therapy (a medical procedure performed outside the body). The method is also used to collect plasma, which is frozen to preserve it for eventual use in the manufacture of a variety of medications.[
Active exercises including breathing exercises

101
Q

Mysthenia Gravis: explain

A

A chronic neuromuscular disorder characterized by progressive muscular weakness on exertion.

Muscle weakness is caused by circulating antibodies that block acetylcholine receptors at the postsynaptic neuromuscular junction,[1] inhibiting the excitatory effects of the neurotransmitter acetylcholine on nicotinic receptors at neuromuscular junctions.
you have a build of ACH in the synaptic cleft.

102
Q

What is the pathopyhsiology of Mysthenia Gravis

Like what Antibody blocks the post synaptic membrane

A

Antibody IgG binds to the acetylcholine receptor sites which impairs normal transmission of impulses from the nerves to the muscles
Approximately 10% of patients develop respiratory involvement

103
Q

Mysthenia Gravis?? Hypoventilation? RR increased yes obvi
CXR: maybe consistent with????

symptoms:: Pa02 increased or decreased

PaCO2

Breath sounds: up or down

Weakness and fatique

Treatments: remember ACH

A

All dynamic lung volumes are decreased
Capacities are decreased
RR increased and tidal volume decreased
Diffusing capacity is decreased due to alveolar hypoventilation
CXR: may be consistent with atelectasis or pneumonia

ABGs: PaO2 is decreased and PaCO2 is increased
Breath sounds: decreased breath sounds are common
Symptoms: weakness and fatigue, unable to focus eyes properly, difficulty swallowing, dyspnea, ineffective cough

Anticholinesterase
Plasmaphoresis
Corticosteroids
Immunosuppressive drugs
Thymectomy
104
Q

What is Tentaus????

A

A disease of the neuromuscular system caused by the neurotoxin Clostridium tetani

105
Q

Etology: think of prolonged muscle contraction due to Clostridium tetnai

Pathophysiology:

A

Neurotoxin binds to the ganglioside membranes of the nerve synapses and blocks release of the inhibitory transmitter

The action of the neurotoxin causes severe muscle spasticity with superimposed tonic convulsions
Chest wall immobility can result in asphyxia and death

106
Q

What is the treatment for tentaus

A

Prevention via immunization
Tetanus antitoxin can be used to neurtalize non fixed toxin in the system.
Once fixed or bound the toxin cannot be neutralized

107
Q

Duchenne’s Muscular dystrphy? Think like what casuses it???? Like its genetic

A

Genetically determined progressive myopathy

Sex-linked (x-chromosome) recessive disorder that occurs only in boys and is transmitted by female carriers. It is the most common of the muscular dystrophies

108
Q

What part of the body is affected first???

What does CX look lije

What is the only factor in the PFT that stays increased?

ABG: of course PaCO2 is increased and PaO2 is decreased.

A

Muscle biopsy shows both muscle fiber hypertrophy and necrosis with regeneration. Muscle innervation is not normal, loss of motor end plates when muscle fibers degenerate. The pelvic girdle is affected first then the shoulder girdle
Respiratory failure/infection is the cause of death in 75% of these patients

All lung volumes are decreased except RV which is usually increased
Increased RR and decreased Tidal volume
Chest wall compliance is decreased
Diffusing capacity is decreased
CXR: atelectasis, infiltrates
ABGs: PaCO2 is increased and PaO2 is often decreased

109
Q

What are some symptoms of Duschene Muscular Dystrophy

A

Breath sounds: often diminished; rales, rhonchi may also be present when there are infiltrates
CV findings: fibrosis of the myocardium can be extensive
Symptoms: waddling gait, toe walking, lordosis, dyspnea, weak and ineffective cough

110
Q

What happens with a paralyzed diaphragm like physiologically? Does the diaphargm get pulled up?

A

The negative pleural space pressure moves the diaphragm in a cephalad direction so that the diaphragm’s resting position is elevated. During inspiration as the pleural space becomes more negative the paralyzed diaphragm is pulled farther upward and the anterior ribs are pulled inward rather than being expanded

111
Q

With a paralyzed diaphargm??? what hapens to the avelovi? remember its elevated?? PaCO2 WNL???

Where are breath sounds decreased??

A

PFTs
All lung capacities and dynamic lung volumes are decreased in proportion to the degree of diaphragmatic dysfunction
CXR: An elevated hemidiaphragm; areas of atelectasis
ABGs: PaO2 is decreased; PaCO2 is usually WNLs
Breath sounds are usually decreased on the side of the paralysis

112
Q

Can Cor pulmonale result in terms of a elevated diaphargm????

Symptoms: include dyspnea and what other type of pnea???

A

CV findings: severe hypoxemia can cause pulmonary hypertension which can progress to cor pulmonale
Symptoms: dyspnea, orthopnea

113
Q

Kyphoscoliosis

What is the etiology: think half vertrbrea

Skeletal abnormalities: is lung compliance increased or decreased and what about the “dead space” increased or decreased???

RR : increased

Diffusing Capacity: decreased, increased or WNL.

CXR: what does it look like???

Will polycytothemia develop hypoventilation

Treatment: Think Kyphoscolosis is like exercise rods so

A

Excessive anteroposterior and lateral curvature of the thoracic spine

Congenital (hemivertebrae)
Develop in response to neuromuscular disease

Skeletal abnormalities decrease chest wall compliance. Lung compliance is also decreased and dead space is increase

PFTs
All dynamic capacities and volumes are decreased
Flow rates are decreased
RR is increased
Diffusing capacity is WNL
CXR: gross abnormalities of the bony thorax

Breath sounds: decreased over the compressed lung
CV findings: hypoventilation; pulmonary hypertension; polycythemia may develop
Symptoms: dyspnea on exertion, decreased exercise tolerance

Treatment: Conservatively: bracing and exercise programs
Surgically: Harrington rods

114
Q

Ankylosing Spondylitis: what is it

Markedly decreased compliance of the chest wall
6% of these patients develop specific fibrosing lesions in the upper lobes

What is the PFT’s

VC and IC are increased or decreased

RV and FRC are increased or decreased thinkfixed

Do you get a hemooptysis??

Treatment:

A

A chronic inflammatory disease of the spine characterized by immobility of the sacroiliac and vertebral joints and ossification of the paravertebral ligaments

PFTs
VC and IC are decreased
RV and FRC are increased
CXR: may show areas of fibrosis
Breath sounds: are normal unless upper lobes are involved when rhonchi may be present
Symptoms: DOE, productive cough, hemoptysis

No curative treatment
Important to maintain good body alignment and as much thoracic mobility as possible
If direct lung involvement, then treatment of infection may be required

115
Q

Pectus Excavatum

A

A congenital abnormality characterized by sternal depression and decreased anteroposterior diameter

116
Q

Pectus Carinatum

A

A structural abnormality characterized by the sternum protruding anteriorly. 50% of patients with ASDs or VSDs have pectus carinatum. It is associated with severe prolonged childhood asthma

117
Q

RA is obvi inflammation of the peripheral joints and affects the joint and surronding structures but, what causes it?

A

Believed to be autoimmune disease but, exact etiology is unknown

118
Q

What are the six ways RA affects the lungs

many inflammation of different areas of the lungs

A
Can effect the lungs in six ways
Pleural involvement
Pneumonitis
Interstitial fibrosis
Development of pulmonary nodules
Pulmonary vasculitis
Obliterative bronchiolitis
Also chest wall compliance may be significantly decreased
119
Q

What are the CV findings with RA and symptoms think inflammation of the joints

What are some treatments mainly medications

A

CV findings: pulmonary hypertension
Symptoms: swollen painful joints; progressive dyspnea, non productive cough

Corticosteriods reduce inflammation
and immunosuppressents decrease the WBC’s accumlmation which in turn will result in decreased inflammation

120
Q

Systemic Lupus Erthymatosus what is it
Etiology
Pathophysiology
Symptoms

Remember that this a systemic thing so it affects more than just the lungs
think white, red, blue (Raynauds)

Treatment

A

A chronic inflammatory connective tissue disorder

Etiology: Unknown, immune system seems to be involved
90% cases in women
More common in black women
Pathophysiology: The most common lung involvement is pleurisy, often with the development of small bilateral exudative pleural effusions
Acute lupus pneumonitismay lead to chronic interstitial pneumonitis and fibrosis
Diaphramatic weakness is common
CV findings: Pericarditis is often present
Pericardial effusions and pulmonary hypertension may also be present

Symptoms: arthralgias and polyarthritis, dyspnea, cough, hemoptysis, pleuritic pain, raynaud’s phenomena

Treatment: Corticosteroids
Plasmaphoresis
Fibrotic changes in the lungs are irreversible supportive therapy

121
Q

Scleroderma What is it
Etiology
Pathophysiology

What about the ABG’s Pa02 and PACO2

What about Symptoms????????? Clubbing of nails???????

Treatment?

A

A progressive fibrosing disorder that causes degenerative changes in the skin, small blood vessels, esophagus, intestinal tract, lung, heart, kidney, and articular structures (basically hardening of the fibrous tissue at skin level and progress to areas like the GI tract and the eshogaus and likes etc.

Etiology: Unknown
4x more common in women
Majority of patients are diagnosed between ages 30-50

Pathophysiology: Within the lung, it appears as progressive diffuse interstitial fibrosis in which collagen replaces the normal connective tissue framework of the lung
Fibrotic replacement of connective tissue within the alveolar walls
Pulmonary arterioles undergo obliterative changes

ABGs: PaO2 is decreased and PaCO2 is usually within normal limits
Breath sounds: bibasilar rales; rhonchi if pulmonary infiltrates are present
CV findings: pulmonary hypertension, cor pulmonale
Symptoms: DOE, non productive cough, clubbing of the digits

Treatment: No effective Treatment supportive care is the best treatment

122
Q

Polymyositis what is it? think proximal and systemic

Etiology?? is it know is it common in women begging to see a pattern here??

Pathopsyhiology??

Treatment??? I think when in doubt corticosteroids?
unless its scleroderma which there is no treatment for

A

A systemic connective tissue disorder characterized by symmetric proximal muscle weakness and pain

Etiology- Unknown, but may involve the immune system
Twice as common in women

Pathophysiology??5% of the patients exhibit involvement of the lung parenchyma
Changes can include
Interstitial pneumonitis and fibrosis
Bronchiolitis obliterans
Aspiration  pneumonia
Diffuse pulmonary infiltrates

Treatment?? Corticosteroids

123
Q

Dermatomyositis what is it? and what percent of the time does it develop in the lungs??? What disease does it mirror?

A

A systemic connective tissue disorder characterized by inflammatory and degenerative changes in the skin.
Pulmonary involvement in this disease mirrors polymyositis
5% of patients have lung involvement

124
Q

Pregnancy What trimester affects the lungs development and what is this process depedent on???

What does this lead to

RR is increased or decreased
what about work rate of breathing

What hormone is responsible for the increase in ventilation during the third trimester to prevent hypoxemia?

A

During the third trimester of pregnancy, ventilation to the dependent regions of the lungs is impaired by the growth and position of the fetus.
Decreased ventilation in the bases of the lungs results in early small airway closure and increased V/Q mismatching

Voluntary lung volumes are decreased
RR is increased
Work of breathing is increased
Progesterone levels increase during the third trimester, increasing the ventilatory drive to prevent hypoxemia

125
Q

Obesity is classified as how much over the ideal body weight???
How does being obese affect the lungs.

A

An increase in weight of 20% or more over the ideal body weight
Excess soft tissue mass on the chest wall decreases the compliance and increases the work of breathing
Excess soft tissue in the abdomen forces the diaphragm into a high resting position

126
Q

Pregnancy What trimester affects the lungs development and what is this process depedent on???

What does this lead to

RR is increased or decreased
what about work rate of breathing

What hormone is responsible for the increase in ventilation during the third trimester to prevent hypoxemia?

A

During the third trimester of pregnancy, ventilation to the dependent regions of the lungs is impaired by the growth and position of the fetus.
Decreased ventilation in the bases of the lungs results in early small airway closure and increased V/Q mismatching

Voluntary lung volumes are decreased
RR is increased
Work of breathing is increased
Progesterone levels increase during the third trimester, increasing the ventilatory drive to prevent hypoxemia

127
Q

Obesity is classified as how much over the ideal body weight???
How does being obese affect the lungs.

A

An increase in weight of 20% or more over the ideal body weight
Excess soft tissue mass on the chest wall decreases the compliance and increases the work of breathing
Excess soft tissue in the abdomen forces the diaphragm into a high resting position