Pneumonia
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Viral, Bacterial, Fungal/parasitic, aspiration
6th leading cause of death, aerosol transmission most common.
Typical: Streptococcus Pneumoniae, HemophilusInfluenzae, Staphylococcus Aureus
Atypical: Legionella Pneumophila, ChlamydophilaPneumoniae, Mycoplasma Pneumoniae,
Viruses
Gram Staining:is a method of differentiating bacterial species into two large groups (Grampositive and Gram-negative).It is based on the chemical and physical properties of their cell
walls. Primarily, it detects peptidoglycan, which is present in a thick layer in Gram positive
bacteria. A Gram positive results in a purple/blue color while a Gram negative results in a
pink/red color.The Gram stain is almost always the first step in the identification of a bacterial
organism.
CXR: consolidation
Symptoms: Cough, fever, increased WBC, Tachypnea, atelectasis, mucus production (bacterial),
Pleuritic chest pain
RT treatment: Bronchial hygiene, also treat any pre-existing chronic lung diseases
Other treatment: Antibiotics or anti-virals, fluid hydration
BACTERIAL PNEUMONIAS:
Streptococcus Pneumoniae:
Gram positive
80% of all bacterial pneumonias
Causes sinusitis, meningitis (brain), endocarditis, sepsis, pericarditis, brain abscess and
pneumonia.
Vaccine exist- recommend old and young, immunocompromised
Part of normal upper respiratory flora becomes pathogenic from immunosuppression
Transmitted through aerosol/ cough or sneeze
Generally acute/ nosocomial acquired
HamophilusInfluenzae:
Gram negative
Affect children primarily 1 month -6 years old
Opportunistic pathogens, live in host, affect immunocompromised
Vaccine exists (HiB)
Most common cause of epiglottitis, rare due to Hib vaccine
Causes bacterial meningitis in children
Transmitted via aerosols
Staphylococcus Aureus:
Gram positive
Part of normal nasal flora and skin flora
Cause of staph infections in skin, blood, lungs, nasal passages
Can lead to sepsis, bactermia, endocarditis
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20% of population are carriers (healthcare providers more like 80%)
One of the most common nosocomial infections, especially post-surgical patients.
MRSA resistant strain of staph. Found all over the community
Treatment of non MRSA is penicillin. With MRSA treatment is a combination antibiotic
Yellow sputum, transmitted via skin to skin contact, blood, sneeze/cough
Legionella Pneumophila:
Gram negative
Legionnaires' disease
Discovered in 1976 during an outbreak of severe pneumonia-like disease at an American
Legion convention
Transmitted via aerosol
Thought to have colonized in the AC units of the convention hall
Community acquired
Pseudomonas aeruginosa
Gram Negative
Water loving organism
Leading cause of hospital acquired pneumonia
Normally colonizes in the GI tract
Frequently found in burns, the respiratory tract of intubated or trached respiratory patients,
catheters, respiratory therapy equipment
Transmitted via aerosol or contact with fomites
Sputum infected is usually sweet smelling and green/bright yellow
Klebsiella pneumonia
Gram Negative
Associated with lobar pneumonia
A normal inhabitant of the GI tract (aspiration)
Transmitted by aerosol or fomites – especially the hands of healthcare workers
Usually a hospital acquired infection
Morality is high because septicemia is a frequent complication
Clostridium difficile (C-diff)
Gram positive
Anaerobic spore-forming organisms
Hospital acquired in patients on antibiotic therapy
Replaces normal flora causing severe gastric instability and diarrhea mimicking flu
Fast becoming antibiotic resistant
Hands MUST be washed with soap and water before and after entering patient room
Mycoplasma pneumoniae
Common cause of mild pneumonia (walking pneumonia)
Smaller than bacteria but larger than viruses
Described as Primary Atypical Pneumonia because the organism escapes ID by standard
bacteriologic tests
Most frequently seen in people younger than 40
Spreads easily where people congregate
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Usually community acquired
Escherichia coli
Gram negative
Normal GI inhabitant (Aspiration)
Usually hospital acquired pneumonia
Moraxella catarrhalis
Naturally inhabits the pharynx
Third most common cause of acute exacerbation of chronic bronchitis
Usually hospital acquired
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VIRAL PNEUMONIAS:
Influenza Virus
Several subtypes in which A and B are the most common causes of viral respiratory tract
infections
Commonly occur in epidemics
Children, young adults and the elderly are most at risk
Transmitted via aerosol
Survives well in conditions of low moisture and humidity
Found also in swine, horses and birds
Respiratory Syncytial Virus (RSV)
Member of the paramyxovirus group along with parainfluenza, mumps and rubella viruses
Most often seen in children under the age of 6
Transmitted via aerosol and direct contact
Old treatment = Ribavirn via SPAG, now treat symptoms, suction.
Associated with bronchiolitis
Parainfluenza Virus
Member of the paramyxovirus group
Type 1 is considered a “croup” type virus seen in the young
Type 2 and 3 present as a severe type of infection
Transmitted via aerosol and direct contact
Severe Acute Respiratory Syndrome (SARS)
First reported in China in 2002
Newly recognized Coronavirus
Transmitted via droplet and aerosol and possibly contaminated objects
Incubation is 2-7 days
10-20% require mechanical ventilation
Community acquired
Other causes: Measles, Chicken Pox, Mumps, Rickettsia, Adenovirus, VAP (keep HOB at 45
degrees, suction above ETT cuff)
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Tuberculosis
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Mycoplasma, diagnosis with acid fast staining (3 tests to R/O TB), symptoms, mantoux/PPD skin
test and CXR
Can present in lungs (most common, aerobic bacterium), brain, kidney, spine
Transmitted via air, stays suspended in air for long periods of time, must wear HEPA mask,
patient kept in airborne isolation (negative pressure rooms, door alarms)
Deadly if left untreated, common among immunosuppressed, HIV/AIDS, chemotherapy…
Widespread throughout world
Vaccine exists (actual weak TB bacterium injected)
Symptoms: Night sweats, hemoptysis, weight loss, fatigue, dysnpnea
Creates cavitation/nodules in lung on CXR, can lead to pneumothorax or pleural effusion
After initial exposure, leads to pulmonary edema/inflammation
Latent TB, may lay dormant in a tubercle for decades, body forms scar tissue/calcification
around TB after initial exposure.
Active TB occurs after immune compromise, or anytime, tubercle ruptures
Treatment: Isoniazid, rifampin, pyrazinamide, ethmabutol
RT treatment: sputum collection, bronchial hygiene, not for pre-tubercle rupture, only treat
active TB
Bronchiolitis
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Primarily caused by RSV
Common viral pathogen of infants-children, under 6 months require hospitalization
Spread by aerosol/ cough and sneezing, keep isolated
Ribarivin old treatment through SPAG, no longer used do to provider side effects
Causes inflammation of small airways, may lead to consolidation, atelectasis, congestion
Diagnosis with nasal swab/ RSV wash, symptoms and CXR
CXR show streaky opacities
May have nasal flaring, retractions, apnea, wheezes, rhonchi, crackles, and mucus
RT treatment: Bronchial hygiene, nasal suctioning, hydration. Bronchodilators are ineffective.
May use Racemic epinephrine, Pulmicort steroid
Emphysema
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COPD 3rd leading cause of death, pink puffers, increased compliance, decreased elasticity
Late onset for smoking induced, 50’s vs 20-30’s for genetic form
Primary cause is cigarette smoking. Less common alpha 1 anti-trypsin, genetic emphysema
Decreased FEV1, FVC, FEV/FEV1 ratio, decreased DLCO, hypercapnic, chronic hypoxemia
Will have compensated respiratory acidosis when not having acute symptoms; know baseline
ABG on your patient
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Increased volumes, RV, FRC, TLC from air trapping from bullae formation from destruction of
alveolar walls
Chronic exposure to the irritants in cigarette smoke (tar) causes constant neutrophil and
macrophage release, causes elastin/collagen destruction as well as cilia malfunction
Clubbed fingers, barrel chest, cough, wheezing, SOB at rest/exertion, corpulmonale,
polycythemia, dyspnea, pulmonary hypertension
Increased mucus production, common pneumonias
Increased VD/VT; decreased VA, PaO2, PAO2
Accessory muscle use, malnutrition/loss of appetite
Bleb formation can lead to pneumothorax
Centrilubar and panlobar emphysema depends on genetic vs self-induced
CXR: hyperluceny, flattened diaphragms, increased rib spacing—AIR TRAPPING
Treatments: fast acting bronchodilators (Albuterol/Xopenex), Anticholinergics (Atrovent or
Spiriva), Steroids (Advair, flovent, Qvar, Symbicort…); low concentration (FIO2 less than 30%) O2
(Nasal cannula or venturi mask); Theophylline (RARE), breathing exercises (pursed lip,
diaphragmatic breathing, huff cough); bronchial hygiene, genetic drugs, surgery (lung transplant,
lung reduction)
Ask patients smoking hx, pack years
Dx: history, PFT showing obstructive pattern and non-reversible airflow obstruction, CXR/CT
Chemoreceptor changes, central to peripheral from desensitized effects from H+ ions
Cystic Fibrosis
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Heredity disease, affecting Caucasians mostly
Disease of viscous mucus, blocking bile ducts, bronchial tubes, reproduction organs and sinuses
Caused by a genetic mutation of the gene coding for a large protein that controls the
movement of chloride ions through the cell membrane.
Movement of chloride is vital to the proper production and regulation of secretions in the lungs,
pancreas, sweat glands
Leaves males sterile, causes frequent pneumonias, scar tissue formationpneumo/bronchiectasis
Mucus plugs lead to atelectasis, air trapping
Diagnosed with sweat chloride test > 60 mEq/L, baby tastes salty; PFT, neonatal screening,
blood testing
Pancreatic insufficiency reduces the number of digestive enzymes. These patients experience
malnutrition, diarrhea, vitamin deficiency and undigested fat in the stool
Each time two carriers of the CF gene have a child, the chances are:25% (1 in 4) the child will
have CF
Patient has malnutrition, has symptoms similar to COPD-late symptoms
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Treatment: Bronchial hygiene (CPT/vest, PD, Flutter, EZPAP, Thera-Pep, IPV, humidity,
suctioning); huff cough; mucolytic pulmozyme, fast acting and long acting bronchodilators,
steroids, antibiotics (Tobi); low FIO2 oxygen; lung transplant; Digestive enzymes, vitamins
Common infections: Staphylococcus; Haemophilus influenza; Pseudomonas aeruginosa
Chronic Bronchitis
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Presence of cough and sputum production for three or more months in two successive years
Primary cause is smoking, blue bloaters
Inflammation in the large airways, increased mucus glands, thickened upper airway on CXR
Air trapping; associated with emphysema
Same FVC results as emphysema
Common pathogens include Haemophilusinfluenzae and Streptococcus pneumonia, Moraxella
catarrhalis
Increase in number of mucus secreting glands; goblet cells increase, causing decrease in ciliated
columnar cells; submucosal glands hypertrophy
Increased JVD, stocky appearance, edema, AP diameter
Mucopurulent infections leading to yellow or green sputum
Mucus thick, gray in color
Symptoms and treatments similar to emphysema
Asthma
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Characterized by airway hypersensitivity with mucosa swelling and bronchial constriction
Types include intrinsic and extrinsic. Extrinsic is allergic, most common. Intrinsic is sports
induced and occupational
Allergens include pollens, molds, cockroach droppings, foods, dust mites, pet dander
Triggers include smoke, weather, emotions, dust, chemicals
Most common pediatric chronic disease
May manifest later in life, from aspirin sensitivity, or environmental changes
Occupational sensitizers include paint, building, farming
Lung produces Ige antibodies in response to antigens. Causes mast cell degranulation of
histamines, neutrophils, esionphiles, leukotriens and other inflammatory mediators
During attack, mediators increase inflammation response, mucus production and capillary
permeability, causing pulmonary edema
Asthma attacks are early and late phase
Treatments include: mast cell inhibitors (intal and tilade), PRN fast acting bronchodilators
(xopenex, and albuterol), inhaled steroids (flovent, pulmicort, qvar…) LABA’s serevent, brovona,
foradil; combo drugs advair, symbicort. Avoiding allergens, allergy shot. Atrovent for acute
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attacks; systemic steroids- solumderol/prednisone; leukotriene inhibitors; bronchial hygiene
after attack from increased mucus
Assess bronchospasm with peak flow
Education is key- air quality, asthma management; house pollutions
Diagnosis through PFT testing pre and post testing, metcholine challenge
Allergy testing (skin and blood)/ atopic response, strong link
Status asthmaticus: attack unresponsive to asthma medications
Risk factors for asthma: obesity, gender, GERD, infections, emotions, night (increased
symptoms)
Symptoms: wheezing, dyspnea, congestion
Asthma classifications:
mild intermittent (Symptoms < 2/week or < 2 times/month at night; Little effect on day to day
activities; Expiratory flow ≥ 80% of predicted)
mild persistent ( Symptoms > 2/week but less than 1/day; < 2 times/month at night;
Exacerbations may affect activity; Expiratory flow ≥ 80% of predicted?
Moderate persistent (Symptoms daily; > 1/week at night; Limitations ≥ 2/week; may last days;
Expiratory flow > 60% but < 80% of predicted)
Severe persistent ( Symptoms continually with frequent symptoms at night; Frequent
exacerbations which limit activity; Expiratory flow < 60% of predicted)
PFT result: FVC changes 12% and at least 200 ml post bronchodilator testing
Bronchiectasis
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chronic dilation and distortion of one or more bronchi as a result of extensive inflammation and
destruction of the bronchial wall cartilage, blood vessels, elastic tissue, and smooth muscle
components
Can affect one or both lungs
Commonly limited to a lobe or segment
Most frequently found in the lower lobes
The smaller bronchi, with less supporting cartilage are predominantly affected
Three forms: saccular (most severe), cylindrical, and varicose
Acquired or congenital
Loss of ciliated epithelium and respiratory unit; Chronic inflammation; Sloughing of mucosa with
ulceration and possible abscess formation; Reduced volume of distal lung and adjacent lung
secondary to scarring and bronchial obstruction; Excessive production of sputum (greater than 1
cup/day)
Sputum is foul-smelling and hemoptysis is common
Hyperinflation of alveoli
Atelectasis, consolidation and parenchymal fibrosis
Sputum separates into three layers: Top layer – thin, frothy; Middle layer – mucopurulent;
Bottom layer – opaque, mucopurulent or purulent with mucus plugs, foul-smelling
Halitosis; possible hemoptysis
Pneumothorax
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Closed or open, depending on cause
Closed from tension, rupture of alveoli (from mechanical ventilation, rupture of a bleb, TB,
fistulas) spontaneous (tall skinny)
Open from blunt trauma, stab/gunshot
Iatrogenic induced from MD’s during line placement, thorencentesis
May push the mediastinum and trachea to the opposite side during a pnuemo, pressure on
heart, and vessels decreases venous return back to the heart, decreasing cardiac output
Symptoms: pleuritic chest pain, tachypnea, tachycardia,
Treatment involves: 100% O2 (nitrogen washout), needle decompression (between 2-3rd rib mid
clavicular line), and chest tube
Mechanical ventilation with positive pressure is contraindicated for untreated pneumos
Symptoms: pleuritic chest pain, SOB/tachypnea, tachycardia, hypotension
Causes atlectasis if left untreated, depresses the diaphragm
CXR: dark area (hyperlucent), decreased vascular markings, Breath Sounds diminished or absent
over affected side
Pleural Effusions
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Fluid in pleural space, caused by pressure or inflammation in or around the pleural space
Ineffectice lymphatic drainage can increase pressure around space and lead to pleural effusion
Common with caners (particularly upper thoracic) and CHF
Two primary types: Transudative (increased pressure) and Exudative (infection)
Transudative: CHF, cirrhosis, lymphatic obstruction
Exudative: cancer, lymphoma, mesothelioma, bacterial infections, TB, fungal infections, viral
Many other causes as well
Transudative effusions: Any effusion that forms while pleural space is undamaged will have
[protein] <50% of serum level and LDH <60% of serum level: Specific causes of transudative
effusions CHF: high hydrostatic pressure increases pleura fluid production, most common cause
of effusions; Nephrotic syndrome: protein loss in urine results in low capillary oncotic pressure
and fluid third spacing; Hypoalbuminemia: different cause but mimics above; Liver disease:
ascites fluid moves through small holes in diaphragm, almost always on right side; Atelectasis:
cause pleural pressures to become more negative resulting in small effusions; Lymphatic
obstruction: blockage prevents drainage and results in accumulation
Exudative effusions: Occur due to inflammation of lung or pleura and will have a higher protein
and inflammatory cell content; Thoracentesis may be performed to determine type.
Specific causes of exudative effusions; Parapneumonic: secondary to lung inflammation
associated with pneumonia; Complicated if clots form and loculate fluid; Perersistent fever may
signal an empyema, which must be drained for recovery
Diagnose with upright CXR and lateral decubitus film and CT scan, shows meniscus shape, will
move on position; ultrasound also used
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Treatment: thorencentesis; between 4-5th rib
Manage with chest tube, pluerodosis (fuse layers); shunts
ARDS
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A severe restrictive disease causing alveolar collapse from non cardiogenic pulmonary edema
Volumes severely decreased/ compliance decreased. PaO2 severely affected; alveoli collapse
creating refractory hypoxemia/shunting
Caused by several factors including sepsis, blood loss, pneumonia, near drowning, aspiration,
burns, inhaled toxic gases
Three phases: exudative 3-5 days, fibroproliferative days to weeks and resolution
Exudative phase: Consolidative process with injury to the alveoli; Inflammatory process
secondary to the presence of activated macrophages; Destruction of type I pneumocytes;
Migration of interstitial fluid, protein, fibrin, neutrophils, and red blood cells through the
damaged alveolar wall
Fibroproliferative phase; Lung repair begins; Macrophage and lymphatic cleanup of cellular
debris; Hyperplasia of alveolar type II pneumocytes, proliferation of fibroblasts within alveolar
basement membrane and intraalveolar spaces. Variable lung fibrosis can occur depending on
the extent of fibroblast involvement
Resolution phase: improvement in compliance, CXR improves
CXR for exudative phase: bilateral infiltrates, atelectasis, ground glass appearance
A-a gradient wide, decreased VC, tachypnea, low BP, pulmonary hypertension, low CO; low DO2
Acute lung injury is the precursor to ARDS, ARDS has a 40% mortality rate
Treatment includes anti-biotics, vasopressors, anti-inflammatory drugs, hydration, nitric oxide
(controversial); ECMO; mechanical ventilation with high FIO2, PEEP and pressure controlled
modes to prevent pneumothorax, possible oscillator; beta adrenergic drugs
High risk of tension pneumo from mechanical ventilation, renal failure from low blood pressure,
tissue and brain damage from low oxygen tensions, heart failure from increased demand, liver
failure from constant sedation and medications, subcutaneous emphysema from air leaks
Interstitial Lung Disease (pulmonary Fibrosis)
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Encompasses many different causes most of which cause progressive scarring of lung tissue. The
scarring associated with interstitial lung disease eventually affects your ability to breathe and
get enough oxygen into your bloodstream.
Fibrosis leads to granulomas, honeycombing and cavitation (can lead to pneumothorax)
In ILD, the inflammatory condition is characterized by edema and the infiltration of a variety of
WBC’s, fibroblasts, interstitial thickening, fibrosis, granulomas and cavitations
Common causes: smoking, environment, radiation exposure, asbestosis, genetics
Once lung scarring occurs, it's generally irreversible. Medications can slow the damage of
interstitial lung disease, but many people never regain full use of their lungs. Lung transplants
are an option for some people who have interstitial lung disease
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Pulmonary fibrosis is the formation or development of excess fibrous connective tissue
(fibrosis) in the lungs. It is also described as "scarring of the lung
The diagnosis can be confirmed by lung biopsy
The removed tissue is examined histopathologically by microscopy to confirm the presence and
pattern of fibrosis as well as presence of other features that may indicate a specific cause e.g.
specific types of mineral dust or possible response to therapy e.g. a pattern of so called nonspecific interstitial fibrosis
On spirometry, as a restrictive lung disease, both the FEV1 (Forced Expiratory Volume in 1
Second) and FVC (Forced Vital Capacity) are reduced so the FEV1/FVC ratio is normal or even
increased in contrast to obstructive lung disease where this ratio is reduced. The values for
residual volume and total lung capacity are generally decreased in restrictive lung disease.
Diseases of the Spine
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Kyphoscoliosis: curved spines and hunch back, alters normal thoracic expansion
Restrictive disease, decreased FVC and FEV1, normal or high FEV1/FVC ratio
Require bronchieal hygiene, trachestomy
Kyphoscoliosis treatable with curvature correction braces if done early in development
Pectus evactum and carinutum
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pectus carinatum usually develop normal hearts and lungs, but the deformity may prevent these
from functioning optimally. In moderate to severe cases of pectus carinatum, the chest wall is
rigidly held in an outward position. Thus, respirations are inefficient and the individual needs to
use the diaphragm and accessory muscles for respiration, rather than normal chest muscles,
during strenuous exercise.
Pectus excavatum is the most common congenital deformity of the anterior wall of the chest, in
which several ribs and the sternum grow abnormally. This produces a caved-in or sunken
appearance of the chest It can either be present at birth or not develop until puberty.
Pectus excavatum is sometimes considered to be cosmetic; however, depending on the severity,
it can impair cardiac and respiratory function and cause pain in the chest and back.[People with
the condition may experience negative psychosocial effects
Flail Chest
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A flail chest is a life-threatening medical condition that occurs when a segment of the rib cage
breaks under extreme stress and becomes detached from the rest of the chest wall. It occurs
when multiple adjacent ribs are broken in multiple places, separating a segment, so a part of the
chest wall moves independently. The number of ribs that must be broken varies by differing
definitions: some sources say at least two adjacent ribs are broken in at least two placessome
require three or more ribs in two or more places
Lung Cancer
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Deadliest type of cancer, caused by smoking, asbestos, arsenic, chromium, radon, air pollution…
The two main types are small cell lung cancer (more deadly) and non-small cell lung cancer.
Non-small cell carcinoma; Squamous cell carcinoma; Adenocarcinoma; Large-cell carcinoma
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Small cell lung cancer (SCLC) is considered distinct from other lung cancers, which are called
non–small cell lung cancers (NSCLCs) because of their clinical and biologic characteristics. Small
cell lung cancer exhibits aggressive behavior, with rapid growth, early spread to distant sites,
exquisite sensitivity to chemotherapy and radiation; usually plays no role in its management
except in rare situations
Small cell carcinomas, or oat cell carcinomas, arise in peribronchial locations and infiltrate the
bronchial submucosa. Widespread metastases occur early in the course of the disease, with
common spread to the mediastinal lymph nodes, liver, bones, adrenal glands, and brain.
Although commonly associated with lung cancer, adenocarcinoma is a type of cancer that
develops in cells lining glandular types of internal organs, such as the lungs, breasts, colon,
prostate, stomach, pancreas, and cervix. Another type of adenocarcinoma, mucinous
adenocarcinoma, accounts for only 10-15% of all adenocarcinomas and is particular to
aggressive carcinomas that are comprised of at least sixty percent mucus.
Squamous cell lung cancer is a form of non-small cell lung cancer. Eighty percent of lung cancers
are non-small cell lung cancers, and of these, about 30% are squamous cell lung cancers.
Squamous cell lung cancers usually begin in the bronchial tubes (large airways) in the central
part of the lungs. Many people have symptoms early on, commonly hemoptysis(coughing up
blood).
Large cell lung cancer is a form of non-small cell lung cancer. Eighty percent of lung cancers are
non-small cell, but only 10% of these are large cell lung cancer. Large cell lung cancers are
named for the large, round cells that are seen under the microscope with this type of cancer.
They usually start in the outer regions of the lungs and tend to grow very rapidly.
Pulmonary embolism
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Presence of occluding emboli within the pulmonary vasculature which leads to obstruction of
blood flow to all or part of the lung
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Typically caused by prolonged bedrest, DVT’s, age, previous CVAs
Causes sudden obstruction of pulmonary artery branch, increases alveolar dead space, patient
develops an increased ventilation efforts
Bronchospasm can occur, V/Q mismatch
May lead to cardiogenic shock, atelectasis
Diagnose with CT scan, VQ scan, ETCO2, history of patient and coagulation
Treat with CPAP, O2, anti-coagulation, thrombolectomy
Pulmonary Hypertension
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Secondary to a cause or primary
Increased PVR, often misdiagnosed
increase in blood pressure in the pulmonary artery, pulmonary vein, or pulmonary capillaries,
together known as the lung vasculature, leading to shortness of breath, dizziness, fainting, and
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other symptoms, all of which are exacerbated by exertion. Pulmonary hypertension can be a
severe disease with a markedly decreased exercise tolerance and heart failure
Mean pulmonary artery pressure greater than 25 mmHg at rest of 30 mmHg during exercise
with increased pulmonary vascular resistance and normal left heart ventricular function
May be secondary to COPD, CDH, cirrhosis, HIV, drugs
Treat underlying cause, O2. Nitric oxide, calcium channel blockers, anti-coagulants
ALS
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Neuromuscular disorder characterized by progressive degeneration of upper and lower motor
neurons leading to loss of skeletal muscle strength, including the respiratory muscles
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ALS (Amyotrophic Lateral Sclerosis), also known as Lou Gehrig's Disease, is an incurable fatal
neuromuscular disease characterized by progressive muscle weakness, resulting in paralysis. The
disease attacks nerve cells in the brain and spinal cord. Motor neurons, which control the
movement of voluntary muscles, deteriorate and eventually die. When the motor neurons die,
the brain can no longer initiate and control muscle movement. Because muscles no longer
receive the messages they need in order to function, they gradually weaken and deteriorate.
The initial signs of ALS may vary. Symptoms include stiffness and increasing muscle weakness,
especially involving the hands and feet. The disease eventually affects speech, swallowing and
breathing. Because ALS only attacks motor neurons that control the body's voluntary muscles,
patients' minds and senses are not impaired.
Most of those who develop the disease are between 40 and 70 years of age. The average
expected survival time for those suffering from ALS is three to five years.
The cause of ALS remains unclear, and no cure exists. Bronchial hygiene
Guillain Barrer Syndrome
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The diagnosis is usually made by nerve conduction studies and with studies of the cerebrospinal
fluid. With prompt treatment by intravenous immunoglobulins or plasmapheresis, together with
supportive care, the majority will recover completely. Guillain–Barré syndrome is rare, at 1–2
cases per 100,000 people annually, but is the most common cause of acute non-trauma-related
paralysis in the world.
a disorder affecting the peripheral nervous system. Ascending paralysis, weakness beginning in
the feet and hands and migrating towards the trunk, is the most typical symptom, and some
subtypes cause change in sensation or pain as well as dysfunction of the autonomic nervous
system. It can cause life-threatening complications, in particular if the breathing muscles are
affected or if there is autonomic nervous system involvement. The disease is usually triggered by
an infection.
Believed to be caused by an autoimmune defect that destroys the myelin sheath of the neuron;
Can have had a history of upper respiratory infection or flu-like illness preceding onset of
symptoms The Epstein-Barr virus may be implicated
Myasthnia Gravis
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Myasthenia gravis is a chronic autoimmune neuromuscular disease characterized by varying
degrees of weakness of the skeletal (voluntary) muscles of the body. The name myasthenia
gravis, which is Latin and Greek in origin, literally means "grave muscle weakness." With current
therapies, however, most cases of myasthenia gravis are not as "grave" as the name implies. In
fact, most individuals with myasthenia gravis have a normal life expectancy.
The hallmark of myasthenia gravis is muscle weakness that increases during periods of activity
and improves after periods of rest. Certain muscles such as those that control eye and eyelid
movement, facial expression, chewing, talking, and swallowing are often, but not always,
involved in the disorder. The muscles that control breathing and neck and limb movements may
also be affected.
Myasthenia gravis is caused by a defect in the transmission of nerve impulses to muscles. It
occurs when normal communication between the nerve and muscle is interrupted at the
neuromuscular junction—the place where nerve cells connect with the muscles they control.
Normally when impulses travel down the nerve, the nerve endings release a neurotransmitter
substance called acetylcholine. Acetylcholine travels from the neuromuscular junction and binds
to acetylcholine receptors which are activated and generate a muscle contraction.
In myasthenia gravis, antibodies block, alter, or destroy the receptors for acetylcholine at the
neuromuscular junction, which prevents the muscle contraction from occurring. These
antibodies are produced by the body's own immune system. Myasthenia gravis is an
autoimmune disease because the immune system—which normally protects the body from
foreign organisms—mistakenly attacks itself.
Diagnosis with tensilon test, symptoms