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
When does compliance start to decrease in an individual and why does compliance start to decrease.
Compliance of the pulmonary system starts to decrease at about age 20 Thorax undergoes changes Decalcification of ribs Calcification of costal cartilage
26
Why does control of ventilation start to decrease what receptors start to lose their abilities
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.
27
what do EEG studies show about OLD.
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.
28
What happens with old age Does TLC change?? Does RV change?? VC? MVV? Flow rates??
``` 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 ```
29
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
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
30
What about cardiovascular changes with old age Does SV, CO, HRmax decrease or increase
Breath sounds: auscultation often reveals slightly diminished breath sounds CV findings: HRmax decreases SV decreases CO decreases
31
Why don't adults realize the decreased lung capacity with old age??? (2 ) reasons
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.
32
How much can a sedentary person improve his or her cardiovascular capabilites once starting a new exercise routine.
A sedentary elderly person beginning a regular exercise routine can improve their maximal oxygen consumption by 5-25%
33
Idiopathic Pulmonary Fibrosis what is?
An inflammatory process involving all the components of the alveolar wall that progresses to gross distortion of the lung architecture.
34
Etiology of idiopathic Pulmonary Fibrosis speculated theroies
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
35
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
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.
36
What are some symptoms of idiopathic pulmonary fibrosis think like dyspnea, weight loss, anorexia etc..
``` Symptoms: Dyspnea Repetitive non productive cough Weight loss Anorexia Sleep disturbances ```
37
What is the typical treatment for idiopathic pulmonary fibrosis
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.
38
Bronchiolitis Obliterans what is?
A fibrotic lung disease that affects the smaller airways. It can produce both restrictive and obstructive lung dysfunction
39
Etiology of Bronchiolitis Obliterans??
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
40
Whats the pathophyisology of the Bronchiolitis obliterans "starts with nercosis"
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
41
Symptoms of the BO what happens to RR, Flow Rate, Lung volume, ??? everything doesn't decrease.
Diffusing capacity is reduced Lung volumes may be normal or decreased RR is increased Flow rates are frequently WNLs, but may be decreased
42
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??
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
43
what does the chest sound like in BO What are the symptoms : hacking???
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
44
What is the treatment for BO???? very similair to idiopathic pulmonary fibrosis?? but watch fluid balance??
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
45
What is pneumonia???? what are its two ways to be caught?
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
46
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???
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
47
What are the ways that a patient may acquire pneuomia in the hospital??? Think tubes
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
48
What part of the lungs usally gets infected first with pneumoia, and does it and how does our body combat the pneuomia??
``` Bacteria and other microbes commonly enter the LRT. Defense mechanisms Cough Bronchoconstriction Angulation of the airways Mucociliary escalator The immune defenses ```
49
What is the most common pathway for pneumoia What does a patient usally present when he or she has pneumoia??
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
50
How does Viral Pneumonia come about???? Does it cause Edema and hemorrhage??
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
51
What happens with Lung voulme and pneumoia What about lung compliance Gas exchange RR Work of breathing
``` PFTs Decreased lung volumes Decreased lung compliance Decreased gas exchange Increased RR Increased work of breathing ```
52
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
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
What the breath sounds like with pneumoia, What about PaCO2 does it increase or decrease
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
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???
CV findings: tachycardia ``` Symptoms: High fever (bacterial); moderate fever (viral) Chills Dyspnea Productive cough myalgias ```
55
What are some treatments think like precussion its not just corticosterioids and supplemental oxygen there are some other alte whrnatives for pneumoia.
``` Drug therapy Antibiotics for bacterial pneumonias Oxygen supplementation Chest PT Postural drainage Percussion vibration Hydration Nutritional support ```
56
Streptococcus Pneumoniae who is it most common in????? What color is the septum in this case liver dysfunction????
``` 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
Legionella Pnuemophila? what is the main anitbiotic for this disease
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
Haemophilus Influenzae what medication do they give you??? Who is most common in????
Signs/Sx: Sore throat Empyema Preferred antibiotic is ampicillin More common in: Alcoholics COPD elderly
59
Klebsiella pneumoniae and how is it acquired in a community based area And who is more prevelant in a hospital or nosocomial based areas
``` Community acquired More common in: Men Alcoholics COPD DM ``` ``` Nosocomial More common in: Debilitate patients Alcoholics DM Malignancy Chronic Renal Disease Cardiopulm disease ```
60
Pseudomonas Aeruginosa --> is this the most common of the nosocimal hospital diseases What are its signs think confusion is one of them
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
Staphylococcus aureus Who is it seen in??? Childern age 2? Whats the signs whats the treatments
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
Mycoplasma Pneumoniae are they bacteria or viral "trick question"
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
Cytomegalovirus
Most common in immunocompromised hosts Persons most at risk Underlying Cardiopulmonary disease Immunosuppressed Pregnant Treated with dehydroxyphenylglycol
64
Pneumocystis Carinii what is this disease usally associated think aids and how is it treated really complicated drug name
Parasitic protozoa which causes pneumonia Most commonly associated with AIDS Treated with trimethoprim-sulfamethoxazole or pentamidine
65
Psittacosis Pneumonias who usally gets pisittacossi What is the treatment think tetra__________?
Causes approximately 12% of community acquired pneumonias in students and 6% in the elderly and Treatment is with tetracycline or chloramphenicol
66
Adult Respiratory Distress Syndrome What is this disease How does it come about think more external like drug abuse, shock not just virus
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
Pathphysiology of Adult Respiratory Distress Syndrome think premability is the big thing here What about the acute phase may it reslove itself???
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
What happens to the FRC, VC RR, Flow rate, VT within Adult respiratory distress syndrome
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
How does the CXR- symetrical for ARDS, is PaO2 decreased what about PaCO2 ???
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
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
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
What are the symptoms of ARDS think like headache rapid shallow breathing etc...
``` Symptoms: Dyspneic at rest Rapid shallow breathing pattern Headache Impaired mental status cyanosis ```
72
How to treat ARDS think supplmental oxygen pretty sevre disease. Remember electrolytes
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
Sarcoidosis
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
Who acquires scaroidosis? black male 20-40
``` 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
Patho of Scarodolosis what the three trademark signs
Three distinctive features: Alveolitis formation of well-defined round or oval granulomas (collection of marcophages) pulmonary fibrosis Disease progression is very variable
76
What does the Chest x-ray look like is it symetrical What happens to TLC, and all lung volumes V/Q ratio lung complance
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
What happens to PaO2 late in the disease with Sacodolosis Breathe Sounds: what about the apicies
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
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
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
What is the treatment for Sacrodoloasis: only mentions one to help decrease the alveolitis
Corticosteroids to suppress the alveolitis and granuloma formation
80
How does the spinal cord get damaged two ways:
Can result from acute trauma or from a pathological process that invades the spinal cord and damages it.
81
What happens over time when a patient has a SCI think avelovi deflation
Paradoxical breathing Over time the pulmonary compliance is decreased due to the shallow breathing and atelectasis within the lung Chronic state of hypoxemia
82
SCI What happnes to TLC, VC, IC ERV - decreases if??? RR- RV- Tidal volume
``` 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
SCI What happens to ribs over time Breathe sounds CV findings Auntnomic Dysreflexia - occurs in lesions above T7
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
SCI whats autonomic dysreflexia good review Symptoms include: fatique, dyspnea, irritable
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
Treatment for SCI think of gary from Helen Hayes Hospital??? Assited Cough, what else think everything a PT could do????
``` Strength and endurance training of the respiratory muscles Active and passive chest wall stretching Assisted cough Postural drainage Chest PT Suctioning ```
86
What is ALS good review
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
How is generally affected by ALS? Males more than Females????
Unknown Onset is usually >40yrs age Males are affected 1.7x as often as females
88
With ALS are males affected more than females?? What causes ALS?
Unknown Onset is usually >40yrs age Males are affected 1.7x as often as females
89
Where does ALS usally affect??? what part of the spinal column
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
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
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
How do the breath sounds? Sound like???
Breath sounds: very decreased breath sounds; possible rales or rhonchi Symptoms: weakness or wasting of muscles; muscular fasciculations
92
What is the treatment for ALS remember its very progressive disease..
the only therapy is supporitive therapy
93
What is poliomyleitis? describe it
viral disease that attacks the motor nerve cells of the spinal cord and brain stem and can result in muscular paralysis
94
How does polymyelitis about? Etiology? Pathophysiology two stages: preparalytic and paralytic:
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
What about the Clinical Mainfestations of Polyio, Tidal voulme, Diffusing capacity, RR: CXR: shows what think avelovi deflation
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
PaO2 is increased or decreased PaCO2 CV: rise in systolic and diastolic What are the symptoms of Polio
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
Can poliomyleitis can be prevented by the use of a vaccine??? What to do in ventilatory therapy: just think like postioning, etc...
``` No specific treatment Prevention through use of vaccine Supportive therapy Positioning Ventilatory support Strengthening exercises after acute phase Bracing ```
98
What is Gullian-Barre Syndrome: ????????? Similair to ALS
A demyelinating disease of the motor neurons of the peripheral nerves
99
Pathophysiology of Gullian Barre Syndrome think PFT: all RV is decreased RR is increased What does the chest x-ray look like: atelectasis, inflrates
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
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What is the CV findings: think like autonomic disorders or postural hypotension Symptoms: of Gullian Barre: weakness, decreased endurance Treatment: .
: 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
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Mysthenia Gravis: explain
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.
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What is the pathopyhsiology of Mysthenia Gravis Like what Antibody blocks the post synaptic membrane
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
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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
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 ```
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What is Tentaus????
A disease of the neuromuscular system caused by the neurotoxin Clostridium tetani
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Etology: think of prolonged muscle contraction due to Clostridium tetnai Pathophysiology:
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
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What is the treatment for tentaus
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
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Duchenne’s Muscular dystrphy? Think like what casuses it???? Like its genetic
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
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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.
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
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What are some symptoms of Duschene Muscular Dystrophy
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
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What happens with a paralyzed diaphragm like physiologically? Does the diaphargm get pulled up?
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
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With a paralyzed diaphargm??? what hapens to the avelovi? remember its elevated?? PaCO2 WNL??? Where are breath sounds decreased??
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
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Can Cor pulmonale result in terms of a elevated diaphargm???? Symptoms: include dyspnea and what other type of pnea???
CV findings: severe hypoxemia can cause pulmonary hypertension which can progress to cor pulmonale Symptoms: dyspnea, orthopnea
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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
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
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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 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
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Pectus Excavatum
A congenital abnormality characterized by sternal depression and decreased anteroposterior diameter
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Pectus Carinatum
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
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RA is obvi inflammation of the peripheral joints and affects the joint and surronding structures but, what causes it?
Believed to be autoimmune disease but, exact etiology is unknown
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What are the six ways RA affects the lungs many inflammation of different areas of the lungs
``` 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 ```
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What are the CV findings with RA and symptoms think inflammation of the joints What are some treatments mainly medications
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
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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 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
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Scleroderma What is it Etiology Pathophysiology What about the ABG's Pa02 and PACO2 What about Symptoms????????? Clubbing of nails??????? Treatment?
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
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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 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
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Dermatomyositis what is it? and what percent of the time does it develop in the lungs??? What disease does it mirror?
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
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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?
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
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Obesity is classified as how much over the ideal body weight??? How does being obese affect the lungs.
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
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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?
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
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Obesity is classified as how much over the ideal body weight??? How does being obese affect the lungs.
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