Test 3 Flashcards
(154 cards)
1
Q
Air moving in and out of the lungs
A
Ventillation
2
Q
Ventilation depends on three things:
A
- Distensibility: the ease of which the lungs can inflate or distend
- Resistance: Amount of force that the lungs have to work against
- Elasticity: How well the lungs can recoil
3
Q
Blood needs to flow to the lungs and provide oxygen. The air needs to be able to flow from the lungs into the blood stream. CO2 needs to be able to leave the blood stream and go to the lungs.
A
Perfusion
4
Q
For every __L of air we inhale we need ___L of blood/min.
A
4L or air, 5L of blood/min
5
Q
Clinical Manifestations of Respiratory Dysfunction
A
Sneezing Dysphagia Dysphonia Dyspnea Abnormal Respiratory Rates -Tachypnea -Bradynea Abnormal Respiratory Patterns -Kussmaul -Cheyne Stokes
6
Q
Caused by Irritation in upper respiratory tract
A
Sneezing
7
Q
difficulty swallowing
A
• Dysphagia
8
Q
coarse voice
A
• Dysphonia
9
Q
protective from irritants. Normal in healthy individuals. Must determine if ______ is productive or not. Persons with decreased _______ reflex have increase chances of infection
A
cough
10
Q
coughing up blood
A
Hemoptysis
11
Q
shortness of breath. (Can still have normal respiratory rate & be in severe respiratory distress)
A
• Dyspnea
12
Q
positional. Person needs to sit up to breath – unable to lie flat & breathe properly
A
o Orthopnea
13
Q
Wake up at night with extreme SOB, gasping for air
A
o Paroxysmal nocturnal dyspnea (PND)
14
Q
slower than normal breathing
A
o Bradypnea
15
Q
faster than normal breathing
A
o Tachypnea
16
Q
Increase in depth of breathing. Increase in tidal volume. (can be normal after exercise, persons at rest should not have this pattern of breathing)
A
o Kussmaul
17
Q
Progressive increase in the rate and depth of breathing followed by a period of apnea. Alternating periods of deep and rapid breathing.
A
o Cheyne Stokes
18
Q
often seen in children. Not often seen in adults as the cartilage of the adult nose is harder than that of a child.
A
o Nasal flaring
19
Q
Suprasternal, supraclavicular, substernal, subcostal, intercostal indrawing – seen in children, _____ _____ ______ ___at the subcostal area below the rib cage
A
chest wall caves in
20
Q
snoring – indicates an obstruction usually in upper respiratory tract
A
o Sonorous breathing
21
Q
Upper respiratory blockage, high pitched musical sound
A
o Stridor
22
Q
Popping sound
A
o Crackles
23
Q
Continuous musical quality
A
o Wheezes
24
Q
Visceral pleura and parietal pleura rub against each other. Inflammation of pleura may cause this.
A
o Friction rub
25
usually from coughing. Cough so hard they strain muscles in the chest.
• Pain in chest
26
Respiratory pain is reproducible (act of coughing will elicit pain). Cardiac pain is described as a pressure and constant.
o Pleuritic
27
________poisoning is the exception person looks red
CO2
28
Sign of hypoxemia. Occurs in cystic fibrosis, COPD
• Clubbing of digits
29
early signs of hypoxemia. You will see this before changes in vitals occur
• Anxiety/Restlessness/Confusion
30
o Elevated carbon dioxide levels in the blood
| o May also be referred to as hypercarbia
• Hypercapnia
31
```
o Decreased O2 concentration in the blood
o Causes:
Hypoventilation
Diffusion abnormalities
Ventilation-perfusion mismatch
```
• Hypoxemia
32
o Inadequate oxygen supply to the cells
• Hypoxia
33
End result of pulmonary disease
Respiratory Failure
34
Respiratory disease interferes with ______ _________or transport and can lead to ________ _______ as defined by either
o Arterial Blood O2 (PAO2) ___ mmhg/pH
Oxygen Intake, and can lead to respiratory failure
| oArterial Blood O2 (PAO2) 45 mmhg/pH
35
Respiratory Failure May also result from
cardiac dysfunction, drugs, prolonged tachycardia in other disorders such as metabolic acidosis
36
Treatment of respiratory failure is based on the:
etiology of respiratory failure. Must treat whatever is causing the respiratory failure.
37
Tests to Evaluate Respiratory Function (6)
* Chest Xray (CXR): easiest & least expensive. Won’t tell you everything.
* Computed tomography (CT scan)
* Blood gas analysis (ABG’s)
* Pulmonary function tests (PFT)/spirometry
* Sputum analysis (C&S, cytology – looking for cancer cells, Acid Fast Bacilli – TB test)
* VQ scan (Ventilation/Perfusion Scan) – done in nuclear medicine. Measuring how well the lungs are being perfused with blood and oxygen
38
Categories of Respiratory Disorders (Diseases)
Disorders affecting the respiratory system may be classified as:
Resistance to air flow. Air has trouble getting in and out of the lungs. Diseases that block the flow of air in and out of the lungs are obstructive disorders
• Obstructive disorders
39
Categories of Respiratory Disorders (Diseases)
Disorders affecting the respiratory system may be classified as:
Air does not have trouble getting in and out of the lungs. The lungs have poor distensibility. Cannot fully expand
• Restrictive disorders
40
Categories of Respiratory Disorders (Diseases)
Disorders affecting the respiratory system may be classified as:
Caused by a pathogen (pneumonia, croup)
• Infectious disorders
41
Categories of Respiratory Disorders (Diseases)
Disorders affecting the respiratory system may be classified as:
Nothing wrong with lungs. There is a problem with blood flow to the lungs. (blood clot, pulmonary embolism)
• Disorders of Vascular Origin
42
Categories of Respiratory Disorders (Diseases)
Disorders affecting the respiratory system may be classified as:
Cancers
• Malignancies
43
OBSTRUCTIVE DISORDERS
| 10
```
Croup
Epiglottitis
Bronchiolitis
Bronchitis
Asthma
COPD: Umbrella term for Chronic Bronchitis & Emphysema
Chronic Bronchitis
Emphysema
Bronchiectasis
```
44
• Caused by parainfluenza virus, influenza A or respiratory syncytial virus (RSV)
o Attacks upper respiratory structures
• Most commonly occurs in 6 months to 5 years age group.
Croup
45
Croup is characterized by ____________ extending from _____ _______to bronchial lumina
inflammation, vocal cords
46
Clinical Manifestation of Croup (6)
```
o catarrhal symptoms: sick looking eyes – red, runny eyes
o rhinorrhea: runny nose
o low-grade fever
o barking cough
o stridor
o nasal flaring
```
47
Croup is not usually fatal; however, more serious in?
<6 months old.
48
• Causative organisms (not viral)
o Haemophilus influenzae type B – immunization helps prevent epiglottitis
o Streptococcus pneumoniae
Epiglottitis
49
Most common in ____ to _____ year age group, but may also affect adults
2 to 6
50
Epiglottitis Clinical manifestations: sudden onset
o sore throat, dysphagia, drooling, fever
o “sniffing position”, muffled voice, anxious
o stridor, respiratory distress
51
Epiglottitis Evaluation: based on symptoms:
o X-ray of soft tissues of neck.
o Characteristic “thumbprint”
o Do not attempt to examine pt’s throat. Depressing the tongue can cause laryngospasm – may not be able to be intubated after.
52
Epiglottitis can be _______________________
• Fatal: death may occur in a few hours
53
Epiglottitis treatment:
IV antibiotics quickly; may require rapid intubation.
54
widespread infection of the bronchioles
Bronchiolitis
55
_______ ______ _____causes bronchiolitis (majority of cases)
respiratory syncytial virus (RSV)
56
True or False
| Bronchiolitis not contagious?
False
| It is highly contagious
57
Bronchiolitis is more prevalent is what age group and what time of year?
2 – 24 month age group, o November to February
58
Clinical manifestations of Bronchiolitis (7)
o Nasal congestion, mild conjunctivitis
o Inspiratory crackles, expiratory wheezes
o Use of accessory muscles, (such as intercostal indrawing), nasal flaring, increased work of breathing
o Tachypnea (with resp rate 50 – 60 per min. Can go up to 80)
o Tachycardia, poor feeding
o Pallor, cyanosis, hypoxemia
o Episodes of apnea
59
Pathogenesis of Bronchiolitis (4)
o Respiratory virus attacks lower bronchioles
o Bronchiole walls become very swollen & obstructed.
o Edema of submucosa, increase in mucus secretion
o Necrosis of bronchial epithelium
Virus causes epithelial layers to slough off
Clogs up bronchioles so air cannot get past them into the alveoli
60
Management of Bronchiolitis
o Humidity, fluids, rest
| o Infection control precautions
61
* Inflammation of the trachea and bronchi
| * Acute or chronic
Bronchitis
62
Etiology of Bronchitis
influenza virus A or B, parainfluenza virus, respiratory syncytial virus (RSV); smoke or inhalation of chemical irritants
63
Pathogenesis of Bronchitis (5)
```
o Bronchi become invaded by viruses
o Edema of mucous membranes
o Increased mucous production
o Loss of ciliary function
o Causing bronchiole irritation
```
64
Manifestations of Bronchitis
o Expiratory wheezing, dyspnea, malaise
o Cough (productive or nonproductive) from increased mucus production
o Chest pain r/t persistent coughing
65
• Treatment – Acute Bronchitis
o Increase fluids, smoking cessation, expectorants(thins out secretions)/antitussives(suppresses cough), antibiotics not routinely prescribed
66
Chronic Bronchitis
permanent increase in thickness of the bronchi, and increase in the number of goblet cells. Which means increased mucus productions, increased cough, decreased cilia
67
• Clinical Manifestations of Asthma (6)
o Dyspnea, with increased respiratory effort
o Wheezing (inspiratory and expiratory), SOB
o Prolonged expiration
o Cough – nonproductive during acute attack; productive with thick mucus as attack resolves
o Use of accessory muscles, respiratory distress with severe attacks
o May lead to respiratory failure
68
treatment of asthma
o Acute attacks: inhaled bronchodilators, oral corticosteroids, oxygen prn
o Chronic management: avoidance of allergens and triggers, patient education, anti-inflammatories (ie. inhaled corticosteroids), antileukotrienes. Airway inflammation & fluid may be still be present in some individuals, even though they are asymptomatic
69
* Permanent damage
* Cannot be cured
* Person must live with symptoms
COPD: Umbrella term for Chronic Bronchitis & Emphysema
70
* Hypersecretion of mucus and chronic productive cough for 3 months a year for 2 consecutive years
* Increase in the size and number of mucous glands and goblet cells
* Airway obstruction caused by chronic infection and injury
Chronic Bronchitis
71
• Clinical Manifestations of Chronic Bronchitis (4)
o increased mucus productions, increased cough
o At risk for recurrent pulmonary infections
o Peripheral & central edema
o Right sided heart failure (blue bloaters)
Edemic, bloated, cyanotic
72
• Loss of elastic recoil occurs from destruction of alveolar walls resulting in permanent enlargement of gas-exchange airways (Like a balloon that has been inflated too many times)
Emphysema
73
In emphysema the _____big, boggy and stretched (ENLARGED)
o Alveoli
74
_____ _ -______protects us from these enzymes that want to destroy our lungs tissue. Emphysema has a deficiency in this which is a primary cause.
Alpha1-antitripsin
75
Secondary cause to emphysema
injury to lungs from inhaled toxins
| o Cigarette smoke – toxins within cigarettes destroys alpha1-antitripsin
76
• Clinical manifestations of emphysema (4)
o Barrel chest (anterior-posterior diameter of chest is larger than it should be because the lungs are always in a state of hyperinflation)
o Pursed lip breathing – they have to make the extra effort to exhale. It isn’t natural for them, they have to force air out of lungs.
o Sit in tripod position – most comfortable way they can breath
o Weight loss – thin, emaciated appearance
77
People with emphysema are at High risk for pneumonia as they cannot _____________ ___________
effectively expectorate
78
* Dilation of the bronchi
| * Pocket forms on side of bronchi and they have different shapes
Bronchiectasis
79
Bronchiectasis can develop _________ ____________ _____________
abscess, infection, burst
80
Bronchiectasis Occurs as a result of __________ of muscle and elastic fibers of bronchial wall
weakening
81
RESTRICTIVE DISORDERS (2)
Pneumonia
| Atelectasis
82
Pneumonia
| • Etiology (3)
o Begins with Inhalation of pathogens. Pathogens then establish themselves inside the lungs
o Aspiration – vomiting and inhaling gastric contents. Burns the bronchi and respiratory passages
o Endogenous – infection that occurs somewhere else in the body. Travels to the lungs and establishes infection there
83
Pneumonia
| • Pathogenesis
o Set off inflammatory reaction
o Alveoli fill with exudate (drainage)
o Consolidation
84
Pneumonia
| • Clinical manifestations may vary with cause, age and severity of illness (3)
o Fever, chills
o Cough (may or may not be productive)
o Dyspnea, crackles over affected lobe
85
collapse of lung tissue
Atelectasis
86
Atelectasis two types:
o Obstruction
| o Compression by external mass
87
Atelectasis • Pathogenesis (3)
o Airless alveoli shrivel due to elasticity – because they are not receiving air
o Interferes with blood flow through lungs (decreased gas exchange & oxygenation)
o Client will become hypoxemic very quickly
88
Atelectasis • Risk factors (2)
o Immobility – secretions pool in lungs and clog small bronchioles. And alveoli that are passed the area of obstruction do not receive air and shrivel. Inhibits blood vessels. If oxygen isn’t restored the tissue becomes necrotic and dies.
o Surgery
89
Atelectasis • Clinical manifestations (9)
```
o Dyspnea
o Cough
o Fever
o Leukocytosis
o Tachypnea
o Focal decreased breath sounds
o Increased crackles at lung bases
o Hypoxemia
o Decreased depth of respiratory excursions
```
90
Chest Wall Structural Abnormalities – prevent lungs from expanding
Hunched back. Elderly with osteoporosis. Inhibits chest expansion
• Kyphosis
91
Chest Wall Structural Abnormalities – prevent lungs from expanding
(chest excavation) Sternum is displaced backwards
• Pectus excavatum
92
Chest Wall Structural Abnormalities – prevent lungs from expanding
Sternum is protruding forward. Bird chest.
• Pectus carinatum
93
Chest Wall Structural Abnormalities – prevent lungs from expanding
spine is ‘S’ shaped. Interferes with movement of ribs and inhibits movement of chest wall.
• Scoliosis
94
Painful interferes with lung expansions. Leading to pneumonia or atelectasis
• Rib fractures
95
o Usually 2 fractures per rib in consecutive ribs or fracture of sternum plus consecutive ribs.
o Results in paradoxical breathing
o Treatment: pain control and management of underlying pulmonary and/or cardiac injury (Chest tubes, mechanical ventilation)
o Can cause pneumothorax
• Flail chest (multiple rib fractures)
96
• An accumulation of air in the pleural space
o Causes atelectasis (greater amount of air = more severe atelectasis)
• May result from underlying disease (such as COPD) or from chest trauma (rib fractures)
Pneumothorax
97
• Types of pneumothorax
```
o Spontaneous
Primary
Secondary
o Open
o Tension
```
98
Pneumothorax: Spontaneous
| • Primary
o Spontaneous rupture of blebs (air blister) on visceral pleura. May occur during rest, exercise, or sleep.
o Usually occurs in men between 20 – 40 yrs
99
Pneumothorax: Spontaneous
| • Secondary
o Resulting from trauma or spontaneous rupture of bleb on visceral pleura secondary to pre-existing pulmonary disease
100
• Opening in chest wall secondary to trauma such as stab wounds, bullet wounds. (CHEST INJURY)
• Air is drawn through the wound into the pleural space during inspiration and forced back out during expiration. Wound in the chest wall appears to be “sucking air” and is visibly bubbling; therefore referred to as “sucking wound”
o Leads to atelectasis
• Pressure in pleural space equals atmospheric pressure
Pneumothorax: Open
101
As person inhales, air is entering through chest wall. The issue is a flap will develop. Air cannot escape bc of flap. Every time they inhale more and more air get into the pleural space. Increases pressure inside thoracic cavity.
Pneumothorax: Tension (WORST PNEUMOTHORAX)
102
• Air enters the pleural space during inspiration; on expiration, opening is sealed and air becomes trapped, increasing the pressure within the thoracic cavity
Pneumothorax: Tension (WORST PNEUMOTHORAX)
103
manifestations of tension pneumothorax
o Initially: Chest pain, dyspnea, tachycardia, decreased breath sounds on affected side,
o As pneumothorax progresses: absent breath sounds on affected side, hypoxemia, laboured breathing, jugular venous distension, hypotension, contralateral tracheal shift.
104
* Accumulation of excessive fluid in the pleural space
| * Fluid is heavy and sits at bottom of pleural space
Pleural Effusion – same principle as pneumothorax but instead of air it is fluid in the pleural space
105
blood in pleural space usually associated with trauma
o Hemothorax
106
watery drainage in pleural space, low protein count (seen in pneumonia)
o Transudate
107
watery but has high protein count (seen in tumors – lung cancer)
Exudate
108
pus in pleural space (seen in lung abscesses)
Empyema
109
lymphatic fluid leaking into pleural space
Chylous pleural effusion
110
• Clinical manifestations are associated with the extent of atelectasis (amount of drainage) Symptoms worsen as drainage increases (3)
o Dyspnea, tachypnea, tachycardia, decreased breath sounds on affected side
o Fever associated with infection (empyema)
o Hypoxemia, laboured breathing, hypotension, contralateral tracheal shift
111
• Form of respiratory failure
• Causes
o Direct – pneumonia, smoke inhalation, chemical inhalation, inhalation of toxic fumes, near drowning
o Indirect – caused by other diseases such as pancreatitis, drug overdose
Acute Respiratory Distress Syndrome (ARDS)
112
Fibroblast cells deposit protein along walls of alveoli occur with the increased inflammation. This increases the thickness of the alveoli and decreases gas exchange.
Prominent fibrosis (thickening)
o Fibroproliferative phase
113
• Pathogenesis of ARDS
o Acute phase
Inflammatory mediators damage structure of alveoli
At the same time we have an increase in coagulation factors
Lots of inflammation at site
Alveolar membrane becomes damage as a result of inflammation & edema
Increase in coagulation factors causes increase in blood clotting inside the lungs
Can recover from this phase If damage isn’t too severe
114
• Clinical manifestations of ARDS
o Dyspnea, tachypnea, tachycardia, increased respiratory effort.
o Hypoxemia unresponsive to increasing fractions of inspired oxygen (Fi02), poor lung compliance
o Can result in respiratory failure and if not reversed – death
o Restlessness, exhaustion, decreased mental status
115
Inherited disease. Genetic abnormality. Respiratory, pancreatic, and GI tract ducts become clogged with a very thick mucus. Normally, we have a little bit of mucus in secretions. In cystic fibrosis, the mucus is so thick it plugs the ducts.
Cystic Fibrosis (cystic = duct)
116
• CF gene located on chromosome __
7
117
• CFTR (cystic fibrosis transmembrane regulator)
Abnormal expression of protein
118
• Characterized by ______ _________ __ ____ _______and concentrated sweat, often causing obstruction of GI and respiratory tracts
excessive secretion of thick mucus
119
CF Respiratory effects (blocks ducts in respiratory tract)
```
o Cough, wheeze, recurrent pneumonia
o Barrel chest, clubbing bc of hypoxemia
o Bronchospasm
o Mucus in lung
o Causes hypoxemia
```
120
CF Gastrointestinal effects (mucus prevents liver and pancreas from secreting enzymes)
o Failure to thrive, malabsorption
| o Diabetes, pancreatitis, hepatic failure
121
No tx for CF only Manage symptoms by supplementing digestive enzymes
Cotezyme
122
• As the client with cystic fribrosis ages they can develop:
o Pancreatitis
o Liver failure
o Diabetes
o Respiratory problems bc lungs begin to fail, become hypoxemic
Can go into respiratory failure
Usually need lung transplant eventually
123
Etiology – Lung disease caused by chronic exposure to industrial products
Pneumoconiosis
124
fine particle silica(dust) inhalation
• Silicosis
125
in buildings in 50s as fire retardant
• Asbestosis
126
coal miner’s lung, accumulation of soot, fine particle dust
• Anthracosis
127
pesticides, fine hay particles
• farmer’s lung
128
• Macrophages (WBCs) secrete____________which destroy alveolar walls
lysozymes
129
• Causative organism: Bordetella pertussis
Pertussis – whooping cough
130
• Droplet infection of Pertussis – whooping cough
highly contagious
131
Pertussis – whooping cough Pathogenesis
o Attached to cilia in respiratory tract produces a toxin which initiates an inflammatory response
Incubation Period 5 – 21 days
Prodrome: 1 – 2 wks; Rhinorrhea (runny nose), fever, malaise (resembles bad cold)
Paroxysm : 1 – 6 wks; Paroxysmal coughing spasm (associated with vomiting)
Convalescence: wks – months
Can be dangerous in infants and babies bc of coughing spams – cause vomiting. This causes increased risk for aspiration.
132
Pertussis – whooping cough Clinical Manifestations
* Bruising around eyes
| * Broken blood vessels in eye from coughing
133
Pertussis – whooping cough • Complication:
o Risk of aspiration in infants ( 1 – 3 infants deaths per year in Canada)
o Petechiae, bruising, fractured ribs, pneumonia
134
Tuberculosis • Mode of transmission
caused by inhalation of bacterium
| o aerosolized droplet
135
Tuberculosis • Populations at risk (large populations living in small areas)
```
o Elderly
o HIV
o Homeless
o Refugee camps
o Travelers
```
136
TB Clinical Manifestations:
• Primary infection may be asymptomatic
• Active disease:
o Fever, fatigue, malaise, weight loss, night sweats, cough (may be productive, may cough up blood), sputum production, hemoptysis
137
• A severe form of pneumonia caused by:
SARS associated coronavirus (SARS-CoV).
138
SARS quickly leads to ___________ ____________
respiratory failure
139
SARS Pathogenesis
o Incubation period 2 to 7 days
o Onset: fever, chills, myalgia, headache
o Nonproductive cough; progresses to pneumonia
o May develop hypoxemia
o Period of communicability:
when pt symptomatic.
CDC recommends isolation for 10 days post symptoms
140
• Mode of transmission for SARS
airborne (CDC) – highly contagious
141
• WHO guidelines: SARS may be suspected in a patient with
o Fever of 38°C and
o History of
travel to high risk areas OR
Contact with someone with a diagnosis of SARS
142
Influenza – respiratory illness. Can have gastro symptoms comes from the
• Orthomyomyxoviridae – family that influenza comes from…. Awe (comes from birds)
143
• Influenza A
• Influenza B
• Influenza C
Which is the most serious
Influenza A – most serious
144
Influenza – respiratory illness Complications
o Croup, viral pneumonia, secondary bacterial infections
o Cardiac complications
o Reye’s syndrome (encephalopathy – brain damage, secondary to infection)
o Guillain-Barre syndrome
145
Blood clots have developed in lungs or develop elsewhere in the body. An embolus (piece of blood clot) breaks off and travels to lungs
Pulmonary Embolism – blood clot to lungs
146
often caused by DVT Prolonged immobility
o Venous stasis (sluggish blood flow)
147
often caused by DVT
Polycythemia vera (increase coagulability)
Medications (birth control)
o Hypercoagulability (promote blood clotting)
148
often caused by DVT
Hyperglycemia can inflame blood vessel
When we start an IV (venipuncture)
Smoking
o Inflammation of blood vessel
149
Pulmonary Embolism – blood clot to lungs Pathogenesis
o Initially a blood clot (thrombus) forms within the deep veins. The clot becomes embolus, by becoming dislodged from its original site and travels through the systemic circulation and into the pulmonary circulation. The clot eventually travels into a branch of the pulmonary circulation. It can either occlude a small vessel causing temporary symptoms until the fibrinolytic system destroys it. It may manifest as multiple small emboli, or it may be large enough to block the flow of blood distal to the obstruction, creating death of pulmonary tissue (an infarction).
o Can have multiple small emboli or one large one
150
Pulmonary Embolism – blood clot to lungs
| • Clinical Manifestations varies with severity
o Initially – anxiety, restlessness
o Dyspnea, tachypnea, chest pain, tachycardia
o As it worsens – May experience hemoptysis
o Hypoxia/cyanosis
o Massive occlusion from poor blood flow to tissue – profound shock
151
Lung Cancer
| • Small cell
```
o Rapid growing
o Unresponsive to treatment
o Grows in central bronchi region
o Grows from the outside of lung inside
o Doubles in size in 33 days
o Usually isn’t found until it has spread considerable
o Has poorest outcome
```
152
Lung Cancer
| • Non-small cell
o Squamous cell
grows centrally
easily found
grows slowly
```
o Adenocarcinoma
Slow growing cancer
Grows peripherally
Grows more quickly than squamous cell
o Large cell carcinoma
Grows in cluster
Grows peripherally
Slow growing
Fairly easy to find & indentify
o If found early there may be success in treating them
```
153
Lung Cancer what is the first sign
Persistent nagging cough
154
Lung Cancer effects
o Obstruction of airflow
o Inflammation
o Pleural effusion, hemothorax, pneumothorax
o Paraneoplastic syndrome (SIADH) – tumors manufactures and secretes ADH
Swelling
Hyponatremia
